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PATH2220 > W3 > Flashcards

W3 Flashcards

1
Q

what is immunity

A

recognition and disposal of foreign or non-self material entering the body

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2
Q

what initiates an immune response

A

recognition of presence of foreign organism or substance, there are certain recognition receptors: different for the innate and acquired immune response may be circulating freely in blood or body fluids, fixed to cell membrane or within the cytoplasm of some cells

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3
Q

what is the innate immune system

A

the paramedics at an accident, react quickly and efficiently, less specific than later “specialists”, includes phagocytes, complement and NK cells

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4
Q

how does the innate immune system recognise pathogens

A

pattern recognition receptors, pathogen associated molecular patterns and soluble recognition molecules

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5
Q

explain recognition receptors

A

e.g. toll like receptors, mannose receptors, acute phase proteins. on phagocytes- recognise structures common to disease causing pathogens. bind pathogen for phagocytes and send signals that lead to release of effector molecules

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6
Q

explain pathogen associated molecular patterns

A

e.g. dsRNA and flagellin. molecular structures on pathogens not shared with host, not shared with many pathogens and are invariable

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7
Q

explain soluble recognition molecules

A

COMPLEMENT- group of serum proteins that are activated in a cascade leading to inflammation and bacterial lysis
INTERFERONS- family of proteins produced rapidly by many cells in response to virus infection. Block viral replication in infected cell and its neighbours. Role in communication between immune cells
DEFENSINS- antimicrobial peptides- important in early protection of lungs and digestive tract against bacteria

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8
Q

what is a lysozyme

A

an enzyme secreted by macrophages that attacks cell wall of some bacteria

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9
Q

what is mannose binding lectin

A

binds the surface of bacteria and fungi. Can activate complement or act directly to assist phagocytosis

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10
Q

what is acute phase proteins

A

serum proteins present at very low levels. Rapidly produced in high amounts by the liver following infection. Contribute to inflammation and immune response.

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11
Q

what are mast cells

A

large tissue cells that release inflammatory mediators when damaged and under influence of IgE

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12
Q

what are polymorphonuclear leucocyte

A

short-liver scavenger blood cells that are around 80% white blood cells. Granules within contain powerful bacterial enzymes

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13
Q

what are macrophages

A

large tissue cells responsible for removal of damaged tissue and cells etc

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14
Q

what are dendritic cells

A

present antigen to T-cells initiating all T-cell dependent immune responses

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15
Q

what is phagocytosis

A

engulfment of particles by a cells -PMNS and macrophages are the most important phagocytic cells

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16
Q

what are natural killer cells

A

lymphocyte like cells capable of killing targets such as virus-infected and tumour cells, without the receptor or specificity of true lymphocytes

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17
Q

what does cytotoxicity mean

A

macrophages and other cells can kill some targets without phagocytosing them

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18
Q

what is the process of antibody-dependent cells mediated cytotoxicity

A
  1. antibodies bind antigens on the surface of target cells 2. NK cell CD16 Fc receptors recognise cell-bound antigens 3. cross-linking of CD16 triggers degranulation into lytic synapse 4. tumour cells die by apoptosis
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19
Q

what are the two functions of phagocytes

A

internalisation and presentation of antigens vis MHC, intracellular killing

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20
Q

describe the process of macrophage phagocytosis

A
  1. macrophage expresses receptor for bacterial constituents: mannose , LPS and glucan . 2 bacterial binding leads to release of cytokines and other mediators of inflammation 3. bound bacteria is engulfed (phagocytksed by macrophages)
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21
Q

what are adhesion molecules

A

traffic cells in inflammation they bring neutrophils and monocytes in inflamed area

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22
Q

what is the complement cascade

A

identifies and opsonises foreign bodies, recruits and activates inflammatory cells, lyses pathogen, clears immune complexes and apoptotic cells. augments and B cells responses

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23
Q

what are the three pathways to the complement cascade

A
  1. classical pathway 2. lectin pathway and 3 alternate pathway
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24
Q

what are the 3 antigen presenting cells

A

dendritic cells, macrophages and B-cell

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25
Q

what are the 2 signals required for t-cell activation

A

HLA-TCR interaction and binding of B7 to CD18

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26
Q

what does the the pathway promote (the complement cascade pathway)

A

production of cytokines that promote B cell growth, mast cells and eosinophils

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27
Q

what are the two types of immunodeficiency disorders

A

primary and secondary

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28
Q

describe primary immunodeficiency disorders

A

deficiency or dysfunction of immune cells or plasma proteins caused by genetic defect, often present in childhood, they are experiments of nature

