immunity part 2 Flashcards
1
Q
immune system dysfunctions:
1
2
3
A
hypersensitivity
autoimmune diseases
immune deficiency diseases
2
Q
lack of response to antigens that is induced by exposure of lymphocytes to these antigens
A
immunologic tolerance
3
Q
ability to discriminate between self and nonself antigens
A
immunologic tolerance
4
Q
if immunologic tolerance fails->
A
autoimmunity
5
Q
with immunologic tolerance:
normally, microbes are immunogenic[cause immune response], and self-antigens are
A
tolerogenic[do not cause immune response]
6
Q
developing lymphocytes encounter self antigens in central lymphoid organs(bone marrow)
A
central tolerance
7
Q
mature lymphocytes encounter self antigens in peripheral tissues (secondary lymphoid organs)
A
peripheral tolerance
8
Q
central t cell tolerance normally deals with
A
cd4 t cells
9
Q
central t cell tolerance->
self reactive tcells:
A
- negative selection or deletion
- development of regulatory t cells
10
Q
peripheral t cell tolerance 3 ways
A
- regulatory t cells
- anergy
- deletion
11
Q
blocks the activation of self-reactive lymphocytes
A
regulatory t cells
12
Q
functional inactivation of t cells (lack of costimulation)
A
anergy
13
Q
apoptosis of self-reactive lymphocytes
A
deletion
14
Q
self polysaccharides, lipids, and nucleic acids: induce tolerance in
A
b cells
15
Q
two types of cell tolerance in b cells
A
- central b cell tolerance
- peripheral b cell tolerance
16
Q
-receptor editing
-negative selection (apoptosis)
what type of b cell tolerance is this
A
central b cell tolerance
17
Q
-anergy
-excluded from lymphoid follicles
what type of b cell tolerance is this
A
peripheral b cell tolerance
18
Q
immune response against self antigens
A
autoimmunity
19
Q
the development of autoimmunity may be related to
A
- inheritance of susceptibility genes
- environmental triggers
20
Q
must autoimmune diseases are
A
polygenic
21
Q
autoimmune diseases often associate with particular HLA(MHC) genes that are inefficient at displaying self antigens:
A
- defective t cell negative selection
- may fail to stimulate regulatory t cells
22
Q
infections may activate self-reactive lymphocytes in autoimmunity by:
A
- increased production of costimulatory molecules on APCs
- molecular mimicry
23
Q
injurious or pathologic immune reactions
-immune response may be inadequately controlled
-directed against normal harmless antigens
A
hypersensitivity
24
Q
what 3 things causes hypersensitivity
A
- autoimmunity :reactions against self antigens (failure of self-tolerance)
- reactions against microbes: excessive reactions or unusually persistent microbes
- reactions against environment: common allergens (pollen)
25
types of hypersensitivity
type I: immediate
type II: antibody-mediated
type III: immune complex-mediated
type IV: cell mediated (with t cells)
26
which types of hypersensitivity
-tissue reaction that occurs rapidly after interaction of antigen with IgE antibody bound to mast cell
-often developed in atopic individuals- sensitized to allergens
-environmental and food allergens
mild to severe reaction (asthma example)
type I
27
mediators that are released by mast cells after activation for type 1 immediate hypersensitivity:
1
2
3
1. vasoactive amines
2. lipid mediators
3. cyotkines
28
causes vasodilation, increased vascular permeability, smooth muscle contraction, and increased secretion of mucus
histamine-> vasoactive amines
[mediator for type I]
29
smooth muscle contraction, vascular permeability
prostaglandins + leukotrienes-> lipid mediators for type I
30
TNF, chemokines, IL-4, IL-5
cytokine mediator for type I
31
anaphlyaxis, bronchial asthma, allergic, rhinitis, sinusitis(hay fever), food allergies
type I
32
development of allergies?
1. susceptibility is genetically determined
2. atopic individuals: 50% have family history of allergy, more TH2 cells, higher serum IgE
3. environmental factors: pollution, infections
33
1. caused by antibodies directed against target antigens on cell surfaces
-target cells for phagocytosis
-activate complement system
-interfere with normal cellular functions
which type of hypersens.
type II: antibody-mediated diseases
34
1. in type II hypersens, cells may be opsonized(coated) by autoantibodies which targets these cells for
phagocytosis
-induces phagocytosis by neutrophils, macrophages
35
2. in type II hypersens, antibodies activate the complement system which _____________=triggers inflammation
recruits neutrophils, macrophages
which then triggers inflammation
36
3. in type II hypersens, antibody-mediated cellular dysfunction ->
impair or dysregulates important functions
37
1. autoimmune hemolytic anemia
2. autoimmune thrombocytopenic purpura
3. pephigus vulgaris
4. vasculitis caused by ANCA
5. goodpasture syndrome
6. acute rheumatic fever
7. myasthenia gravis
8. graves disease
9. pernicious anemia
types of type II hypersens
38
-antigen-antibody complex formed (immune complexes)
-deposit in blood vessels-> complement activation and acute inflammation
-antigen may be foreign protein or endogenous (autoimmunity)
-soluble antigens!!!!!!!!!
