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Tolerance & Autoimmunity Flashcards

1
Q

what is tolerance induction?
how is tolerance induction conducted by the immune system?

A
  • tolerance induction: induces tolerance to self antigens to prevent autoimmunity. done by two primary methods
    • clonal deletion: central tolerance
      • self reactive T and B lymphocytes are killed by apoptosis in the bone marrow & thymus
    • anergy: peripheral tolerance
      • self reactive lymphocytes are alive but cannot respond to antigen (via Treg)
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2
Q

what is auto-immunity?

A
  • failure of tolerance induction d/t
    • failure to delete T and B cell cells in bone marrow thymus (central tolerance)
    • reactivation of previously anergic T and B cells (peripheral tolerance)
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3
Q
  • what is the means by which central T-cell tolerance in induced?
    • outline the steps of this process
A

central T-cell tolerance = T-cell education: T-cells are selected for in the thymus in four main phases.

  • double negative T-cells
    • cells have neither CD4 nor CD8
    • in subscapular region (outer cortex) of thymus
  • double positive T-cells
    • in the cortex of the thymus:
      • adopt TCR + CD3 + CD4 + CD8
      • undergo-positive selection:
        • exposed to self MHC-I & MCH-II by cortical epithelial cells → those that show moderate affinity advance
    • at the corticomedullary junction
      • undergo 1st round of negative selection
        • exposed to thymic self antigen by IDCS
  • single positive T-cells
    • in the medulla
      • undergo 2nd round of negative selection
        • exposed to non-thymic self antigens by medullary epithelial cells
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4
Q

double negative T-cells

  • found where in the thymus?
  • have what features / undergo what changes
A
  • in subscapular region (outer cortex) of thymus
  • have neither CD4 or CD8
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5
Q

double positive T-cells

  • found where in the thymus?
  • have what features / undergo what changes
A
  • first seen in the cortex of the thymus:
    • adopt TCR + CD3 + CD4 + CD8 markers
    • undergo positive selection (in cortex) → 1st round of negative selection (corticomedullary junction)
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6
Q

positive selection

  • occurs where?
  • involves which cell types?
  • involves what steps?
A
  • in the cortex
  • to DP T-cells, by cortical epithelial cells
    • DP cells exposed to self MHC-I & MCH-II by cortical epithelial cells →
      • those that show MODERATE AFFINITY → advance (“positively selected”
      • those that show too high / too low affinity → apoptosis
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7
Q

negative selection

  • occurs where?
  • to which cell types?
  • involves what steps?
A

occurs in two phases

  • 1st phase
    • in the corticomedullary junction
    • to DP T-cells cells by interdigitating dendritic cells (IDCs)
      • IDCs expose DPs to THYMIC SELF ANTIGENS
  • 2nd phase
    • in the medulla
    • to single positive T-cells by medullary epithelial cells
      • medullary epithelial cells, under regulation of AIRE transcription, expose cells to NON-THYMIC SELF ANTIGEN

cells that do not recognize thymic or non thymic self antigen → leave thymus and populate peripheral lymphoid organs

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8
Q

AIRE transcription regulator- what is its role & clinical significance?

A
  • role: regulates the second round of negative selection, wherein medullary epithelial cells expose single positive cells to non-thymic self antigens
    • clinical significance: a defect in the AIRE gene results in APS (autoimmune polyendocrine syndrome-1)
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9
Q

what is the role of each of these cells in the central tolerance induction of T-cells?

  • cortical epithelial cells
  • interdigitating dendritic cells (IDCs)
  • medullary epithelial cells
A
  • cortical epithelial cells - positive selection: exposes DPs to MHC-I & MCH-II
  • interdigitating dendritic cells (IDCs) - negative selection: expose DPs to thymic self antigen
  • medullary epithelial cells - negative selection: expose SPs to non-thymic self antigen
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10
Q

discuss the mechanism of peripheral T-cell tolerance

A

= anergy: suppression of T-cells that reacted to self antigen but still made it thru T-cell education

  • conducted by T-reg cells
    • that detect self reactive T-cells via detecting T-cells that react with APCs without a B7 receptor - i.e., host cells
    • then release IL-10 & TGF-B → suppression of T-cell
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11
Q

what is the means by which central B-cell tolerance is induced?

A
  • occurs the bone marrow
    • immature B-cells (IgM + and IgD -) are presented with self antigen by stromal cells
    • those that interact with self antigen → deleted
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12
Q

what are the means of peripheral tolerance induction to B-cells?

