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review / wrong answers > DIT review - Immunology > Flashcards

DIT review - Immunology Flashcards

1
Q

What are the 3 functions of antibodies?

A

Opsonization, neutralization, complement activation

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2
Q

What holds the antibody structure together?

A

Disulfide bonds

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3
Q

What is the normal ratio of Lambda to Kappa immunoglobulin light chains?

A

K:L = 2:1

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4
Q

What is the mechanism behind antibody diversity?

A

V(D)J random recombination

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5
Q

What are the surface markers on T-cells

A

CD3, TCR, CD28, CD8 (cytotoxic), CD4 (helper), CD40L (helper)

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6
Q

What are the surface markers on B-cells

A

CD19, CD20, CD21, CD40, MHC II, B7, IgM, IgD

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7
Q

What are the surface markers on macrophages

A

CD14, CD40, MHC I, MHC II, B7

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8
Q

What are the surface markers on NK cells

A

CD16 (Binds to constant region of antibodies to antibody-dependent cell-mediated cytotoxicity - ADCC), CD56

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9
Q

Describe thymus-dependent vs. thymus-independent antigens

A

Thymus-independent antigens lack a peptide component and therefore cannot be presented by MHC to T-cells in order to create lasting immunity (e.g. LPS from gram - bacteria) Thymus-dependent antigens contain a peptide component so can be presented on MHC cells in order to create lasting immunity

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10
Q

What appears with apple green birefringence under Congo red stain?

A

Amyloid deposits

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11
Q

What disorder has anti-centromere antobodies?

A

Limited scleroderma (CREST syndrome - calcinosis, Ranyouds, Esophageal dysmotility, Sclerodactyly, Telangiectasia)

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12
Q

What disorder is associated with anti-desmoglein?

A

Pemphigus vulgaris

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13
Q

What auto-antibody is associated with bullous pemphigoid?

A

Anti-hemidesmosome

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14
Q

What antibodies are associated with SLE?

A

Antinuclear (ANA - nonspecific), anti-dsDNA, anti-Smith

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15
Q

What antibody is associated with drug-induced lupus?

A

Anti-histone

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16
Q

What disorder is associated with anti-Scl-70 (anti-DNA topoisomerase)

A

Diffuse scleroderma

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17
Q

What type of antibody is rheumatoid factor?

A

IgM against Fc portion of IgG

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18
Q

What antibodies are associated with Sjogren syndrome?

A

Anti-SSA, anti-SSB

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19
Q

What antibody is associated with polymyositis and dermatomyositis

A

Anti-Jo-1

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20
Q

What antibody is associated with mixed connective tissue disease?

A

Anti-U1 RNP (ribonucleotide protein)

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21
Q

What type of HSR is contact dermatitis?

A

HSR Type IV

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22
Q

What type of HSR is serum sickness?

A

Type III

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23
Q

What type of HSR is PPD test?

A

Type IV

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24
Q

What type of HSR is acute hemolytic transfusion reaction?

A

Type II

25
Q

What type os HSR is acute rheumatic fever?

A

Type II

26
Q

What type of HSR is rheumatoid arthritis?

A

Type III

27
Q

What type of HSR is SLE

A

Type III

28
Q

What complement factors are responsible for opsonization?

A

C3b

29
Q

What complement factors make up MAC?

A

C5b, C6, C7, C8, C9

30
Q

What complement factors are responsible for neutrophil chemotaxis?

A

C3a and C5a

31
Q

Describe the defect in hereditary angioedema

A

Deficiency in C1 esterase inhibitor, leading to overactivation of complement and increase in bradykinin

32
Q

Describe the defect in paraxoysmal nocturnal hemoglobinuria

A

Deficiency in GPI (protein that anchors DAF/CD55 to RBCs in order to protect from complement-mediated damage)

Leads to chronic intravascular hemolysis and thrombosis (platelets are also destroyed and release their contents, inducing thrombosis)

33
Q

Describe the different parts of the spleen and what cells are located in what parts

A

Red pulp: RBCs

White pulp:

Follicle - B-cells

PALS - T-cells

Marginal zone (between red and white pulp) = antigen presenting cells

34
Q

What is the function of interferons

A

Interferons are anti-viral cytokines

Glycoproteins synthesized by virus-infected cells that act locally on uninfected cells, “priming” them for viral defense by helping to selectively degrade viral nucleic acid and protein

35
Q

What are the factors that are chemotactic for neutrophils?

A

IL-8, C5a, and Leukotriene B4

36
Q

What is the funciton of IL-2?