type III hypersens: immune complex mediated diseases
39
type III immune complex mediated diseases mechanism:
1. formation of immune complexes
2. deposition of immune complexes
3. inflammation and tissue injury
40
antibodies secreted in blood- react with antigen- form antigen-antibody complexes
formation of immune complexes in type III
41
circulating antigen-antibody complexes deposited in tissues
deposition of immune complexes in type III hypersens
42
once deposited, immune complexes initiate inflammation via complement or engagement of leukocytes
inflammation and tissue injury in type III hypersens
43
1. systemic lupus erythematosus
2. poststreptococcal glomerulonephritis
3. polyarteritis nodosa
4. reactive arthritis
5. serum sickness
6. arthus reaction!!!!!!!!
type III hypersens
44
-cd4 t cells: cytokine mediated inflammation
-cd8 t cells: direct cell cytotoxicity
-many chronic inflammatory diseases are t cell mediated
type IV: cell mediated disease
45
1. cytokines produced induce inflammation-> tissue destruction
2. delayed-type hypersens: occurs 48-72 hours after subsequent antigen
3. most reactions are TH1 mediated, some Th17
type IV: CD4 t cell mediated
46
CD8 t cells kill antigen-expressing target cells
-effective in virus-infected cells
type IV CD8 t cell
47
poison ivy= lesion
type IV examples
48
1. rheumatoid arthritis
2. multiple sclerosis
3. type I diabetes!!!!
4. inflammatory bowel disease
5. psoriasis
6. contact sens. (like poison ivy)
type IV
49
immunodeficiency syndromes can either be primary(congenital) or secondary (acquired):
primary: inherited genetic disorders
secondary: acquired after challenge to immune system such as cancer or environmental factors
50
clinically manifested by increased infections
immunodeficiency syndromes
51
-may affect innate or adaptive immunity
-usually detected in infancy
-most involved disorders of B and T lymphocytes
primary immunodeficiencies
52
encompasses 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 transplantation
severe combined immunodeficiency (SCID)
53
-deletion on chromosome 22
-caused by congenital defect in thymic development-> deficient t cell maturation
-infants are especially vulnerable to viral, fungal, protozoal infections
-also may include development malformation with parathyroid gland, heart defects, cleft palate, behavioral problems
digeorge syndrome
54
CATCH 22
Cardiac abnormality
Abnormal facies
Thymic aplasia
Cleft palate
Hypocalcemia/Hypoparathyroidism
for digeorge syndrome
55
-inability of t cells to activate b cells
-production of normal to high levels of IgM antibody!!
-decreased levels: IgG, IgA, IgE!!
-recurrent pyogenic infections, susceptibility to pneumonia
hyper-IgM syndrome
56
two examples of defects in innate immunity that may affect leukocyte function:
1. leukocyte adhesion deficiencies (LADs)
2. Chediak-Higashi syndrome
57
defects in adhesion molecules, impair leukocyte recruitment to site of infection -> increased bacterial infections
leukocyte adhesion deficiencies LADs
(defect in innate immunity)
58
defective phagocyte function due to impaired lysosomal trafficking-> recurrent infections
Chediak-Higashi syndrome
(defect in innate immunity)
59
dchediak-higashi syndrome causes:
1. defective platelets- easy bruising
2. melanocyte abnormalities- albinisim
3. nervous system abnormalities- peripheral neuropathy
60
defects in innate immunity also affect the complement system:
C2 deficiency is the most common- increased bacterial and viral infections
61
may be encountered in individuals with cancer, diabetes, malnutrition, chronic infection, patients receiving chemo/radiation therapy, immunosuppressive medications
-more common than primary immunodeficiencies
secondary immunodeficiencies
62
caused by human immunodeficiency virus (HIV)- SSRNA
transmission by blood or body fluids by sexual contact, parental, perinatal
AIDS
acquired immunodeficiency syndrome
63
what is the primary target for HIV
CD4 helper t cells
64
has a viral RNA genome
-reverse transcribed into complementary DNA
-integrates into host cell DNA
HIV/AIDS
65
are there antibodies against HIV?
yes developed but not protective
66
AIDS/HIV life cycle steps:
1. binding
2. fusion (to cd4 cell)
3. reverse transcription
4. integration
5. replication
6. assembly
7. budding
67
AIDS/HIV clinical features
1. asymptomatic
2. acute retroviral syndrome: 50-70%
-1-6 weeks after exposure
-sore throat, fever, rash, headache, diarrhea
-oral changes like erythema and ulcerations(candidiasis)
-viremia
3. latency period
-several months to 15 years
-progression affected by patient age, host immune response, treatment
68
AIDS diagnosis
1. CD4 t cell count declines to 200 cells/nm
2. CD4 t cell count <14% total lymphocyte
69
HIV treatment
1. anti-retroviral therapy (ART): administered in combination to reduce viral resistance
-viremia declines: reduction in risk for transition to AIDS, death, transmission
70
