Immunology, Serology and Blood Banking Flashcards by KM Guntayon

antibody heterogeneity: variations between light and heavy chains; constant regions of all antibodies and kappa and lambda light chains

isotypes

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antibody heterogeneity: species-specific variations in the constant domains of heavy or light chains; different alleles of heavy chains

allotypes

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antibody heterogeneity: variation in the variable region; produced by a single clone of cells

idiotypes

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links multiple monomers of IgM and IgA

joining (J) chain

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predominant serum antibody, approximately 75% of immunoglobulins in the blood
only Ig that crosses placenta
produced in secondary (anamnestic) antibody response

IgG

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IgG subclasses

IgG1, IgG2, IgG3, IgG4

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IgG subclasses that activate the classical complement pathway

IgG1, IgG2, IgG3

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five monomers linked together by a J chain and interchain disulfide bonds
10% of total serum Ig
first antibody produced against an immunogen
produced in high levels in the primary response
best activator of the classical pathway of complement only one molecule is required

IgM

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2 forms of IgA

serum IgA
secretory IgA

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IgA: single Ig molecule; antigen clearance and immune regulation

serum IgA

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IgA: dimer held together by a J-chain; block attachment of viruses, bacteria and toxins to host cells

secretory IgA

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2 subclasses of IgA

IgA1 and IgA2

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accounts for 15-20% of total serum antibody

IgA

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primarily a cell membrane surface component of beta-lymphocytes
short half-life (2-3 days)

IgD

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responsible for allergic (type 1 hypersensitivity) reactions
Fc portion binds to receptors on mast cells and basophils
once attached to mast cells, binding to an allergen triggers degranulation of the cell and release of allergic mediators, such as histamine and leukotrienes
elevated concentrations are often found during parasitic infections

IgE

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identical antibodies that are produced from a single clone of plasma cells
found in individuals with multiple myeloma
produced in industry by fusing an antigen-sensitized, splenic beta-lymphocyte with non secreting myeloma cell thus creating an immortal cell line that secretes an antibody of a single idiotype

monoclonal antibodies

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quantitation on antibodies

radial immunodiffusion
nephelometry
turbidimetry

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immune system: responsible for non specific response
phagocytosis of invaders
present immunogens to T helper cells, the first step in an immune response
release cytokines that affect other cells’ activities

myeloid cells

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myeloid cells in the peripheral blood

monocytes

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myeloid cells in the tissue

macrophage

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macrophages have these on their surface

major histocompatibility complex class II
complement receptors
antibody Fc receptors

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granulocytes: 60-70% of WBCs in circulation; phagocytosis and contributes to inflammatory response

neutrophils

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granulocytes: 1-3% of circulating wbcs; mediate IgE allergic response

eosinophils

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granulocytes: 0-1% of circulating wbcs, has receptors for IgE and granules responsible for allergic reactions

basophils

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20-40% of circulating wbcs

lymphocytes

20% of circulating lymphocytes express surface molecules such as CD19 and CD20 mature in the bone marrow

b cells

b cells differentiate into:

plasma cells memory b cells

produce antibody

plasma cells

80% of circulating lymphocytes express surface molecules such as cd2 and cd3 lyse host cells infected with viruses and tumor cells and also produce lymphokines

t cells

slightly larger than t or b cells and have cytoplasmic granules

nk cells

present antigens to T cells

dendritic cells

dendritic cells in the dermis and squamous epithelia

langerhans cells

granulocyte resembling basophil that contains many chemicals that affect the immune response

mast cells

soluble protein molecules secreted by one cell type that affect other cells turn on genes in target cells

cytokines

antiviral proteins that inhibit viral replication and activate NK cells produced by virally-infected cells

interferon-alpha and -beta

antiviral effects, activate macrophages and NK cells, stimulates b cells to produce antibodies produced by TH1 cells

interferon-gamma

produced by macrophages, lymphocytes, and NK cells when encountering bacteria, viruses, tumor cells, toxins, and complement protein C5a

tissue necrosis factor-alpha

produced by cd4 and cd8 positive cells after exposure to a specific antigen

tnf-beta

cytokine cellular source: macrophages, b cells, fibroblasts primary targets: t cells, b cells, macrophages, endothelium

IL-1

cytokine cellular source: t cells primary targets: t cells

IL-2

cytokine cellular source: t cells primary targets: stem cells

IL-3

cytokine cellular source: t cells primary targets: b cells, t cells

IL-4

cytokine cellular source: t cells primary targets: b cells

IL-5

cytokine cellular source: t cells, b cells, fibroblasts, macrophages primary targets: b cells, hepatocytes

IL-6

cytokine cellular source: bone marrow, stromal cells primary targets: pre-b cells, t cells

IL-7

cytokine cellular source: monocytes primary targets: fibroblasts

IL-8

cytokine cellular source: t cells primary targets: t cells, mast cells

IL-9

cytokine cellular source: t cells primary targets: TH1 cells

IL-10

cytokine cellular source: macrophages, mast cells, lymphocytes primary targets: macrophages, granulocytes, tissue cells

TNF

cytokine cellular source: leukocytes, epithelia, fibroblasts primary targets: tissue cells

INF-alpha

cytokine cellular source: fibroblasts, epithelia primary targets: tissue cells, leukocytes

