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Mechanisms of Disease Exam #2 > Pathology of Immunity (Part I) > Flashcards

Pathology of Immunity (Part I) Flashcards

1
Q

What are some examples of Pattern Recognition Receptors? (3)

A

TLRs
NOD-like receptors and inflammasome
C-type lectin receptors

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2
Q

What are the 2 generative organs and what do they produce?

A

Bone marrow - lymphocyte stem cells and B cell maturation.

Thymus - maturation of T cells.

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3
Q

What are the 3 peripheral organs/tissues and what happens there?

A

Lymph nodes - lymphocytes can interact w/ APCs and Ags in circulating lymph.

Spleen - lymphocytes can interact w/ blood-borne Ags.

MALT - allows lymphocytes and plasma cells to be in the vicinity of Ags within the mouth and GI tract.

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4
Q

What is contained within the medulla of the thymus? (3)

A

Maturing T cells
Dendritic APC w/ lots of MHC I and II.
Hassall corpuscles (squamous cell nests)

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5
Q

What is the path that immature T cells take from the bone marrow to the place of maturation?

A

Bone marrow -> peripheral cortex of the thymus -> central medulla of the thymus

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6
Q

Where do T and B cells predominate in the peripheral lymphatic organs?

A

T cells - paracortex

B cells - germinal centers

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7
Q

What occurs in the peripheral lymphatic organs? (3)

A

T and B cell clonal expansion.

B cell differentiation.

Migration of T cells and plasma cells out of lymph nodes and into circulation.

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8
Q

MHC I are on:

What do they recognize?

Ags are processed by:

What cells do they present to?

A

All nucleated cells.

Intracellular Ags (viral, tumors, etc.).

Proteasome.

CD8+ cells (cytotoxic).

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9
Q

MHC II are on:

What do they recognize?

Ags are processed by:

What cells do they present to?

A

APCs.

Extracellular Ags.

Endolysosomal enzymes.

CD4+ cells (helper T cells).

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10
Q

Which chromosome code for HLA molecular structure?

A

Chr 6

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11
Q

What is the significance of the extensive heterogeneity of HLA haplotypes?

What is the clinical importance?

A

Differences in fighting off illnesses.
Differences in allergic sensitivities.

Transplanted organs.
Associated AI diseases.

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12
Q

MHC I evoke ______ of ______ pathogens.

MHC II evoke a response to ______ pathogens by ________.

A

Killing of intracellular pathogens.

Extracellular pathogens by CD4+ recruitment of Mo and T cells.

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13
Q

Humoral immunity can be T cell dependent or T cell independent. T cell independent responses can use: (2)

A

Isotype switching

Increasing affinity

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14
Q

IgM (2)

A

First Ig produced.

Pentamer - huge!

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15
Q

IgG (2)

A

Longest half-life.

Important in fetal protection.

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16
Q

IgA (2)

A

Mucosal defense.

Present in high levels in colostrum.

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17
Q

IgE (3)

A

Shortest half life.
Regulates hypersensitivity reactions.
High affinity binding to FC receptor on MCs, basophils, eosinophils.

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18
Q

NK cells destroy: (2)

Do they have TCRs or Ig?

What turns them off?

A

Stressed or abnormal cells.

No.

MHC I class expression turns them off.

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19
Q

What activates NK cells?

What inhibits NK cells?

A

+ Damaged cells recognized by NKG2D receptors.

  • Self MHC molecules.
  • Class I MHC (on all nucleated cells).
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20
Q

BCRs and TCRs are products of:

A

Multiple germline and randomized somatic genetic programming.

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21
Q

What happens if a large population of cells w/ the exact same genes is identified? (3)

A

Abnormal clone
Neoplasia
Lymphoma

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22
Q

What is the “backstory” of type 1 hypersensitivity (what you do NOT see)? (5)

A
  1. DCs present to naive T cell.
  2. T cells differentiate to Th2 cells.
  3. B cells undergo class-switching to IgE.
  4. Interleukins get involved
    - IL-4: class switching, IL-5: eosinophil activation, IL-13: enhanced IgE production.
  5. MCs get prepared by binding IgE to their FceRI receptor.
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23
Q

What DO you see in a type 1 hypersensitivity? (4)

A

MC activation:

  • Degranulation: histamine release.
  • Lipid mediators: LTB4, LTC4, LTD4, PG D2, PAF.
  • Cytokines and chemokines: leukocyte recruitment (late phase).
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24
Q

Immediate vs. late reactions in type 1 hypersensitivity?