A

Produced by T-cells in order to stimulate growth of more T-cells (helper, cytotoxic, regulatory) and NK cells

37
Q

What is the function of TNF-a

A

Secreted by macrophages

Mediates septic shock

Causes WBC recruitment

38
Q

What is the function of IL-8

A

Chemotaxis of neutrophils

39
Q

What is the function of IFN-y

A

Produced by Th1 cells

Stimulates macrophages to kill phagocytosed pathogens

40
Q

What is the function of IL-10

A

Secreted by Th2 cells

Inhibits macrophages and dendritic cells

41
Q

What are the different HSR involved in hyperacute, acute, and chronic transplant rejection

A

Hyperacute - Type II (preformed antibodies)

Acute - Type IV (cellular and humoral - but antibodies develop after transplant)

Chronic - Type II and IV

42
Q

What is graft-vs-host disease

A

Donor (foreign) bone marrow is transplanted into the patient, and then the donor cells begin to attack the host

Type IV HSR

Presents as: maculopapular rash, jaundice, diarrhea, hepatosplenomegaly

43
Q
  • Infliximab
A
  • TNF-a inhibitor
    • Recall: TNF-a is an acute phase reactant produced by activated macrophages to mediate inflammation by accelerating neutrophil migration, and facilitate lymphocyte proliferation; TNF-a is responsible for fever, anorexia, corticotropin releasing hormone, septic shot, and cachexia
  • Mechanism of action:
    • Is a monoclonal antibody to TNF-a
  • Uses:
    • Used for autoimmune conditions due to anti-inflammatory effect
    • Rheumatoid arthritis, psoriasis, ankylosing spondylitis
44
Q
  • Etanercept
A
  • TNF-a inhibitor
    • Recall: TNF-a is an acute phase reactant produced by activated macrophages to mediate inflammation by accelerating neutrophil migration, and facilitate lymphocyte proliferation; TNF-a is responsible for fever, anorexia, corticotropin releasing hormone, septic shot, and cachexia
  • Mechanism of action:
    • Mimics TNF-a receptor (aka it intercepts TNF-a before it can reach its target)
  • Uses:
    • Used for autoimmune conditions due to anti-inflammatory effect
    • Inflammatory bowel disease, rheumatoid arthritis, ankylosing spondylitis, psoriasis
45
Q
  • Cyclosporine
A
  • Immunosuppressant
    • Blocks lymphocyte activation and proliferation
  • MOA:
    • Binds cyclophilin (protein within cytosol of T-cells)
    • Inhibits calcineurin (which stimulates IL-2) à prevention of IL-2 transcription
  • Uses:
    • Transplant rejection
    • Psoriasis
    • Rheumatoid arthritis
  • Toxicity
    • Nephrotoxicity
46
Q
  • Tacrolimus
A
  • Immunosuppressant
    • Blocks lymphocyte activation and proliferation
  • MOA:
    • Binds FK506 binding protein
    • Inhibits calcineurin à prevention of IL-2 transcription
  • Uses:
    • Transplant rejection prophylaxis
47
Q

Sirolumus (aka Rapamycin)

A
  • Immunosuppressant
    • Blocks lymphocyte activation and proliferation
  • MOA:
    • Binds FKBp12 à inhibition of mTOR
    • Prevents response to IL-2
48
Q
  • Dacluzimab
A
  • Immunosuppressant
    • Blocks lymphocyte activation and proliferation
  • MOA:
    • Binds CD25 (IL-2 receptor) à preventing response to IL-2
49
Q
  • Azathioprine
A
  • Immunosuppressant
    • Blocks lymphocyte activation and proliferation
  • MOA:
    • Precursor of 6-mercaptopurine
    • Blocks nucleotide synthesis, thus preventing cells division and replication
  • Toxicity increased by allopurinol
    • 6-MP is degraded by xanthine oxidase and allopurinol blocks xanthine oxidase
50
Q
  • Mycophenolate mofetil
A
  • Immunosuppressant
    • Blocks lymphocyte activation and proliferation
  • MOA:
    • Inhibits IMP dehydrogenase à prevents synthesis of guanine
51
Q

What is a major cause of SCID

A

SCID = defect in early stem cell differentiation

Caused by adenosine deaminase deficiency (leads to increased dATP which is cytotoxic to lymphocytes)

52
Q

What are the two immunodeficiencies that present with an absent thymic shadow?

A

DiGeorge

SCID

53
Q

Describe Wiskott-Aldrich syndrome

A

XLR immunodeficieny - due to T cells unable to reorganize actin skeleton

WATER - Wiskott Aldrich, Thrombocytopenia, Eczema (especially truncal), Recurrent infections

54
Q

What is the cause and presentation of ataxia telangiectasia

A

Immunodeficiency - decreased T-cells and IgA

Defect in ATM gene - failure to repair DNA double strand breaks - cell cycle arrest

Triad: Cerebellar defects (ataxia), Spider angiomas (telangectasia), IgA deficiency

55
Q

Deficient enzyme in CGD

A

NADPH oxidase

56
Q

Presentation of Chediak Higashi syndrome

A

Remember that it is a defect in protein trafficking:

Recurrent infections

Partial albinism

Peripheral neuropathy

57
Q

Cause and presentation of Hyper-IgE (Job syndrome)

A

o Deficiency in IFN-y lead to impaired neutrophil recruitment

o Presentation à FATED

§ F – coarse Facies

§ A – Abscesses

§ T – retained primary Teeth

§ E – increased IgE (all other immunoglobulins are normal)

§ D – dermatologic problems (eczema)

58
Q

Cause and presentation of leukocyte adhesion deficiency

A

o Defect in integrin (CD18) leading to impaired neutrophil migration and chemotaxis

o Leads to recurrent bacterial infections and delayed separation of umbilical cord

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