INF-beta

cytokine cellular source: T cells, NK cells, epithelia, fibroblasts primary targets: leukocytes, tissue cells, TH2 cells

INF-gamma

produced by macrophages, B cells, and other cell types activates T helper cells, increase number of B cells, activates vascular endothelium, causes fever and acute phase protein synthesis and induces T cells to produce lymphokines

IL-1

produced by T helper cells causes proliferation of activated t and b cells

IL-2

produced by activated T cells causes increases in the number of mast cells in skin, spleen and liver

IL-3

produced by activated T cells induces proliferation of T cells and class switching from IgM to IgG1 and IgE

IL-4

primary lymph tissues of adults

bone marrow and thymus

secondary lymphoid organs: in the lymph nodes, ___ migrate to the cortex and ___ to the paracortex

b cells t cells

secondary lymphoid organs: in the lymph nodes: ____ there are many small b cells, and after stimulations becomes ____

primary follicle secondary follicle

secondary lymphoid organs: has small and large lymphocytes, blast cells, macrophages and dendritic cells

germinal center

secondary lymphoid organs: contains plasma cells and large lymphocytes

medulla

secondary lymphoid organs: filters blood, contains both t and b cells

spleen

secondary lymphoid organs: found in submucosa in gastrointestinal tract and urogenital tract, these surfaces interact with the environment and can begin the immune response early

mucosal associated lymphoid tissue

specialized MALT found in the lower ileum

Peyer's patch

cell surface markers that allow immune cells to distinguish self from nonself first described on white blood cells and are coded for by genes in the MHC located on the chromosome six

human leukocyte antigens

MHC found on nearly every nucleated cell surface antigen presenting cells with MHC I molecules present antigens to CTLs

class I loci

HLA-A HLA-B HLA-C HLA-E HLA-F HLA-G HLA-I

molecules located on the surface of monocytes, macrophages, b cells, activated t cells, dendritic cells, langerhans cells and some epithelial cells antigen presenting cells with MHC II molecules present antigen to T helper cells HLA-DM, HLA-DO, HLA-DP, HLA-DQ, HLA-DR

class II

complement proteins, TNF-alpha and beta, and other proteins not associated with cell membrane surfaces

class III

combination of inherited HLA alleles

true or false: transplants last longer if the HLA antigens from the recipient and the donor are closely matched

true

true or false: although poor response to platelet transfusion is multifactorial, antibodies to class I HLA antigens are the primary cause of immune-mediated platelet transfusion refractoriness

true

true or false: 46 haplotypes are a genotype

false, only 2 (one from each parent)

true or false: HLA loci are polymorphic and recombination is rare. HLA inheritance patterns can exclude fathers with approximately 99%

true

HLA antigen associated with ankylosing spondylitis

HLA B-27

involved in nonspecific response by attachment to damaged epithelium, migration into tissue chemotaxis, phagocytosis, and digestion of target cells, increased metabolism, and degranulation

PMNs

defect in oxidative pathway (respiratory pathway) that phagocytes use to create hydrogen peroxide, which is used to kill bacteria

chronic granulomatous disease

granules contain acid phosphatase, peroxidase, histamine and several other types of molecules clearing immune complexes, limiting inflammatory reactions, protein in granules toxic to parasites

eosinophils

release substances that mediate immune reaction causing increased vascular permeability, smooth muscle contraction, chemotaxins for phagocytes, increased inflammatory response

mediator cells

mast cells basophils platelets

degranulate when membrane-bound IgE binds an allergen or by non immunologic mechanisms such as surgical incisions, heat and skin or mucous membrane infection

mast cells

amplify the reactions that start with the mast cells at the site of entry of the antigen play a role in anaphylactic reactions

basophil

mononuclear phagocyte system

alveolar macrophages splenic macrophages Kuppfer cells

sequenced evens following tissue damage that protect the host from foreign invaders and attempt to minimize tissue damage increased vascular permeability which then causes fluid to move from the circulation to the space around the injury site

inflammation

PMNs move between the endothelial cells to the site of tissue damage

diapedesis

components on of the complement system are synthesized by the liver, except ___, which is synthesized in the epithelial cells of the intestines

complement system: five proteins unique to the classical pathway

C1q C1r C1s C4 C2

complement system: three proteins unique to the alternative pathway

factor B factor D properdin

complement system: six proteins common to both pathways

C3 C5 C6 C7 C8 C9

activation of the complement: classical pathway

immune complexes, require one IgM or two IgG molecules

activation of the complement: alternative pathway

antibody-independent, microbial components such as lipopolysaccharide, polysaccharide, teichoic acid, and peptidoglycan

activation of the complement: lectin pathway

binding of mannose-binding lectin to mannose residues on glycoproteins or carbohydrates on the surface of microorganisms

true or false: C4a, C5a, C6a causes basophils and mast cells to release histamine and also cause smooth muscle contraction and increased vascular permeability

false, C3a, C4a, C5a

true or false: C3a adheres to immune complexes and surfaces of substances to facilitate clearing of these molecules

false, C3b

true or false: if C3b is attached to a cell, phagocytosis is enhanced

true

true or false: C5b is an anaphylatoxin and induces the migration of neutrophils and monocytes to the site

false, C5a

true or false: cell lysis through the formation of the membrane attack complex

true

components of the membrane attack complex (MAC)

