Immunology Flashcards

(70 cards)

1
Q

What cytokine is primarily responsible for Th1 differentiation from Th0 cells?

A

IL-12

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2
Q

What cytokine is primarily responsible for Th2 differentiation from Th0 cells?

A

IL-4

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3
Q

Describe reciprocal inhibition

A

IL-10 from Th2 inhibits Th1 cell activity; IFN-gamma from Th1 inhibits Th2 activity

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4
Q

What is CD25?

A

Il-2 receptor

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5
Q

What does IPEX stand for? What causes it?

A

Immunodysregulation polyendocrinopathy enteropathy X-linked syndrome; dysfunction of transcription factor Foxp3 (necessary for Treg cell differentiation)

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6
Q

What MHC class do Treg cells bind in the thymus?

A

MHC II

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7
Q

How does antigen dose relate to immune system tolerance?

A

High dose leads to B and T cell tolerance (“exhaustion”), low dose leads to T cell tolerance, intermediate dose is immunogenic

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8
Q

Toleragenic and immunogenic routes of antigen administration

A

Toleragenic: IV and oral
Immunogenic: subcutaneous, IM, intradermal

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9
Q

Why are soluble antigens generally good toleragens?

A

They bypass antigen processing and fail to cross-link antigen receptors (indicated by “disaggregated,” “monomeric,” “incomplete”)

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10
Q

What does IL-2 do, broadly?

A

T cell activity

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11
Q

Type I (“insulin-dependent”) diabetes pathogenesis

A

Cell-mediated autoimmune disease: Mononuclear infiltrates incr. MHC I and II expression in pancreatic beta islet cells, leading to chronic inflammation (antigen presentation, cytokines, adhesion molecules)

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12
Q

Rheumatoid arthritis pathogenesis

A

Cell/antibody mediated: Mononuclear cell and PMN infiltrates in joints with immune complex deposition and complement activation

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13
Q

Pernicious anemia (autoimmune disease) pathogenesis

A

Antibody/cell mediated: AutoAb against parietal cells/intrinsic factor interfere with absorption of vitamin B12

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14
Q

SLE pathogenesis

A

Antibody mediated: UV light causes thymidine dimers in DNA, which are recognized as foreign and lead to autoantibodies against nuclear material

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15
Q

What types of infections generally are evident in patients with defects in T cells or phagocytes?

A

Disseminated candidiasis

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16
Q

An increase in the relative risk of autoimmune disease is most often associated with the expression of what types of HLA genes?

A

HLA class II genes

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17
Q

Pathogens associated with Th2 inflammation?

A

Helminths, mites, ticks

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18
Q

Pathogens associated with Th1 inflammation

A

Viral infections

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19
Q

Pathogens associated with Th17 inflammation

A

Bacterial/autoimmunity

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20
Q

Where is CD40 found? What happens when it is activated?

A

B cells; 3 things - “affinity maturation” (B cells with highest specificity receptors preferentially reproduce), class switching, production of memory B cells

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21
Q

Basophil function, generally

A

“Back up” mast cells

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22
Q

Mediators of type I hypersensitivity reactions

A
Recall: IgE, mast cell, histamine
New: PGD2 (chemotaxis for each granulocyte, Th2 chemotaxis), LTC4, IL-4 (Th2 promotion, class switching in B cells, up regulates MHC II), TNF
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23
Q

What causes the itch scratch reflex? When is this beneficial?

A

Mast cells release histamine, which binds to venue receptors to cause swelling and C-fiber receptors (mechanosensitive) to cause pain and itch; e.g. Lyme disease, because the tick takes 24 hrs to engorge

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24
Q

What type of hypersensitivity is serum sickness?