A

Immediate - MC mediators cause vasodilation, vascular leakage and SM spasm.

Late - inflammatory cells cause epithelial damage.

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25
Q

Eosinophilic esophagitis (3)

A

Food antigen-driven disease of childhood.
Recurrent dysphagia.
Weight loss - can’t swallow, hurts to swallow.

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26
Q

Type 2 hypersensitivity reactions can be due to: (2)

A

Autoantibodies

Exogenous antigens bound to cell surfaces.

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27
Q

What are the 3 mechanisms of type 2 hypersensitivity reactions?

A

Phagocytosis
Inflammation
Cellular dysfunction

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28
Q

Autoimmune hemolytic anemia
Target Ag:
Mechanism of disease:

A

Target Ag: RBC membrane proteins (Rh blood group Ags, I Ag).

Mechanism of disease: opsonization and phagocytosis of RBCs.

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29
Q

Autoimmune thrombocytopenia
Target Ag:
Mechanism of disease:

A

Target Ag: platelet membrane proteins (GpIIb: IIIa integrin).
Mechanism of disease: opsonization and phagocytosis of platelets.

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30
Q

What is unique about the basic mechanism of opsonization/phagocytosis in type 2 hypersensitivity reactions?

A

It does not require any cells (anemia, thrombocytopenia).

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31
Q

What is the mechanism of complement and Fc receptor-mediated inflammation in type 2 hypersensitivity reactions?

A

Damaged tissue allows for exposure of basement membrane.

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32
Q

What is Rheumatic Heart?

What sensitivity type?

A

AI dz of the heart.
Cross-reactive Abs that use molecular mimicry w/ streptococcal Ag and myocardial Ag.

Type 2.

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33
Q

What is the basic mechanism of antibody-mediated cellular dysfunction in type 2 reactions?

A

Dysfunction due to receptor blockage from disrupted endocrine or neural signaling.

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34
Q

Myastenia gravis
Target Ag:
Mechanism of disease:

A

Target Ag: Ach receptor.
Mechanism of disease: Ab inhibits binding of of ACh and down-regulated the receptors.

Type 2.

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35
Q

Graves disease
Target Ag:
Mechanism of disease:

A

Target Ag: TSH receptor.
Mechanism of disease: Ab-mediated stimulation of TSH receptors.

Type 2.

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36
Q

Insulin-resistant diabetes
Target Ag:
Mechanism of disease:

A

Target Ag: insulin receptor.

Mechanism of disease: Ab inhibits binding of insulin.

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37
Q

Serum sickness: acute and chronic types

Hypersensitivity type:

A

Acute form classically due to non-human protein Ag (diphtheria antitoxin).

Chronic form is from self-Ags (lupus, etc.).

Type 3.

38
Q

Arthus reaction

Hypersensitivity type:

A

Seen in rabbits injected w/ horse serum.
Rare local effect of vaccination.

Type 3.

39
Q

How does post-streptococcal cross-reactive Abs act at the heart versus the kidneys?

A

Heart - cross-reactive Abs directly act on myocardium -> type 2.
Kidneys - cross-reactive Abs are forming immune complexes that deposit in the glomeruli -> type 3.

40
Q

T1DM is what hypersensitivity?

A

Type 4.

41
Q

Examples of type 4 hypersensitivities (6)

A 
RA
MS
T1DM
IBD
Psoriasis
Contact dermatitis
42
Q

Tuberculin skin test (4 steps)

What does it indicate?

A

PPD is intradermally injected.
Reaction is reassessed 48-72 hrs later.
Sensitized T cells begin inflammatory response.
Local swelling results.

Indicates prior TB exposure.

43
Q

What happens to self-reactive T cells in the thymus?