C5 through C9

C1 inhibitor combines with C1r and C1s to block ___

C1 activities

deficiency in C1INH autosomal dominant disease unregulated classical pathway activation resulting in vascular permeability, and swollen mucous membranes in airways which can become blocked

hereditary angioehema

removes a single amino acid from C4a, C3a and C5a, rendering them useless as anaphylatoxin

anaphylatoxin inactivator

MAC inhibitors

S protein binds to C5b-C7 complex

CRI binds C3b and C4b and inhibits the amplification loop

complement receptor type I

acute-phase reactants: activate the classical pathway of complement and can also bind to NK cells and monocytes, stimulating them to target tumor cells may also be increased during acute coronary heart diseases

c-reactive proteins (crp)

acute-phase reactants: removes free hemoglobin from circulation

haptoglobin

acute-phase reactants: converted to fibrin to heal the injury

fibrinogen

acute-phase reactants: family of serine protease inhibitors synthesized in the liver, deficiency causes premature loss of elasticity in the lung and liver damage

alpha-1 antitrypsin

acute-phase reactants: principal copper-transport protein, vital in aerobic energy production, collagen formation, and protection against superoxide ions

ceruloplasmin

deficiency of ceruloplasmin

wilson disease

acute-phase reactants: protease inhibitor, complexes are phagocytized by macrophages and fibroblasts

alpha-2 macroglobulin

phagocytic cells that process antigen and express it on the cell surface associated with MHC class I and II molecules

monocyte/macrophages dendritic cells

nonphagocytic cells that attach to antigens in their native form, process antigens and express them on their surface associated with MHC II molecules

b cells

true or false: b cell antigen receptor is monomeric IgM and IgG

false, IgM or IgD

b cell surface receptors have two identical antigen-binding pockets

Fab portion

t cell receptor consists of two non identical _____

peptides cd3

t helper cells have ____ on their surface that interacts with MHCII on the antigen presenting cell

cd4

ctls have ___ on their surface that interacts with ___ on the antigen presenting cell

cd8 mhcI

mediated by TH1 cells monocytes and macrophages are stimulated by cytokines from TH1 cells ctls are activated by cytokines from TH1 cells and then destroy targets by cell-to-cell contact, main function is to destroy infected cells nk cells kill target cells without being previously sensitized

cell-mediated immunity

subset of T helper cells that secrete cytokines that activate other cells involved in the response

TH1 cells

b cell activation begins when antigen binds to antibody on B cell surface and the antigen is internalized and linked to an MHC II molecule on the cell's surface

humoral mediated immunity

antibodies can be produced that recognize an unlimited number of antigens but there are a limited number of B cells due to recombination events that occur during b cell maturation

antibody diveristy

produce antibodies with the same specificity of antibodies that were on the surface of the b cell

plasma cells

produced when host first encounters antigen no antibody is produced for about 5-7 days during this time, the host is producing plasma cells that will secrete antibodies antibody production starts, slowly peaks, levels off then declines

primary antibody response

first antibody produced during the primary antibody response

IgM

produced after the host has previously been exposed to an antigen short lag phase (3-5 days) higher antibody concentration IgG produced due to class switching, and persists longer in circulation than IgM

secondary antibody response

cytolytic effector cells can lyse antibody coated target cells if there is direct contact

antibody-dependent cell-mediated cytotoxicity

occurs when an an individual produces antibodies or a t cell response to his/her own antigens there is a loss of self-tolerance antibody-cell surface component interaction > formation of autoantigen-autoantibody complexes > sensitization of t cells

autoimmune disease

diseases and conditions associated with hla types: HLA-B8

graves disease type I disease

diseases and conditions associated with hla types: HLA-DR2

SLE multiple sclerosis hashimoto disease myasthenia gravis

diseases and conditions associated with hla types: HLA-DR3

sjogren syndrome myasthenia gravis SLE graves disease type I disease

diseases and conditions associated with hla types: HLA-DR4

rheumatoid arthritis type I diabetes pemphigus vulgaris

autoimmune theories: burnet postulated that when an error in self-recognition occurs during the fetal life and lymphocytes against an autoantigen are not destroyed, then autoantibodies are produced

forbidden-clone theory

autoimmune theories: clones developed during fetal life are not stimulated by low doses of antigens. the ability to produce antibodies against higher doses of antigens is still preset

clonal energy

autoimmune theories: some antigens are hidden from the immune system during fetal development. when the tissue is damaged, the "hidden cells" are exposed to the immune system and antibodies are produced against these cells

sequestered-antigen theory

autoimmune theories: suppressor t cells control antibody production by b cells. if suppressor t cell exhibit decreased activity, then antibodies against autoantigens are produced

immunologic deficiency theory

autoimmune theories: an individual can make antibodies or reactive t cells to an infectious agent that cross react with self-antigens

molecular mimicry

autoimmune theories: a number of bacteria and viruses are known to non specifically stimulate b cells. if these b cells have activity against self antigens, an autoimmune disease

polyclonal b cell activation

diagnostic tests for non-organ specific autoimmune diseases: associated with SLE, mixed connective tissue disease and rheumatoid arthritis

anti-nuclear antibodies (ANA)

techniques used to detect ANA

agglutination indirect immunofluorescence enzyme immunoassay

interpretation of indirect immunofluorescence results: evenly stains the nuclei and is associated with anti-dna antibodies and histones

