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Infectious Disease (Phase II) > Immunology > Flashcards

Immunology Flashcards

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
Q

What type of hypersensitivity is Celiac disease?

A

IgA mediated

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26
Q

Difference between eradication and elimination?

A

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

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27
Q

Examples of live attenuated vaccines

A

MMR, VZV, yellow fever, rotavirus, intranasal influenza (all viral)

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28
Q

Examples of inactivated viral vaccines

A

Polio, hepatitis, rabies

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29
Q

Examples of inactivated fractional toxoid vaccines

A

Tetanus, diphtheria, pertussis

30
Q

Examples of inactivated fractional subunit vaccines

A

HPV, influenza, hep B, anthrax

31
Q

Examples of inactivated pure polysaccharide vaccines

A

Pneumococcal, meningococcal, Salmonella?

32
Q

Examples of inactivated conjugated polysaccharide vaccines

A

Pneumococcal, meningococcal, H influenzae

33
Q

What are adjuvants used for? What are some applications with respect to vaccines? What is the most commonly used adjuvant today?

A

Enhancing the immunogenicity of antigens; increased vaccine efficacy in an at-risk population, dose-sparing; Aluminum substances

34
Q

What effector mechanisms are triggered by vaccines?

A

Production of Ab, CD8+ cytotoxic T cells, CD4+ helper T cells (for cytokine production, CD8+ and B cell proliferation)

35
Q

Define concomitant immunity. What infection is this associated with historically? How does this related to cancer

A

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
Q

What type of mutations lead to tumor antigens?

A

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
Q

Types of tumor antigens recognized by the immune system

A

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
Q

5 ways cancer “evades” immune system

A

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
Q

“Most important type of immunotherapy for cancer?” Give examples.

A

T cell modifying Ab; anti-CTLA-4 Ab blocks CTLA-4 (“turns T cells back on”), anti-PD-1/PDL-1 activates CTLs

40
Q

3 most important warning signs of immunodeficiency

A

Failure to thrive, needing IV abs to clear infections, family history of immunodeficiencies

41
Q

What is by far the most common cause of immunodeficiencies?

A

Antibody deficiency or dysfunction

42
Q

Immunodeficiency affecting what cell type(s) would predispose someone to bacterial infections?

A

B cells, phagocytes, complement

43
Q

Immunodeficiency affecting what cell type(s) would predispose someone to viral infections?

A

B cells, T cells

44
Q

Immunodeficiency affecting what cell type(s) would predispose someone to infection by encapsulated bacteria?

A

Antibody deficiencies

45
Q

Immunodeficiency affecting what cell type(s) would predispose someone to fungal infections?

A

T cells, phagocytes

46
Q

Immunodeficiency affecting what cell type(s) would predispose someone to infection by intracellular pathogens?

A

T cells, macrophages

47
Q

What causes X-linked agammaglobulinemia? When do symptoms usually appear? What pathogens are associated?

A

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
Q

What is the most common immunodeficiency?

A

Selective IgA deficiency

49
Q

What causes Hyper-IgM? What are the symptoms? When do they usually present?

A

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
Q

Leukocyte Adhesion Deficiency cause and symptoms

A

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
Q

DiGeorge syndrome cause and clinical indications

A

22q11 deletion; thymus absent (no peripheral T cells), hypocalcemia (d/t parathyroid impariment), congenital heart defects (baby has murmur)

52
Q

Chronic Granulomatous Disease cause, symptoms, diagnosis and associated pathogens

A

Defect in NADPH oxidase compromises respiratory burst (H2O2 gone); Nitroblue tetrazolium test; Catalase-positive organisms (staph, Pseudomonas cepacia, Serratia marcescens, aspergillus, nocardia)

53
Q

SCID cause, clinical indications, testing and treatment

A

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
Q

What specific components of the immune system could be deficient in (recurrent) mycobacterium infections?

A

IFN-gamma receptor, IL-12/IL-12 receptor, T cells and macrophages

55
Q

Effect(s) of booster vaccines, generally

A

Stimulate clonal expansion AND affinity maturation

56
Q

Advantages and disadvantages of live attenuated vaccines

A

Provide cell-mediated and humoral immunity, but with risk to immunosuppressed or immunodeficient individuals

57
Q

Problems with vaccines

A

Inadvertent harm (e.g. oral polio, earlier rotavirus), ineffective (persistent infection resistant to clearance, rapidly mutating pathogen)

58
Q

Global immunosuppressant classes

A

Corticostreroids, inhibitors of T cell proliferation, inhibitors of T cell activation

59
Q

Immunosuppressant methods of treating asthma

A

Anti-IgE Ab, Anti-IL-5 Ab, desensitization (food, e.g. peanuts)

60
Q

How could juvenile arthritis be treated?

A

TNF inhibitors

61
Q

How could systemic juvenile arthritis be treated?

A

IL-1 or IL-6 inhibitors, blocking CD28 interaction with B7, blocking CD20 (blocking production of Ab)

62
Q

How are helminths used to treat Crohn’s disease?

A

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
Q

What type hypersensitivity reaction is primary (first-set) graft rejection?

A

Type IV hypersensitivity

64
Q

What type hypersensitivity reaction is secondary (second-set) graft rejection?

A

Type III hypersensitivity (“white graft”)

65
Q

What type hypersensitivity reaction is hyperacute transplant rejection? How quickly does it occur? What is the underlying mechanism?

A

Type II hypersensitivity reaction; minutes to hours; preformed humoral antibodies

66
Q

How quickly does accelerated transplant rejection occur? What is the underlying mechanism?

A

Days; reactivation of sensitized T cells

67
Q

What type hypersensitivity reaction is acute transplant rejection? How quickly does it occur? What is the underlying mechanism?

A

Type IV hypersensitivity reaction; weeks; primary activation of T cells

68
Q

What type hypersensitivity reaction is chronic transplant rejection? How quickly does it occur?

A

Type II, IV hypersensitivity reactions; months to years

69
Q

What allorecognition pathway leads to alloantibodies in chronic transplant rejection?

A

Indirect allorecognition

70
Q

What allorecognition pathway occurs in the initiation phase of GVHD?

A

Mainly direct allorecognition but also indirect allorecognition

Infectious Disease (Phase II) (2 decks)

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