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Pathology I > Immunity II > Flashcards

Immunity II Flashcards

1
Q

what is immunologic tolerancr

A

-lack of response to antigens that is induced by exposure of lymphocytes to these antigens
- ability to discriminate between self and nonself antigens

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2
Q

normally microbes are:
- self antigens are:

A

immunogenic; tolerogenic

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3
Q

what is central tolerance

A

developing lymphocytes encounter self antigens in central lymphoid organs

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4
Q

what is peripheral tolerance

A

mature lymphocytes encounter self antigens in peripheral tissues

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5
Q

what do self reactive T cells do in central T cell tolerance

A
  • negative selection or deletion
  • development of regulatory T cells
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6
Q

what do regulatory T cells do in peripheral T cell tolerance

A

block the activation of self reactive lymphocytes

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7
Q

what is anergy

A

functional inactivation of T cells

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8
Q

what is deletion

A

apoptosis of self reactive lymphocytes

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9
Q

what induced tolerance in B cells

A

self polysaccharides, lipids and nucleic acids

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10
Q

what does central B cell tolerance undergo

A
  • receptor editing
  • negative selection
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11
Q

what does peripheral B cell tolerance undergo

A
  • anergy
  • excluded from lymphoid follicles
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12
Q

what is autoimmunity

A

immune response against self antigens

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13
Q

what might the development of autoimmunity be due to

A
  • inheritance of susceptibility genes
  • environmental triggers
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14
Q

most autoimmune diseases are______

A

polygenic

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15
Q

what are autoimmune diseases often associated with

A

particular HLA genes that are inefficient at displaying self antigens
- defective T cell negative selection
- may fail to stimulate regulatory T cells

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16
Q

how might infections activate self reactive lymphocytes

A

-increased production of costimulatory molecules on APCs
- molecular mimicry

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17
Q

what are hypersensitivity reactions

A

injurious or pathologic immune reactions

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18
Q

what is autoimmunity

A
  • reactions against self antigens
  • failure of self tolerance
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19
Q

what does hypersensitivity cause

A
  • autoimmunity
  • reactions against microbes
  • reactions against environmental antigens
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20
Q

describe type I immediate hypersensitivity

A
  • tissue reaction that occurs rapidly after interaction of antigen with IgE antibody bound to mast cell
  • often develop in atopic individuals
  • environmental and food allergens
  • mild to severe reaction
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21
Q

what is the mechanism of type 1 immediate hypersensitivity

A
  • activation of Th2 cells and IgE class switching in B cells
  • production of IgE
  • binding of IgE to Fc on mast cells
  • repeat exposure to allergen
  • activation of mast cell and release of mediators
  • mediators could be vasoactive amines or cytokines
  • vasoactive amines cause immediate hypersensitivity reaction
  • cytokines cause late phase reaction
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22
Q

what is an example of a vasoactive amine and what does it do

A

histamine: causes vasodilation, increased vascular permeability, smooth muscle contraction and increased secretion of mucus

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23
Q

what are the lipid mediators and what do they cause

A
  • prostaglandins and leukotrienes: smooth muscle contraction and vascular permeability
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24
Q

what are the cytokines released in immediate hypersensitivity

A

TNF, chemokines, Il4 and IL5

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25
Q

what are the clinical syndromes and manifestations of type I immediate hypersensitivity reactions

A
  • anaphylaxis: fall in BP, vascular dilation, airway obstruction due to laryngeal edema
  • bronchial asthma: airway obstruction due to smooth muscle hyperactivity
  • allergic rhinitis: increased mucus secretion, inflammation of upper airways and sinuses
  • food allergies: increased peristalsis causes vomiting and diarrhea
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26
Q

how do allergies develop

A
  • genetically determined
  • environmental factors: environmental pollutants, infections
  • atopic individuals
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27
Q

describe atopic individuals

A
  • higher serum IgE
  • more TH2 cells
  • 50% have fam hx of allergies
28
Q

what is the hygiene hypothesis

A
  • allergies decreasing in developing countries: too much hygiene can cause allergies
  • early childhood exposure is good
29
Q

what happens in type II antibody mediated diseases

A
  • opsonized by autoantibodies -> targets cell for phagocytosis by neutrophils and macrophages
  • antibodies activate the complement system and recruit neutrophils, macrohpases to trigger inflammation
  • antibody mediated cellular dysfunction -> impair or dysregulate important functions
29
Q

what is Type II antibody mediated disease caused by

A

-antibodies directed against target antigens on cell surfaces
- target cells for phagocytosis
- activate complement system
- interfere with normal cellular functions

29
Q

what are the diseases associated with type II hypersensitivity

A
  • autoimmune hemolytic anemia
  • autoimmune thrombocytopenic purpura
  • pemphigus vulgaris
  • vasculitis caused by ANCA
  • goodpasture syndrome
  • acute rheumatic fever
  • myasthenia gravia
  • graves disease
  • pernicious anemia
30
Q

describe type III immune complex mediated diseases

A

-antigen- antibody complex formed
- deposits in BV -> complement activation and acute inflammation
- antigen may be foreign protein or endogenous (autoimmunity)
- soluble antigens

31
Q

what is the mechanism of type III diseases

A
  • formation of immune complexes: ABs are secreted in blood, react with antigen and form antigen- antibody complexes
  • deposition of immune complexes: circulating antigen- antibody complexes deposited in tissues
  • inflammation and tissue injury: once deposited, immune complexes initiate inflammation via complement or engagement of leukocytes
32
Q

what are the diseases associated with type III

A
  • systemic lupus erythematosus
  • poststreptococcal glomerulonephritis
  • polyarteritis nodosa
  • reactive arthritis
  • serum sickness
  • arthrus reaction
33
Q

what is the arthrus reactino from

A

vaccines which cause antibodies to form immune complexes that activate complement and enhance localized inflammation