diffuse or homogenous

interpretation of indirect immunofluorescence results: stains the edge of the nuclei and is associated with anti-dna antibody and antibi-lamins (proteins found in the nuclear membrane) antibody

peripheral

interpretation of indirect immunofluorescence results: numerous evenly distributed stained speckles within the nuclei associated with antibodies to extractable nuclear antigen-nucleanribonucleoprotein (anti-RNP) and anti-smith

speckled

interpretation of indirect immunofluorescence results: stains two or three large areas within the nucleus and is associated with anti-RNP antibody

nucleolar

interpretation of indirect immunofluorescence results: stains as a discrete speckled pattern due to anti-centromere antibody

centromere

autoantibodies and associated disorders: centromere

CREST (calcinosis cutis, raynaud syndrome, esophageal hypomotility, sclerodactyly and telangiectasia) syndrome

autoantibodies and associated disorders: dsDNA

found in SLE and low titers found in rheumatoid arthritis and sjogren syndrome

autoantibodies and associated disorders: histone

drug-induced SLE

autoantibodies and associated disorders: nuclear RNP

SLE and mixed connective tissue disease

autoantibodies and associated disorders: Scl-70

scleroderma (systemic sclerosis)

autoantibodies and associated disorders: Sjogren syndrome A (SSA [Ro])

sjogren syndrome and SLE

autoantibodies and associated disorders: Sjogren syndrome B (SSA [LA])

sjogren syndrome and SLE

autoantibodies and associated disorders: Sm

diagnostic for SLE (high specificity) if present but low sensitivity

diagnostic tests for non-organ specific autoimmune diseases: anti-antibody, typically IgM, that binds the Fc portion of IgG; usually detected by latex agglutination, positive for 75% of patients with rheumatoid arthritis and also noted in chronic hepatitis, SLE and syphilis

rheumatoid factor (RF)

diagnostic tests for non-organ specific autoimmune diseases: proteins that reversibly precipitates at 4degC, and associated with autoimmune diseases such as vasculitis, glomerulonephritis, SLE, RA and sjogren syndrome

cryoglobulins

chronic, non infectious inflammatory disease involving many organs more likely to occur in women than men and in black than whites tissue injury is caused by autoantibodies and immune complexes deposited in the tissues depressed suppressor T cell function allows production of antibodies against self symptoms include fever, weight loss, malaise, weakness, arthritis, skin lesions, photosensitivity, butterfly rash, renal disease, pericarditis, seizures, ocular changes, pancreatitis, and small-vessel vasculitis

SLE

chronic, non infectious, systemic inflammatory disease that primarily affects the joints women are affected 2-3 times more often than men due to production of IgM antibodies against IgG in the synovium > immune complexes form > activates complement > inflammatory response proceeds and damages the synovium > attract neutrophil and macrophages to the joint that degranulate and contribute to tissue destruction symptoms: fatigue, weight loss, weakness, mild fever, anorexia, morning stiffness, joint pain, vasculitis, rheumatoid nodules lab: elevated ESR, elevated CRP, positive RF, cryoglobulins and sometimes ANAs, synovial fluid is cloudy with a WBC count between 5000-20,000/microliters, elevated protein, poor mucin clot development, decreased complement and positive RF

rheumatoid arthritis

an inflammation of the salivary and lacrimal glands causing dryness of the mouth and eyes lab: polyclonal hypergammaglobulinemia, autoantibodies against the salivary glands and positive RF, ANA (speckled or diffuse pattern), anti-SSA and anti-SSB

sjogren syndrome

increased rate of RBC destruction results in a normocytic, normochromic anemia autoantibody is directed against RBC antigens lab: positive direct antiglobulin test and sometimes cold agglutinins

autoimmune hemolytic anemia

humoral and cellular immunity are activated and destruction of normal thyroid tissue leads to hypothyroidism, loss of thyroid function and low levels of thyroid hormone in the blood antithyroid antibodies detected include antithyroglobulin, antithyroid peroxidase (microsomal antigen), and second colloid antigen (CA-2)

hashimoto disease

hyperplasia and diffuse goiter caused by autoantibody reacting with thyroid receptor on cells that overstimulates the thyroid gland autoantibody mimics the activity of thyroid stimulating hormone thyrotoxicosis results from overstimulation; both free and total T3 and T4 are elevated and TSH is decreased symptoms: exophthalmos and infiltrative dermopathy

graves disease

neuromuscular disease in which the nerve muscle do not function normally most patients exhibit antibodies to acetylcholine receptors autoantibodies block nerve impulses and can initiate damage to neurons

myasthenia gravis

considered a chronic progressive inflammatory disease with demyelinization of the nerves active lesion contains CTLs, helper T cells and macrophages most patients have increased IgG concentrations in the cerebrospinal fluid oligoclonal bands in CSF on high resolution electrophoresis are also indicative

multiple sclerosis

islet cell destruction in the pancreas results in insulin-dependent autoantibodies and CTLs reactive against pancreatic beta cells produce marked atrophy and fibrosis of the islet cells > insulin deficiency viruses can trigger autoantibody production by molecular mimicry

type I diabetes

overreactive immune responses to innocuous substances on re-exposure that can result in tissue damage involve humoral (types I-III) and cell-mediated (IV) responses