A

Type III hypersensitivity

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25
What type of hypersensitivity is Celiac disease?
IgA mediated
26
Difference between eradication and elimination?
Eradication refers to the reduction to zero new cases of a disease worldwide; elimination refers to the reduction to zero or very few cases of a disease in a defined geographic area
27
Examples of live attenuated vaccines
MMR, VZV, yellow fever, rotavirus, intranasal influenza (all viral)
28
Examples of inactivated viral vaccines
Polio, hepatitis, rabies
29
Examples of inactivated fractional toxoid vaccines
Tetanus, diphtheria, pertussis
30
Examples of inactivated fractional subunit vaccines
HPV, influenza, hep B, anthrax
31
Examples of inactivated pure polysaccharide vaccines
Pneumococcal, meningococcal, Salmonella?
32
Examples of inactivated conjugated polysaccharide vaccines
Pneumococcal, meningococcal, H influenzae
33
What are adjuvants used for? What are some applications with respect to vaccines? What is the most commonly used adjuvant today?
Enhancing the immunogenicity of antigens; increased vaccine efficacy in an at-risk population, dose-sparing; Aluminum substances
34
What effector mechanisms are triggered by vaccines?
Production of Ab, CD8+ cytotoxic T cells, CD4+ helper T cells (for cytokine production, CD8+ and B cell proliferation)
35
Define concomitant immunity. What infection is this associated with historically? How does this related to cancer
Immune response to antigen in one part of the body prevents antigen presentation in a another part of the body; Leishmania (parasite); this is one reason why cancer won't metastasize early on (initial tumor prevents other tumors)
36
What type of mutations lead to tumor antigens?
Point mutation allows binding of new peptide to MHC class I; point mutation in self-peptide creates new epitope for recognition by T cells
37
Types of tumor antigens recognized by the immune system
Product of oncogene or mutated tumor suppressor gene; mutated self-protein (tumor specific); over expression or aberrant expression of self-protein (tumor associated); oncogenic viruses
38
5 ways cancer "evades" immune system
Low/no immunogenicity; lack of co-stimulation leads to tumor antigens treated as self; antibody-mediated endocytosis selects for tumor cells without antigen; tumor-induced suppression (cytokines); tumor-induced privileged site
39
"Most important type of immunotherapy for cancer?" Give examples.
T cell modifying Ab; anti-CTLA-4 Ab blocks CTLA-4 ("turns T cells back on"), anti-PD-1/PDL-1 activates CTLs
40
3 most important warning signs of immunodeficiency
Failure to thrive, needing IV abs to clear infections, family history of immunodeficiencies
41
What is by far the most common cause of immunodeficiencies?
Antibody deficiency or dysfunction
42
Immunodeficiency affecting what cell type(s) would predispose someone to bacterial infections?
B cells, phagocytes, complement
43
Immunodeficiency affecting what cell type(s) would predispose someone to viral infections?
B cells, T cells
44
Immunodeficiency affecting what cell type(s) would predispose someone to infection by encapsulated bacteria?
Antibody deficiencies
45
Immunodeficiency affecting what cell type(s) would predispose someone to fungal infections?
T cells, phagocytes
46
Immunodeficiency affecting what cell type(s) would predispose someone to infection by intracellular pathogens?
T cells, macrophages
47
What causes X-linked agammaglobulinemia? When do symptoms usually appear? What pathogens are associated?
Defect in Bruton's Tyrosine Kinase causes an issue with pre-B cell differentiation, leading to an absence of mature B cells (all Ig's reduced); 4-6 months (maternal IgG wanes); Enterovirus and giardiasis
48
What is the most common immunodeficiency?
Selective IgA deficiency
49
What causes Hyper-IgM? What are the symptoms? When do they usually present?
Defect in CD40 ligand compromises interaction of CD4+ T cells with B cells, thus no isotype class switching can occur; Oral ulcers, bacterial infections (especially Pneumocystis carnii); Pre-school aged boys (X-linked)
50
Leukocyte Adhesion Deficiency cause and symptoms
Defect in CD18 subunit of several adhesion molecules (LFA-1, CR3, CR4); delayed separation of umbilical cord, recurrent bacterial infections (esp periodontal ulcers) without pus formation in spite of high WBCs
51
DiGeorge syndrome cause and clinical indications
22q11 deletion; thymus absent (no peripheral T cells), hypocalcemia (d/t parathyroid impariment), congenital heart defects (baby has murmur)
52
Chronic Granulomatous Disease cause, symptoms, diagnosis and associated pathogens
Defect in NADPH oxidase compromises respiratory burst (H2O2 gone); Nitroblue tetrazolium test; Catalase-positive organisms (staph, Pseudomonas cepacia, Serratia marcescens, aspergillus, nocardia)
53
SCID cause, clinical indications, testing and treatment
Gamma chain defect (most common) or ADA deficiency; low T and B cells (no Ig's), candida infections; T cell Receptor Excision Circles (will be low in T cell lymphocytopenia); bone marrow transplant only long term option
54
What specific components of the immune system could be deficient in (recurrent) mycobacterium infections?
IFN-gamma receptor, IL-12/IL-12 receptor, T cells and macrophages
55
Effect(s) of booster vaccines, generally
Stimulate clonal expansion AND affinity maturation
56
Advantages and disadvantages of live attenuated vaccines
Provide cell-mediated and humoral immunity, but with risk to immunosuppressed or immunodeficient individuals
57
Problems with vaccines
Inadvertent harm (e.g. oral polio, earlier rotavirus), ineffective (persistent infection resistant to clearance, rapidly mutating pathogen)
58
Global immunosuppressant classes
Corticostreroids, inhibitors of T cell proliferation, inhibitors of T cell activation
59
Immunosuppressant methods of treating asthma
Anti-IgE Ab, Anti-IL-5 Ab, desensitization (food, e.g. peanuts)
60
How could juvenile arthritis be treated?
TNF inhibitors
61
How could systemic juvenile arthritis be treated?
IL-1 or IL-6 inhibitors, blocking CD28 interaction with B7, blocking CD20 (blocking production of Ab)
62
How are helminths used to treat Crohn's disease?
T cell infiltrates in intestinal mucosa part of Crohn's, and Trichiursuis suis induces Treg cells in colon (infection cleared by the body in a few weeks)
63
What type hypersensitivity reaction is primary (first-set) graft rejection?
Type IV hypersensitivity
64
What type hypersensitivity reaction is secondary (second-set) graft rejection?
Type III hypersensitivity ("white graft")
65
What type hypersensitivity reaction is hyperacute transplant rejection? How quickly does it occur? What is the underlying mechanism?
Type II hypersensitivity reaction; minutes to hours; preformed humoral antibodies
66
How quickly does accelerated transplant rejection occur? What is the underlying mechanism?
Days; reactivation of sensitized T cells
67
What type hypersensitivity reaction is acute transplant rejection? How quickly does it occur? What is the underlying mechanism?
Type IV hypersensitivity reaction; weeks; primary activation of T cells
68
What type hypersensitivity reaction is chronic transplant rejection? How quickly does it occur?
Type II, IV hypersensitivity reactions; months to years
69
What allorecognition pathway leads to alloantibodies in chronic transplant rejection?
Indirect allorecognition
70
What allorecognition pathway occurs in the initiation phase of GVHD?
Mainly direct allorecognition but also indirect allorecognition