What happens to self-reactive B cells in the bone marrow?

A

Apoptosis.

Can undergo receptor editing or apoptosis.

44
Q

What can happen to the T cells that are self-reactive in the periphery? (2)

A

Anergy

Suppression by Tregs.

45
Q

2 inhibitory receptors in T cells

What do they do?

Who takes advantage of this?

A

CTLA, PD-1.

Help T cells downregulate when self-Ags are presented.

Tumors and viruses can utilize this to evade immune destruction.

46
Q

How does blocking the action of CTLA and PD-1 w/ Abs affect cancer cells?

A

The immune response becomes amplified against the cancer cells.

47
Q

Most common Tregs are induced by:
Positive for:
Express: (2)

A

Induced by TGF-beta.
Positive for CD4.
Express CD25 and FOXP3*.

48
Q

What are 2 actions of Treg cells?

A 
Cytokine immunosuppression (IL-10, TGF-beta).
Inhibition by CTLA-4.
49
Q

How can Tregs suppress naive T cell activation?

A

They block and move B7 on APCs (which would bind CD28 on naive T cells)

50
Q

Mutations in the AIRE gene can lead to:

A

Polyendocrine disorders due to autoimmunity.

51
Q

IPEX can cause:

A

Systemic disease in humans

52
Q

3 characteristics of defining an autoimmune disease

A

The immune reaction is directed against a self-Ag.
The immune reaction is primarily responsible for a pathologic condition.
No other pathophysiology is responsible.

53
Q

Ankylosing spondylitis

What is it associated with?

A

Hereditary inflammatory condition of the joints of the spine.
Inflammation leads to degeneration and then fusion of the vertebrae.

Class I HLA allele B27, but it is not definitive of having or not having the disease.

54
Q

Crohn disease cause:

What does it lead to?

A

Polymorphisms in NOD-2 gene that renders Paneth cells in intestinal epithelium ineffective at micorbial killing.

Defective killing and clearance leads to accumulation of bacteria and an exaggerated immune response.

55
Q

What is the initial T cell response in Oral Lichen Planus? What is epitope spreading?

A

Initial T cell response leads to keratonic lesions in oral and conjunctival mucosa.

Epitope spreading occurs when the basement membrane disruption exposes antigenic proteins which leads to a secondary B cell response.

56
Q

ANA can be used to detect: (3)

What does its presence prompt?

A

Systemic lupus erythematosus (discoid lupus, drug-induced lupus).
Sjogren syndrome
Systemic sclerosis

More specific testing to confirm the diagnosis.

57
Q

What tests are most specific for people with lupus? (2)

A

Anti DS DNA

Anti Smith

58
Q

What tests are most specific for people with Sjogren’s? (2)

A

Anti Ro/SS-A

Anti La/SS-B

59
Q

What tests is most specific for people with systemic sclerosis? (1)

A

Anti DNA topoisomerase

60
Q

What are 3 genetic and environmental influences that degrade self-tolerance in SLE?

A

Genetic association: familial patterns, HLA-DQ.
Female bias: X chr.
UV light

61
Q

Immune cells/complexes involved in SLE (3)

A

B cells
CD4+ T cells
Immune complex formation

62
Q

To call it SLE, ___ characteristics of a list including which criteria? (11)

A

4.

Malar rash
Discoid rash
Photosensitivity
Oral ulcers
Arthritis
Serositis
Renal d/o
Neurological d/o
Hematologic d/o
Immunologic d/o
Antinuclear antibodies
63
Q

When should you suspect Lupus?

A

Younger females.

Arthritis, skin rahses, fevers, fatigue, hemolytic anemia, edema.

64
Q

What occurs first in Lupus Nephritis?

What happens last?

What is seen often as an end-stage process?

A

Minimal mesangial.

Sclerosing lupus nephritis.

Fibrosis.

65
Q

Diffuse Lupus Nephritis (class IV)

Sx:

The glomeruli show:

Type of hypersensitivity?

A

Most common pattern of lupus nephritis.

Pts are symptomatic (hematuria and proteinuria).

Glomeruli show increased cellularity.