hypersensitivity

classified as an immediate hypersensitivity reaction because it occurs within minutes after re-exposure to an allergen after the first exposure, basophils and mast cells are sensitized with IgE, upon second exposure, IgE binds to a specific allergen and chemical mediators are released from those cells (degranulation), which causes allergic symptoms

type I hypersensitivity reaction

systemic form of the type I hypersensitivity shock or edema of the upper respiratory tract

anaphylaxis

type I hypersensitivity mediators: causes contraction of bronchioles and smooth muscle of blood vessels, increases capillary permeability, increases mucus secretion int he airway

histamine

type I hypersensitivity mediators: cause vasodilation and increased vascular permeability

prostaglandins

type I hypersensitivity mediators: erythema and wheal formation, 30-1000 times the ability of histamine to cause bronchospasm and also stimulate mucus secretion in the airways

leukotrienes

methods used to measure total serum IgE levels

competitive radioimmunosorbent test (RIST) non competitive RIST double-antibody radioimmunoassay (RIA) sandwich enzyme-linked immunosorbent assay (ELISA)

due to IgG or IgM antibodies directed against cell surface antigens immediate hypersensitivity reaction antibody-mediated tissue damage: PMNs bind to antibody-sensitized cells and destroy the cells by phagocytosis or antibody-dependent cellular cytotoxicity reaction complement-mediated cell lysis: antibody-antigen complex on cell surface activates the complement pathway to cause lysis incompatible blood transfusion damage to sensitize tissue cells causes inflammation which, in turn causes damage to normal tissue cells

type II hypersensitivity

immune complex reactions, immune complexes are deposited on tissue causing inflammation immediate hypersensitivity reaction circulating immune complexes SLE, RA, serum sickness, arthus reaction

type III hypersensitivity

two sites where immune complexes are often deposited in type III hypersensitivity

heart valves renal glomerulus

type III hypersensitivity: an allergen injected intradermally

arthus reaction

type III hypersensitivity: patients develop antibodies against heterologous serum proteins

immune complex disorders

type III hypersensitivity: immune complexes are deposited on renal glomeruli, causing inflammation of the kidney and possibly renal failure

glomerulonephritis

type III hypersensitivity: inflammation of the blood vessel wall

vasculitis

caused by soluble factors or lymphokines released by T cells > antibody and complement are not involved in this reaction lymphokines are produced by T cells these chemicals attract macrophages that become activated, causing them to degranulate as more macrophages arrive at the site, ulceration and necrosis occur

type IV hypersensitivity

subcutaneous injection of tuberculosis antigen is sued as a diagnostic skin test swelling occurring at the site within 24-72 hours indicates previous infection

tuberculin-type hypersensitivty

allergens from poison ivy and poison oak cause sensitization resulting in edema in the skin with the formation of microvesicles and itching on subsequent exposure

contact sensitivity (dermatitis)

marked deficiency of all classes of Ig is detected after about 6 months of age recurrent, life-threatening infections occur with encapsulated influenzae, manifested as pneumonia, sinusitis, bronchitis, otitis, furunculosis, meningitis, and septicemia b cells are markedly decreased or absent

bruton x-linked agammaglobulinemia

x-linked genetic disease serum IgM is increased; IgG and IgA are markedly decreased or absent defect in CD40 ligand on T helper cells prevents class switching from IgM to IgG, IgA or IgE affected individuals are prone to respiratory tract infections, often have autoantibodies to platelets, red blood cells and neutrophils

hyper IgM syndrome

patients present with small amounts or absence of serum and secretory IgA usually caused by a genetic defect or by drugs (phenytoin and penicillin) anaphylaxis may result if IgA is administered to someone with this deficiency

selective IgA deficiency

autosomal recessive disorder that presents with ataxia, telangiectasia, recurrent sinopulmonary infections, a high incidence of malignancy, and variable immune defects typically present with an IgA and sometimes IgE deficiency defect in a kinase gene that regulates the cell cycle b and t helper cells are affected

ataxia-telangiectasia

because T cells are involved in both humoral and cell mediated responses, individuals with ____ can have a severe combined immunodeficiency

T helper deficiencies

hypocalcemic tetany, due to underdevelopment of the thymus and heart disease immune defect is variable, from slight decrease in T cells to no T cells in the bloodstream very susceptible to opportunities infections and have a poor prognosis

congenital thymic hypoplasia digeorge syndrome

group of diseases with different causes, that affect T and B cell function, resulting in a suppression of humoral and cell mediated immune responses

severe combined immune deficiency

absence of these enzymes causes an accumulation of nucleotide metabolites in all cells which is particularly toxic to T and B cells very low number of T cells is present, and children often have an underdeveloped thymus-lack of tonsil or lymph nodes, hypogammaglobulinemia, and lymphopenia

adenosine deaminase or purine nucleotide phosphorylase

with an mhc class II deficiency, t helper cells fail to develop patients present with hypogammaglobulinemia and no cell-mediated immune response mhc class I deficiency is less severe loss of ctls and response to intracellular pathogens

bare lymphocyte syndrome

defect prevents t helper cells from delivering lymphokines to b cells, macrophages and other target cells patients demonstrate eczema, thrombocytopnenic purpura, and increased risk of infection platelets are small and defective

wiskott-aldrich syndrome

protein involved with cytoskeletal reorganization necessary for delivering cytokines

wiskott aldrich syndrome protein

complement deficiencies: patients with defects in early ______ such as factor D and properdin, are susceptible to infections by Neisseria meningitidis