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29
Q

describe secondary immunodeficiency disorders

A

deficiency or dysfunction of immune cells or proteins cause by infections, disease or medical treatments

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30
Q

what are some of the things antibodies can do

A

neutralisation of microbes and toxins, opsonisation and phagocytosis of microbes, antibody-dependent cellular cytotoxicity, lysis of microbes, phagocytosis of microbes opsonised with complement fragments, inflammation and also complement activation

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31
Q

what is X-linked agammaglobuliaemia (XLA)

A

mutations of Btk gene on X chromosome (deficiency of B cell tyrosine kinase that is crucial for B cells to develop in the bone marrow). defective maturation of B in the BM. B cell deficiency in blood and lymphoid tissue (leads to no tonsils or palpable lymph nodes and can’t produce B cells). Deficiency of plasma cells leading to impaired antibody response

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32
Q

what is common variable immunodeficiency disorder

A

various defects of B cell activation and survival ( deficiency of switched memory B cells and impaired differentiation of B cells into plasma cells). Low serum levels of IgG, IgA and IgM of variable severity. Imparied antibody responses resulting in an increased susceptibility to infection. may present at any age but usually during first 3 decades of life

33
Q

what are marginal zone B cells

A

encounter antigens in marginal zone of spleen and some regions of lymphoid tissue. rapid production of IgM and IgG antibodies in a T-cell independent manner

34
Q

what are follicular B cells

A

encounter antigens in germinal centres of follicles in lymphoid tissues. Require T-cell help to produce antibodies that are high affinity and isotope switches as well as memory B cell. These are longer to produce but are better quietly than marginal zone B cells

35
Q

describe hyper-IgM immunodeficiency syndrome

A

defect in switching from B cells producing IgM to B cells producing IgG, IgA and IgE. High serum levels of iGM and low IgG and IgA. impaired IgG antibody responses. CD40 ligand deficiency is most common causes

36
Q

what happens if there is a deficiency in the classical pathway

A

immune complex disease, occasionally increased infection susceptibility

37
Q

what happens if there is a deficiency in the alternative pathway

A

increased susceptibility to infections with neisseria sp. particularly minigococci.

38
Q

what happens if there is a problem in the mannose binding lectin pathway

A

increased suscepitilbity to infections, mainly when associated with other immune defects

39
Q

what happens if there is a problem with the membrane attack complex int he complement cascade

A

increased suscepitilibty to infection with neisseeria sp. particularly meningococci

40
Q

what is thymus aplasia/ hypoplasia in 22q11.2

A

deletion syndrome, embryonic map-development of 3rd and 4th brachial pouches associated with deletions of chromosomes 22q11.2. thymus aplasia or hypoplasia (deficiency of all T-cells), variable associated defects (digeorge syndrome), parathyroid hypoplasia and micrognathia

41
Q

what can cause a decrease in the CD4 t cell leaves

A

HIV

42
Q

what are combined immunodeficiency disorders

A

severe combined immunodeficiency disorder, combined defects of B cells and T cells +- NK cells resulting in impaired antibody and cells mediated immune responses. Often fatal during first two years of life if not treated. treatment often requires allogenic haemopoitic stem cells transplantation.

43
Q

what are some immune defects causing severe combined immunodeficiency disorders

A

adenosine deaminase deficiency, cytokine receptor common Y chain deficiency.

44
Q

describe the primary response of immunological memory

A

there is a time lag between antigen exposure and antibody titre. Initially IgM, followed by IgG that is higher and persists longer than IgM

45
Q

describe the secondary response of immunological memory

A

appears quicker (due to memory) and lasts longer, higher titre and predominantly IgG

46
Q

what are most autoimmune disease associated with

A

autoantibody production and some due to cell mediated immune response.

47
Q

what is the mechanism for autoimmune diseases

A

unclear, probably multifactorial and may be caused by drugs or viral illness.

48
Q

what is the aetiology of autoimmunity

A
  1. cooperation between auto reactive B-cells and non-autoreactive T-cells, 2 molecular mimicry 3 polyclonal lymphocyte activate
49
Q

describe cooperation between auto reactive B-cells and non-autoreactive T-cells,

A

autoreactive B-cells - efficient antigen presenting cells. May present antigen to non-autoreactive T-cells. Processed antigen is capable of stimulating antigen-specific T-cells and provide help for auto reactive B-cells

50
Q

what is molecular mimicry

A

T-cells may be induced to provide help to infecting organism with a cross-reactive T-cell epitope. Immune system recognises virus and self the same, immune response directed towards itself on the tissue

51
Q

describe polyclonal lymphocyte activation

A

viruses and bacterial products may because polyclonal B-cell activation. There may be a degree of polyclonal activation in many autoimmune diseases.