A
  • anergy: immature B-cells that react to soluble self antigen but made it through negative selection in bone marrow are made unreactive
  • receptor editing: RAG genes reactivated and B-cell antibodies specificity are changed from self → non self reactive
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13
Q

what are the immunologically privileged sites? what does this mean?

A

T-cell x tissue interactions don’t occur in these sites because they are inhibited by a blood-tissue barrier

  • brain
  • anterior chamber of eye
  • placenta / pregnancy uterus
  • testis
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14
Q

T-reg cells

  • have what markers?
  • secrete what cytokines?
  • have what role (s)?
A
  • CD4, CD25, FoxP3
  • secrete IL-10, TGF-B
  • role: conduct peripheral T-cell anergy to → prevent autoimmunity
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15
Q

autoimmune polyendocrine syndrome - 1

  • pathogenesis
  • presentation
A
  • d/t defect in AIRE gene: regulates negative selection (exposure of T-cells to non-thymic self antigens by medullary epithelial cells)
  • clinical presentation
    • mucocutaneous candidasis
    • hypoparathyroidism / thyroiditis
    • type I DM
    • ovarian failure
    • alopecia
    • vitiligo
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16
Q

IPEX

  • pathogenesis
  • presentation
A

= immunodysregulation, polyendocrinopathy, and enteropathy X-linked (autoimmune disease)

  • pathogenesis: mutation of Foxp3 gene (codes for FoxP3 marker on T-reg cell)
  • presentation
    • classic triad = enteropathy + endocrinopathy + dermatitis
      • enteropathy: severe diarrhea
      • endocrinopathy: TIDM, thyroiditis
      • dermatitis - eczema, psoriasis
    • bullous phempigoid
    • high IgE
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17
Q

induction of auto-immunity is influenced by..?

A
  • inheritance of HLA genes (B27, DR2, DR3, DR4)
  • environmental: molecular mimicry
  • physical trauma that breaks immunological privileges
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18
Q

HLA-B27 is associated with development of what autoimmune diseases?

A
  • psoroiasis
  • ankylosing spondylitis
  • IBD: crohns, UC
  • reiter’s syndrome

“PAIR”

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19
Q

HLA-DR2 is associated with development of what auto-immune diseases?

A
  • MS (type IV)
  • SLE (type III)
  • goodpasture (type II)
  • hay fever / allergic rhinitis (type 1)
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20
Q

HLA-DR3 & DR4 are associated with what autoimmune diseases?

A
  • both HLA-DR3/DR4: T1DM
  • HLA-DR4: rheumatoid arthritis
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21
Q

what autoimmune disease is an example of molecular mimicry?

A
  • rheumatic fever following s. pyogenes infection (IgG/IgM made against cardiac myosin that resembles M-protein - Type II hypersensitivity)
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22
Q

what is an example of autoimmunity to trauma?

A
  • sympathetic ophthalmia - antigens released from (anterior chamber of eye) - reacts with T-cells who have never been exposed to them
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23
Q

pernicious anemia

  • molecular target
  • organ target
  • hypersensitivity type
A
  • molecular target: intrinsic factor / parietal cells
  • organ target: stomach
  • hypersensitivity type II
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24
Q

pernicious anemia - mechanism

A
  • Abs made against intrinsic factor / parietal cells (parietal cells produce intrinsic factor). this leads to
    • megoblastic anemia
      • intrinsic factor needed for Vit B12 → Vit B12 malabsorption → dysfunctional RBC production
    • chronic hylicobacter pylori infection
      • parietal cell destruction → achlorhydria → infection
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25
Q

pernicious anemia - clinical presentation

A
  • class triad
    • weakness
    • paresthesia
    • tongue - sore, beefy red
  • “megoblastic madness”
    • delusions / paranoia
  • ataxia
  • chronic H. pylori infections
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26
Q

pernicious anemia - diagnosis

A
  • presence of Abs to intrinsic factor
  • gastric gland atrophy
  • achlorydia
  • abnormal RBCs
    • megoblastic RBCs
    • oval macrocytic RBCs
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27
Q
A

presence of oval macrocytic RBCs

pernicious anemia (autoimmune, type II)

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28
Q
A

megoblastic RBCs

pernicious anemia (autoimmune, type II)

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29
Q
A

Abs to parietal cells

pernicious anemia (type II,

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30
Q
A

sore tongue

  • part of pernicious anemia triad
    • weakness
    • paresthesia
    • sore tongue
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31
Q

pernicious anemia - tx

A

Vitamin B12 (cobalamin)