alternative complement proteins

complement deficiencies: patients with a ______ have the most severe clinical manifestations

c3 defects

decline in serum immunoglobulins during the first few months of life individuals eventually produce normal amounts of immunoglobulins

transient hypogammaglobulinemia

certain viruses impair the function of the immune systems

human immunodeficiency virus epstein barr virus cytomegalovirus

tremendous amounts of several classes of immunoglobulins to several specific antigens are produced, resulting in a broad spike in the gamma region on serum protein electrophoresis

polyclonal hypergammaglobulinemia

causes of polyclonal hypergammaglobulinemia

infectious diseases inflammatory responses liver disease

malignant transformation of a clone of b cells that produce identical antibodies narrow peak on serum protein electrophoresis

monoclonal hypergammaglobulinemia

lymphoproliferative disease in which plasma cells produce a high concentration of immunoglobulin approximately 50% of patients have Bence Jones proteins weakness, anorexia, weight loss, skeletal destruction, plasma cell infiltrate in bone marrow

multiple myeloma

light chain fragments

bence jones proteins

diagnostic of multiple myeloma, waldenstrom macroglobulinemia, chronic lymphocytic leukemia or lymphoma immunoglobulin type determination is necessary for diagnosis and prognosis

monoclonal immunoglobulins (m protein)

uncontrolled proliferation of a clone of b cells that synthesize a homogenous IgM cause unknown hyperviscosity of plasma causes heart failure, headache dizziness, partial or total loss of vision, bleeding and anemia weakness, fatigue, headache and weight loss lab: a spike in the beta or gamma region on serum protein electrophoresis, increased plasma viscosity, and abnormal accumulation of lymphoid cells in the bone marrow and tissues

waldenstrom macroglobulinemia

non structural protein that becomes insoluble after an alteration in its secondary structure

amyloid protein

monoclonal plasma cell disorder in which abnormal immunoglobulin or bence jones protein or less commonly heavy chain fragment is produced insoluble proteins are deposited in some of the tissues: skin, liver, nerves, heart, kidney results in progressive loss of organ function lab: frequent abnormalities of serum Ig and presence of bence jones proteins

primary amyloidosis

transfer of tissue from one site to another within an individual

autograft

transfer of tissue between genetically identical individuals

isograft (syngraft)

transfer of tissue between two genetically non identical individuals of the same species

allograft

transfer of tissue between two individuals of different species

xenograft

revascularization and healing lead to a repaired site in about 2 weeks

graft acceptance

first time a graft is encountered, the immune system attacks and ultimately destroys (rejects) the nonself tissue occurs 10-14 days after transplantation

first set rejection

the second time non self tissue with the same or similar antigens is encountered rejected within 6 days

second set rejection

clinical indications of graft rejection: occurs within 24 hours of transplantation rejection is caused by a pre-existing antibody to antigens on the grafted tissue tissue never becomes vascularized caused by ABO blood group antibodies and MHC class I antibodies

hyperacute rejection

clinical indications of graft rejection: occurs within weeks of transplantation due to cell-mediated response histopathology reveals massive infiltration of lymphocytes and macrophages

acute rejection

clinical indications of graft rejection: occurs months to years after transplantation mechanisms of rejection include both humoral-mediated and cell-mediated immunity

chronic rejection

abnormal mass of tissue that results from the uncontrolled growth of normal cells even after the growth stimulus is removed

neoplasm

typically a mild and non progressive tumor that pushes aside normal tissue, but does not invade it, as the tumor expands

benign tumor

generally consisting of poorly differentiated cells that grow rapidly and invade surrounding tissue, robbing the normal tissue of nutrients

malignant tumor

secondary tumor derived from a malignant primary tumor

metastatic tumor

intracellular proteins expressed on the surface of a tumor due to interaction with MHC class I and II moleculues

tumor-specific peptides

occurs when macrophages come in close contact with tumor cells

macrophage-mediated cytotoxicity

kills those cells with mutations leading to decreased MHC class I products expressed on their surfaces

NK cells

antibodies can be produced to antigens found on the surface of tumor cells, which then can be lysed by complement activation or antibody dependent cellular cytotoxicity reactions involving NK cells, PMNs and macrophages

humoral-mediated immunity

activates t cells, b cells and nk cells and induces a fever

IL-1

destroys tumor cells

TNF alpha

produced by activated t cells and nk cells

INF-gamma

glycoproteins found in small amounts in normal serum but elevated in certain types of cancers used to screen for cancer but more commonly are used to monitored therapeutic response or to determine tumor burden

tumor markers

used in management of gastrointestinal tumors (colon cancers) and adenocarcinomas of the colon, pancreas, liver and lungs can also be found in inflammatory bowel disease, ulcerative colitis, crohn disease, polyps tumors of the GI tract, and cigarette smokers

carcinoembryonic antigen (CEA)

produced during embryonic and fetal development high in patients with hepatocellular carcinoma, hepatoblastoma, testicular and ovarian cancer can also be elevated in viral hepatitis, cirrhosis and ulcerative chelitis temporary marker for monitoring cancer therapy

alpha fetoprotein (AFP)

composed of two subunits: alpha and beta found in serum and urine during pregnancy may be produced by neoplastic cells of testicular cancer and various other tumors levels are useful in evaluating patients with gestational trophoblastic disease, testicular tumors and ovarian germ cell tumors