34
Q

describe type IV cell mediated disease

A
  • CD4 T cells: cytokine mediated inflammation
  • CD8 T cells: direct cell cytotoxicity
  • many chronic inflammatory diseases are T cell mediated
  • most are TH1 mediated, some are TH17
35
Q

what is the mechanism of TYpe IV

A

cytokines produced induce inflammation and cause tissue destruction

36
Q

when do type IV diseases happen

A

delayed-type: 48-72 hours after exposure

37
Q

what does the CD8 t cell do in type IV

A

kill antigen expressing target cells
- effective in virus infected cells

38
Q

what are the diseases in type IV

A
  • RA
  • MS
  • type I DM
  • IBS
  • psoriasis
  • contact sensitivity
39
Q

what mediated type I DM

A

CD8 t cells

40
Q

what are primary/ congenital immunodeficiency syndromes

A

inherited genetic disorders

41
Q

what are secondary immunodeficiency syndromes

A

after challenge to immune system such as cancer or environmental factors

42
Q

describe primary immunodeficiencies

A
  • may affect innate or adaptive immunity
  • usually detected in infancy - 6 months-2 years of age
  • most involve disorders of B and T lymphocytes
43
Q

what is severe combined immunodeficiency (SCID)

A

-encompassed many genetically distinct syndromes with defects in both cell mediated immunity and humoral immunity
- children are susceptible to severe recurrent infections
- death within first year without stem cell transplant

44
Q

what is digeorge syndrom

A
  • deletion of chromosome 22
  • caused by congenital defects in thymic development -> deficient T cell maturation
  • infants are vulnerable to viral, fungal, protozoal infections
  • may include developmental malformation with prathyroid gland, heart defects, cleft palate, behavioral problems
45
Q

what are the features of Di george syndrom

A
  • cardiac abnormailty
  • abnormal facies
  • thymic aplasia
  • cleft palate
  • hypocalcemia
46
Q

what is hyper IGM syndrome

A
  • inability of T cells to activate b cells
  • production of normal to high levels of IgM antibody
  • decreased levels of IgG, IgA and IgE
  • recurrent pyogenic infections, susceptibility to pneumonia
47
Q

describe activation and class swtiching of B cells

A
  • APC presents antigen to T helper cells
  • B7 is expressed and interacts with CD28 activating T helper cells
  • activated Th cells interact with B cells via CD40 ligand, activating B cells to proliferate, differentiate, and secrete antibodies
  • th cells secrete cytokines that determine class switching
48
Q

what is leukocyte adhesion deficiencies (LADs)

A

defects in adhesion molecules, impair leukocyte recruitment to site of infection -> increased bacterial infections

49
Q

what is chediak higashi syndrome

A

defective phagocyte function due to impaired lysosomal trafficking -> recurrent infections

50
Q

what are the symptoms of chediak higashi

A
  • defective platelets- easy bruising
  • melanocyte abnormailities - albinism
  • nervous system abnormalities- peripheral nueropahty
51
Q

what is the most common defect in complement function

A

C2 deficiency- increased bacterial and viral infections

52
Q

when would secondary immunodeficiencies be encounters

A

cancer, diabetes, malnutrition, chronic infection, patients receiving chemo/radiation therapy, immunosuppresive meds

53
Q

describe AIDS

A
  • caused by HIV- SSRNA
  • 1981 first reported
  • > 80 million infection, >35 million deaths
54
Q

what is the transmission of AIDS

A
  • blood or body fluids
  • sexual contact
  • parenteral
  • perinatal
55
Q

what is the pathogenesis of AIDS/HIV

A
  • targets CD4+ T cells
  • viral RNA genome: reverse transcriptase transcribed into complementary DNA. integrates into host cell DNA
  • antibodies against HIV develop but not protective
  • HIV virus- cell death with subsequent release of the virus or latency
56
Q

what receptors and coreceptors does HIV bind to on CD4 cells

A
  • CXCR4 coreceptor
  • CD4 receptor
  • CCR5 coreceptor
57
Q

what is the life cycle of the HIV virus

A
  • binding
  • fusion
  • reverse transcription
  • integration
  • replication
  • assembly
  • budding
58
Q

what are the clinical features of AIDS/HIV

A
  • asymptomatic
  • acute retroviral syndrome
  • latency perios
59
Q

describe acute retroviral syndrome and how many patients experience it

A
  • 50-70%
  • generalized lymphadenopathy, sore throat, fever, rash, headahce, myalgia, arthralgia, diarrhea, photophobia, and peripheral neuropathies
  • oral changes are erythema and ulceration
  • viremia
60
Q

dscribe latency period of HIV

A
  • several months to 15 years
  • progression affected by patient age, host immune response, treatment
61
Q

how is AIDS diagnoses

A
  • CD4 T cell count declines: 200 cells/mm^3
  • CD4 T cell count < 14% total lymphocytes
    -AIDS defining condition
62
Q

what are aids defining conditions

A
  • candidiasis
  • lymphomas
  • weakened immune systems that cause opportunistic infections
63
Q

what are the HIV treatments

A

-anti retroviral therapy (ART)
- viremia declines

64
Q

what are the 6 broad categories of antiretroviral therapies

A
  • nucleoside reverse transcriptase inhibitors
  • nonnucleoside reverse transcriptase inhibitors
  • protease inhibitors
  • fusion inhibitors
  • integrase inhibitors
  • CCR5 inhibitors
65
Q
A

Pathology I (24 decks)

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