52
Q

what are environmental factors suggested to trigger autoimmunity

A

viral infection, viral and/or bacterial super-antigen, dietary components and environmental toxins

53
Q

what is the auto antigen to systemic lupus erythematosus

A

nuclear antigens, cellular cytoplasmic antigens, phospholipids, red blood cell and platelet antigen

54
Q

what is the auto antigen to rheumatoid arthritis

A

immunoglobulin

55
Q

what is the auto antigen to sicca syndrome

A

components of exocrine and nuclear antigens

56
Q

what is a systemic autoimmune disease

A

AI response against auto-antigens not restricted to single organ

57
Q

what is a organ specific AI disease

A

AI response against auto-antigens present in single organ or system

58
Q

what is the auto antigen for the following organ specific disease : graves disease

A

TSH receptor of thyroid

59
Q

what is the auto antigen for the following organ specific disease : myasthenia gravis

A

actyl choline receptor of skeletal muscle

60
Q

what is the auto antigen for the following organ specific disease : diabetes mellitus

A

components of pancreatic islets cells

61
Q

what is the auto antigen for the following organ specific disease : pemphigus

A

intracellular substance of epidermis and mucous stratified epithelium

62
Q

what is systemic lupus erythematosus (SLE)

A

chronic multi0system inflammtory disorder, unknown aetiology, occurs predominately in females,

63
Q

what is systemic lupus erythematosus associated with

A

uncontrolled interaction between T and B cells. anti-nuclear antibodies and probably defects in regulation of Bcells +- T cells

64
Q

what is the immunopathogenesis of SLE

A

predisposition to develop SLE appears to be multifactorial. strong genetic basis, the development is multi step. there is a presence of numerous autoantibodies, particularly die to breakdown of immune surveillance and loss of self tolerance

65
Q

what is the hallmark for SLE

A

production of anti-nuclear antibodies ANA are IgG antibodies directed against nuclear antigens

66
Q

what is the detection for SLE

A

add patients serum to Hep-2 cels and if serum contains ANAs then immunoglobulins present in serum will bind to the nucleus of cell. The add anti-IgG and ANA can not be detected through florescent light

67
Q

what are the patterns of ANA

A

homogenous, rim/peripheral, speckled and nucleoar

68
Q

describe ANA testing and SLE diagnosis

A

need other testing because 1/3 people have ANA but they are still healthy.

69
Q

what are the key concepts of SLE

A

autoantibodies mediate pathology of SLE by binding to cell surface antigens, by forming immune complexes that are then deposited in tissue and interfere with function or cause tissue damage by complement activation. by poorly understood mechanisms of disease association

70
Q

when is the peak incidence of graves disease

A

3rd and 4th decade

71
Q

what are the predisposing factors to graves disease

A

being female and living in high areas of iodine intake

72
Q

what is the pathogenesis of Graves disease

A
  1. IgG compete for receptors with TSH and keep on binding to produce thyroxin. TSH is usually keep in close regulation but IgG is not and thyroxin is overproduced. 2. dense lymphocytic infiltrate , CD4 AT cells help B cells to produce IgG antibodies
73
Q

what is hashimotos thryroiditis

A

chronic inflammatory disease of thyroid-autoimmune factors play a prominent role.

74
Q

when is the peal incidence of hashimotos thryroiditis

A

middle age, females are much more likely than males

75
Q

what are the characteristics of hashimotos thryroiditis

A

high titre of anti-TPO antibody

76
Q

what is the pathogenesis of hashimotos thryroiditis

A
  1. dense lymphocytic infiltrate. CD4 t cells may help B cells to produce anti-thyroid antibodies . 2 autoantibodies, antibodies expressed on surface of thyroid follicular cells. 3. Complement fixation-IgG autoantibodies 4. Antibody dependent cytotoxicity
77
Q

what are the two main type of autoantibodies in hashimotos thryroiditis

A

anti-thyroid peroxidase (has 2 pathogenic roles, 1. kill thyroid cells in presence of complement and 2. bind to and interfere with function of peroxidase and anti-throglobulin (unlikely to have pathogenic role). more than 98% of people with thyroiditis have one or both of these antibodies

78
Q

true or false. autoantibodies to receptors alter receptor function causing disease: stimulating (hyperthyroidism) and blocking (hypothyroidism)

A

true

PATH2220 (14 decks)

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