human chorionic gonadotropin (hCG)

glycoprotein that dissolves seminal gel formed after ejaculation normal prostate tissue contains this but it is present in extremely low amounts in blood increased in prostrate cancer, benign prostatic hypertrophy, and acute or chronic prostatitis levels correlate with prostrate size, stage of prostate cancer and response to treatment used to screen for prostate cancer in conjunction with a digital rectal examination

prostate specific antigen (PSA)

antigen-antibody interactions: positively charged portions of one molecule are attracted to negatively charged portions of another molecule affected by the pH and ionic strength of the environment increases as the two molecules get closer together

electrostatic force or ionic bonding

antigen-antibody interactions: binds to an electronegative atom such as oxygen or nitrogen weak bond, but it contributes greatly to the antigen-antibody interaction maximum binding strength occurs below 37degC

hydrogen bonding

antigen-antibody interactions: attraction between non polar groups non polar groups tend to aggregate to reduce surface area, and this increased the strength of the bond

hydrophobic bonding

antigen-antibody interactions: a weak, attractive force between an electron orbital of one atom and the nucleus of another atom

van der waals force

antigen-antibody interactions: strength of interaction between an antibody binding site and a single epitope

affinity

antigen-antibody interactions: describes whether the antigen-antibody complex is highly complementary, and therefore would not bind readily

affinity constant

antigen-antibody interactions: affinity for multivalent antigens and multiple antibodies to combine; the extent of bindings capacity greater than the cumulative affinity constants for all antigen-antibody pairs

avidity

antigen-antibody interactions: antibody's greatest affinity for a particular antigen

specificity

antigen-antibody interactions: occurs when the antibody combines with an antigen that is structurally similar to the immunogen that stimulated the antibody production or the antigen that the antibody has the greatest affinity

cross reactivity

assays involving antibody-antigen reactions

immunoassays

soluble antigen and soluble antibody reacts to form an insoluble product, such as gel diffusion, radial immunodiffusion, immunoelectrophoresis, immunofixation, nephelometry and turbidity

precipitation reaction

soluble antibody reacts with insoluble antigen or soluble antigen reacts with insoluble antibody; reactants are made insoluble by combining with latex particles, rbcs, dyes, liposomes

agglutination

antigen-antibody interactions: a label producing a measurable end product is attached to an antibody or antigen; labels include fluorochromes, enzymes, chemiluminescent molecules, and radionuclides

labeled reaction

precipitation reactions: maximum precipitation occurs when the concentration of the antigen and antibody are about equal

zone of equivalence

precipitation reactions: occurs when excess amount of antibody is present, and the antigen and antibody do not combine to form precipitates - the complexes remain soluble; results in a false negative result

prozone

precipitation reactions: occurs when excess amount of antigen is present, and the antigen and antibody do not combine to form precipitates - the complexes remain soluble; results in a false negative result

postzone

types of precipitation reactions: passive diffusion of soluble antigen and antibody

fluid-phase precipitation

measurement of light transmitted through a suspension of particles; formation of immune complexes decreases the amount of light passing through a suspension the more immune complexes are formed, and the larger they are, the greater the decrease in light able to pass through

turbidimetry

direct measure of light scattered by particles suspended in solution scattering of light is proportional to the size and the amount of immune complexes formed

nephelometry

types of precipitation reactions: antigen and antibody diffuse through the agar gel and precipitate when they reach the zone of equivalence; molecular size determines the speed of travel through the gel

precipitation reactions in agar gel

types of precipitation reactions: antigen and antibody are placed in wells in the gel and diffuse towards each other, when optimum concentrations are met, a precipitate line forms can be used to determine if a specific antibody is present in serum

double immunodiffusion (oachterlon) technique

types of precipitation reactions: on an agar gel plate or slide, antigen is added to one well, and antibody is added to another well an electric current accelerates the movement of the antigen and antibody toward each other, resulting in precipitation sooner than if an electric current is not applied can be used to detect antibody to infectious agents and microbrial antigens

contercurrent immunoelectrophoresis

serum urine, or CSF, is electrophoresed antisera contained in a cellulose acetate strip are then placed on top of the electrophoresis gel the antibodies diffuse into the electrophoresis detects the presence of an immunoglobulin in serum or urine

immunofixation electrophoresis

used to quantify antigens antigens are electrophoresed in agar-containing antibody a pH is selected so that the antibodies are immobile antibody and antigen combine to form precipitates in the shape of a rocket height is proportional to the concentration of antigen in the specimen

rocket immunoelectrophoresis

occurs when particles in suspension clump together due to antibody-antigen interaction uses an antigen or antibody attached to a particle (insoluble)

agglutination

antibodies that participate in agglutination reaction

IgM IgG

this method uses antigens naturally occurring on a particle to demonstrate agglutination

direct agglutination

naturally occurring process in which in virus will agglutinate RBCs by binding to surface receptors

viral agglutination

technique in which soluble antigen is attached to a particle, producing agglutination with specific soluble antibody

passive agglutination

a technique in which an antibody is attached to a particle, producing agglutination with a specific soluble (antigen)

reverse passive agglutination

sometimes used to detect antibody in patient sera serum is mixed with a specific known antigen if antibody to the antigen is present, immune complexes forms complement is added, and if an immune complex is present, it will bind the complement detect antibodies to viruses, rickettsia, and fungi