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32
Q

good-pasture syndrome

  • molecular target
  • organ target
  • hypersensitivity type
A
  • molecular: type IV collagen in basement membrane
  • organ: lungs, kidneys
  • hypersensitivity Type II
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33
Q

good-pasture syndrome - mechanism

A
  • type II sensitivity → smoking / solvent in the context of HLA-DR → Abs made against type IV collagen in the basement membrane of
    • lungs → pulmonary hemorrhage
    • kidneys → glomerulonephritis
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34
Q

good pasture syndrome - presentation

A

main manifestations are

  • lungs → pulmonary hemorrhage
    • dyspnea + cough
    • chest pain
    • worse case: respiratory failure → death
  • kidneys → glomerulonephritis
    • dysfunction of nephron leads to
      • HTN
      • edema
      • hematuria
      • proteinuria
    • worst case: ESRD
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35
Q

good-pasture syndrome - diagnosis

A
  • CXR: lung consolidations
  • kidney defects:
    • inc BUN & creatinine
    • hematuria, proteinuria
  • immune:
    • circulating anti-GDM antibodies
      • form linear bands
      • are “ribbon like”
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36
Q

what immunological findings in the blood help dx good-pastures?

A
  • circulating anti-GBM antibodies
    • linear bands → look “ribbon like”
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37
Q

what is the m/c cause of death in good-pastures syndrome?

A

pulmonary hemorrhage → respiratory failure → death

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38
Q
A
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39
Q

tx of good-pasture syndrome?

A
  • acute phase tx
    • intubation / assisted ventilation
    • hemodialysis
  • long term tx
    • pharmaceutical
      • plasmapheresis → removes Abs
      • immunosuppression
        • corticosteroids
        • cyclophosphamide
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40
Q

Type I DM

  • molecular target
  • organ target
  • hypersensitivity type
A
  • molecular target: beta cells
  • organ target: pancreas
  • hypersensitivity type IV
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41
Q

type I DM mechanism

A
  • autoimmune cell mediated killing of beta cells (Type IV)
    • viral infection (possibly Cocksackie virus) has “molecular mimicry” with GAD45 receptor on B-cell
      • Th1 vs Treg “fight” over GAD45 on B-cell
        • If Treg wins: IL-10/TGF-B made → anergy of T-cells
        • if Th1 wins: INF-y → Tc activated → kill host B-cells:
          • Tc bind:
            • IGRP
            • Fas

often occurs in the context of HLA-DR3/DR4

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42
Q

T1DM - presentation

A
  • juvenile onset
  • THIN
  • hyperglycemia:
    • → polydipsia, polyuria
    • → ketoacidosis
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43
Q

myasthenia gravis

  • molecular target
  • organ target
  • what type hypersensitivity
A
  • molecular target: AChR
  • organ target: skeletal muscle
  • type II hypersensitivity
44
Q

myasthenia gravis - presentation

A
  • muscle weakness that
    • affects one muscle in particular
    • is worse in the pm
    • results in
      • eye defects:
        • ptosis
        • incomplete closure
        • diplopia
        • limited adduction
      • difficulty chewing / swallowing
45
Q

neonatal myasthenia

  • mechanism
  • presentation
A
  • passively transferred anti-AChR IgG
  • presenattion - general weakness
46
Q

addison’s disease

  • molecular target
  • organ target
  • what type hypersensitivity?
A
  • molecular target: adrenal cell components
  • organ target: adrenal gland
  • type II + type IV hypersensitivity
47
Q

Addison’s disease - mechanism

A
  • type II + type IV
    • auto-Ab against adrenal cell components
    • cortex atrophy
    • insufficiency aldosterone
      • BP drop
      • ACTH → MSH accumulates
48
Q

addison’s disease - presentation

A
  • HYPOTENSION
    • often orthostatic
  • MSH ACCUMULATION:
    • hyperpigmentation
    • vitiligo
  • weight loss + fatigue + abdominal pain
49
Q

bullous pemphigoid

  • molecular target
  • organ target
  • what hypersensitivity type
A
  • molecular target: hemidesmosome antigens - BPAg1 & BPAg2 at dermal-intradermal junction
  • organ target: SKIN
  • hypersensitivity type II
50
Q

bullous pemphigoid - mechanism

A
  • type II
    • IgG antibody made against hemi-desmosomal antigens - BPAg1 & BPAg2 - along basement membrane →
      • SKIN BLISTERING
      • rarely involves mucous membranes
51
Q