  • proliferation of endothelial, mesangial and epithelial cells.
  • EM shows immune deposits in subendothelium.

Type 3, granular pattern of IgG Ab-containing complexes.

66
Q

What happens in the skin changes in SLE?

A

Basal layer degenerates leaving vacuolated spaces between degenerating cells.

Positive immunofluorescence.

67
Q

Libman-Sacks endocaditis

A

A CV complication from SLE.
Contains “verrucuos” (warty) valve deposits composed of fibrin.
Not infective.
Rarely embolize, but can happrn.

68
Q

What are 2 CV complications from SLE?

A

Libman-Sacks endocarditis

CAD

69
Q

What is an L-E cell?

A

A neutrophil or Mo that ingests the nucleus of a damaged cell.

Not used for DX anymore, but may be seen in blood or body fluids.

70
Q

Discoid lupus erythematosis includes what 3 characteristics?

A

Discoid rash
Positive ANA
Positive immunofluorescence

71
Q

Discoid lupus affects what area of body?

What tests are positive and negative?

What is possible from its onset?

A

Usually only affects face and scalp.

Positive ANA.
Negative Anti-DS DNA.

Progression is possible.

  • disseminated skin lesions.
  • systemic organ involvement (late occurrence)
72
Q

Drug-induced lupus (DIL) cause:

What meds? (2)

What is positive? (2)

Does it resolve?

A

Medication-induced breakdown of self-tolerance.

Procainamide, Hydralazine.

Positive ANA (arthralgias, fever), anti-histone Ab.

Yes, once the meds stop.

73
Q

HLA high-risk linkages in drug-induced lupus for Hydralazine and Procainamide

A

Hydralazine: HLA-DR4

Procainamide: HLA-DR6

74
Q

What happens in Sjogren syndrome (generally)?

A

Destruction of lacrimal and salivary gland tissue

75
Q

What is the pathogenesis of Sjogren syndrome?

A

B and T cell mediated inflammatory reaction to target tissues with inflammatory damage followed by fibrotic destruction.

76
Q

Major sx of Sjogren syndrome (3)

A

Dry eyes
Root caries
Smooth tongue w/ candida infection from dry mouth

77
Q

What test evaluates for tear production?

A

Schirmer’s test

78
Q

How is Sjogren syndrome diagnosed? (2)

A

Anti-Ro/SS-A and Anti-La/SS-B

Bx of lip to look for inflammation of minor salivary glands.

79
Q

What are some complications of Sjogren syndrome?

A

Extraglandular disease: pulmonary fibrosis.

Lymphoid proliferation becoming clonal: Lymphoma*

80
Q

What triggers the following pathways?

Alternate
Classical
Lectin

A

Alternate - microbe/pathogen
Classical - antibody
Lectin - mannose binding lectin (MBL)

81
Q

Roles of C3b and C5a/C3a

A

C3b: phagocytosis

C5a/C3a: inflammation

82
Q

Which cytokines are essential for class switching?

A

IL-4 and IFN-y

83
Q

Immediate response from PGD2 and LTB, C, D in allergy:

A

Bronchoconstriction
Increased bowel peristalsis
Vascular leakeage

84
Q

Role of the doctor after allergen is identified (2):

A

Block His and provide airway support

85
Q

Which hypersensitivities are insulin resistant DM vs T1DM?

A

Insulin resistant DM: type 2

T1DM: type 4

86
Q

Type 2 hypersensitivity

A

Abs react w/ Ags on cells or ECM

87
Q

Type 3 hypersensitivity

A

Ab-Ab complexes form and cause damage

88
Q

Fluoresence for type 2 vs type 3

A

Type 2 is smooth/liner

Type 3 is grainy/granular

89
Q

Hypersensitivity for Goodpasture syndrome

A

Type 2

90
Q

ANA patterns for:

SLE:
Centromere:
Systemic sclerosis:
Sjogren syndrome:

A

SLE: speckled, but can be homogenous, rim/peripheral or nuclear.
Centromere: CREST syndrome
Systemic sclerosis: speckled
Sjogren syndrome: speckled

Mechanisms of Disease Exam #2 (10 decks)

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