complement fixation assays

antibodies labeled with fluorescent dye are used to detect an antibody or antigen

immunofluorescence

conjugated reagent antibody reacts with an antigen in a clinical sample to form an antigen-antibody complex

direct immunofluorescence

antigen reacts with unlabeled antibody forming an antigen-antibody complex that is then complexed with a labeled antihuman antibody, creating an antibody, antigen, antibody sandwich

indirect immunofluorescent assay

this is an indirect assay in which the detection system is modified by using biotin-labeled antibody followed by avidin-labeled fluorochrome

biotin-avidin-immunofluorescence

antibodies to nuclear antigens are present in many systemic autoimmune diseases, such as SLE, mixed connective tissue disease, rheumatoid arthritis

antinuclear antibodies

enzyme-labeled reagents are used to detect antigens or antibodies colorless substrate is metabolized by the enzyme into a colored compound the intensity of the color is directly proportional to the amount of enzyme present

enzyme-linked immunosorbent assays (ELISA)

cellular assays: enumeration of t cells is important in assessing immune response monoclonal antibodies are used in conjunction with flow cytometry to identify cell markers such as CD1, CD2, CD3, CD4

T cell subsets

cellular assays: classical test for labeled antibody to surface membrane immunoglobulin; monoclonal antibodies are now used in conjunction with flow cytometry to identify CD19, CD20

b cell subsets

cellular assays: NK cells, macrophages, neutrophils

CD16

cellular assays: immature cells

CD34

cellular assays: B cells, monocytes, myeloid cells, and erythroid precursors

HLA-DR

cellular assays: erythroid cells

glycophorin A

cellular assays: myelomonocytic cells

CD14

cellular assays: platelet and megalokaryocytes

CD41

causes pharyngitis, pyoderma, puerperal sepsis, and necrotizing fasciitis, scarlet fever

streptococcus pyogenes (group A streptococci)

post-streptococcal sequelae

rheumatic fever glomerulonephritis

sx: carditis, chorea, erythema marginatum, polyarthritis, and/or subcutaneous nodules occurs 3-4 weeks after infection m protein of S. pyogenes shares antigen epitopes with proteins found in synovium, heart muscle, and heart valve, suggesting that the damage is from an AI due to molecular mimicry

rheumatic fever

sx: proteinuria, hematuria, hypertension, impaired renal function and edema occurs about 10 days after pharyngitis or 15-21 days after a skin infection circulating Ag-Ab complexes are deposited on the GBM, where complement is activated and damage to the membrane results platelet aggregation and fibrin and fibrinogen build up, causing capillary obstruction and impaired renal function

glomerulonephritis

hemolysin produced by most beta-hemolytic group A streptococci

streptolysin O

a ___ increase in titer between acute and convalescent samples indicates a recent group A infection

fourfold

neutralization assay antibodies to streptolysin O prevent hemolysis serial dilutions of patient serum are prepared, the titer is the last tube with no hemolysis

ASO neutralization test

latex particles coated with streptolysin O agglutinate when mixed with patient's serum containing ASO antibody

ASO rapid latex agglutination test

reference range for ASO rapid latex agglutination test: titers considered indicative of a group A streptococcus for preschool children

> 85

reference range for ASO rapid latex agglutination test: titers considered indicative of a group A streptococcus for school-age children

> 170

reference range for ASO rapid latex agglutination test: titers considered indicative of a group A streptococcus for adults

> 85

screening test produced by wampole laboratories that detects antibodies to five s. pyogenes proteins: DNAse, b hyaluronidase, NADase, streptokinase, and streptolysin O four-fold rise in titer between acute and convalescent sera is indicative of an infection passive hemagglutination assay

streptozyme

antibody peaks at 4-6 weeks after group A streptococcal infection and lasts for moths latex agglutination or immunonephelometry

anti-DNAse B test

causative agent of syphilis

treponema pallidum subsp. pallidum

MOT of syphilis

direct contact across the placenta

painless, non-bleeding ulcer of syphilis

chancre

initial lesion is chancre, 1 week later, lymph nodes enlarge antibodies are produced 1-4 weeks after darkfield analysis of lesion demonstrates spirochetes

primary syphilis

symptoms include skin rash, low-grade fever, malaise, pharyngitis, weight loss, arthralgia, and lymphadenopathy, and las 4-6 weeks spirochetes are present throughout the body ulcers develop on mucous membranes serologic tests are positive

secondary syphilis

stage of syphilis with no signs or symptoms non treponemal and treponemal serologic tests are positive

latency

one in four individuals relapses into secondary syphilis

early latency

patient is resistant to reinfection and to relapses

late latency

symptoms occur 2-40 years after initial infection gummas found throughout the body syphilitic aortitis, aortic valve insufficiency and thoracic aneurysm are possible neurosyphilis can cause blindness and senility

tertiary syphilis

syphilis lesions due to hypersensitivity reaction to treponemal antigens

gummas

infection of the fetus causes late abortion, still birth, neonatal death, neonatal disease or latent infection presents in the neonates as diffuse maculopapular desquamatous rash (perioral, palmar or sole area), hemolytic anemia, jaundice, hepatosplenomegaly, abnormal cartilage, and bone involvement and mental retardation

congenital syphilis

Immunology, Serology and Blood Banking Flashcards

(300 cards)