bullous pemphigoid -presentation

A
  • blisters that are
    • TENSE
    • PRECEDED BY URTICARIA
52
Q

bullous pemphigoid- diagnosis

A
  • IgG
    • in linear band dermal-epidermal junction
    • on blister roof
    • circulating, against BPAg2 & BPAg2
53
Q

pemphigous vulgaris

  • molecular target
  • organ target
  • sensitivity type
A
  • molecular target: keratinocyte desmogleins
  • organ target; SKIN + mucous membranes
  • type II hypersensitivity
54
Q

pemphigous vulgaris mechanism

A
  • type II hypersensitivity
    • IgG or IgM made against keratinocyte desmogleins
    • leads to → flaccid blisters
55
Q

pemphigous vulgaris - presentation

A
  • blisters that
    • are PAINFUL
      • not pruritic
    • slough off
    • penetrate into mucous membranes
56
Q

pemphigous vulgaris diagnosis

A
  • IgG/IgM on the surface of keratinocytes, or
  • circulating IgG that bind the epidermis

“fish net appearance”

57
Q
A

pemphigous vulgaris - painful (not pruritic) blister that penetrates skin & mcuosa

58
Q
A

bullous pemphigoid - TENSE, preceded by urticaria

59
Q
A

linear band of IgG at dermal-epidermal junction

bullous pemphigoid

60
Q
A

salt-split skin: IgG on blister roof

bullous pemphigoid

61
Q
A

IgG/IgM on the surface of keratinocytes (on epidermis)

“fishnet appearance”

pemphigous vulgaris

62
Q
A

hyperpigmentation (MSH acculuation)

Addison’s disease

63
Q

compare and contrast the two bullous diseases - in terms of mechanism, presentation, dx

A

both type II diseases

bulloid pemphigous

  • presentation:
    • tense, preceded by urticaria
    • ONLY SKIN AFFECTED
  • dx: IgG that is
    • in a linear band at dermal-epidermal junction
    • on blister roof
    • circulating, anti-BPAg1 & BPAg2

pemphigous vulgaris

  • presentation:
    • painful (not itchy)
    • SKIN + MUCOUS MEMBRANES AFFECTED
  • dx: IgG/IgM
    • on keratinocytes (in epidermis) -“fishnet appearance”
64
Q

Grave’s Disease

  • molecular target
  • organ target
  • hypersensitivity type
A
  • molecular target: TSH receptor
  • organ target: thyroid
  • hypersensitivity type II
65
Q

Grave’s Disease - mechanism

A
  • type II hypersensitivity
    • auto-Ab made against TSH receptor → is agonistic → hyperthyroidism
66
Q

grave’s disease - presentation

A
  • triad
    • goiter
    • exopthalmos
    • pretibial myxedema: “orange peel” skin under the knee
  • hyperthyroidism (hyper-metabolic state)
    • sweating
    • heat intolerance
    • tachycardia
    • inc GI - diarrhea, weight loss
    • restless / anxious
67
Q

Grave’s disease - dx

A
  • anti-TSH receptors - diagnostic
  • also
    • TSH LOW
    • T3, T4 ELEVATED
    • inc radioactive iodine uptake in thyroid
68
Q

hashimoto thyroiditis

  • molecular target
  • organ target
  • hypersensitivity type
A
  • molecular target: thyroid globulin & thyroperoxidase
  • organ target: thyroid
  • type II hypersensitivity
69
Q

hashimoto thyroiditis - mechanism

  • molecular target
  • organ target
  • what type of hypersensitivity?
A
  • molecular: thyroglobulin & thyroid peroxidase (necessary for T3 & T4 synthesis)
  • organ: thyroid
  • Type II & Type IV hypersensitivity
70
Q

hashimoto thyroiditis - mechanism

A
  • Th1 infiltration of thyroid gland, which triggers
    • B-cell production of antibodies made against thyroid peroxidase & thyroglobulin
    • cytotoxic T-cell activation
  • leads to
    • formation of lymphoid follicles
    • lack of T3,T4 → hypothyroidism
71
Q

hashimoto’s thyroiditis - presentation

A
  • hypothyroidism (hypo-metabolic state)
    • cold intolerance
    • dry scaly skin (no sweating)
    • bradycardia
    • dec GI → constipation, weight gain
72
Q

hashimoto thyroiditis - dx

A
  • antibodies to thyroid peroxidase & thyroglobulin - diagnostic
  • also
    • elevated TSH level
    • low T3, T4
    • decreased uptake of radioactive iodine
  • histology: lymphoid follicles
73
Q

what is the most common autoimmune disease of the skin?

74
Q

psoriasis - mechanism

A

Th1 and Th17 cytokines induce keratinocytes

75
Q

psoriasis - presentation

A
  • scaly plaques - over elbows, knees, scalp, lower back
    • + blisters that: are filled with STERILE, PUSTILE FLUID (vs bullous pemphigus & pemphigus vulgaris)
    • auspitz sign: punctate bleeding
76
Q

psoriasis - presentation

A
  • scaly plaques - over elbows, knees, scalp, lower back
    • + blisters that: are filled with STERILE, PUSTILE FLUID (vs bullous pemphigus & pemphigus vulgaris)
    • auspitz sign: punctate bleeding
77
Q
A

psoriasis - scaly plaques on knees/elbows, scalp & back - blisters filled with sterile, pustule fluid

78
Q

psoriasis - dx

A
  • RF negative
  • elevated uric acid
  • clinical: scaly plaques, blisters with PUS, auspitz sign
79
Q

rheumatoid arthritis

  • molecular target
  • organ target
  • hypersensitivity type
A
  • molecular target: synovial components
  • organ target: joints - synovial membrane / cartilage / ligaments / tendons
  • type IV hypersensitivity
80
Q

rheumatoid arthritis - mechanism

A
  • type IV hypersensitivity
    • CD4 T-cells → stimulates synovial cells

often in the context of HLA-DR4 mutation

81
Q

rheumatoid arthritis - presentation

A
  • arthritis of 3+ joint areas
    • especially of
      • HANDS
      • FEET
    • also elbows, knees, hips spine, ect.
82
Q

rheumatoid arthritis -diagnosis

A
  • ESR and CRP elevated
  • +/- circulating RF
  • radiographs show:
    • erosions
    • decalcifications
83
Q

tx or rheumatoid arthritis?

A
  • rituximab (targets CD20)
  • anti-TNF-a inhibitors
    • infliximab (same as IBD)
    • adalimumab (same as IBD)
    • etanercept
84
Q

SLE

  • molecular target
  • organ target
  • hypersensitivity type
A
  • molecular target: DNA/nucleoproteins
  • organ targets: several - skin + kidneys + joints
  • type III hypersensitivity
85
Q

SLE - mechanism

A
  • type III hypersensitivity
    • immune complexes form against DNA/nucleoproteins in the skin + kidney + joints
    • worsened by complement deficiency
86
Q

SLE - presentation

A
  • triad
    • ERYTHEMA - BUTTERFLY RASH
    • GLOMERULONEPHRITIS
    • ARTHRITIS
  • sometimes discoid rash
87
Q

what increases the risk of SLE?

A
  • complement deficiency
  • increased estrogen
88
Q
A

butterfly rash

SLE

89
Q
A

discoid rash

SLE

90
Q

which autoimmune diseases can cause mouth rashes?

A
  • pemphigus’ vulgaris (type II) - painful blisters
  • SLE - (type III) discoid rash
91
Q

SLE - diagnosis

A
  • lumpy-bumpy pattern on IF
  • antibodies that indicate kidney involvement
    • anti-dsDNA antibodies
    • anti-smith antibodies
  • +/- RF (less common that RA)
92
Q

SLE - tx

A
  • avoid sunlight to prevent flares
  • NSAIDS
  • steroids
93
Q

sjogren syndrome (sicca syndrome)

  • target molecule
  • target organ
  • hypersensitivity type
A
  • target molecule: n/a
  • target organ: exocrine glands - salivary, lacrimal
  • mechanism: type IV hypersensitivity
94
Q

sjogren syndrome - presentation

A
  • DRY EYES (XEROPHTALMIA) + DRY MOUTH (XEROSTOMIA) - m/c
    • can cause dryness of other mucosa - skin, nasal, laryngeal, vaginal
  • parotid swelling (esp. in children)
95
Q

sjogren syndrome - diagnosis

A
  • type IV hypersensitivity
    • CD4 cells infiltrate exocrine glands → impedes secretion
96
Q

sjogren syndrome - dx

A
  • Shirmer test - tear production
  • salivary / parotid gland biopsy → CD4 cell infiltrate
  • +/ RF
97
Q

guillane barre syndrome (GBS)

  • molecular target
  • organ target
  • hypersensitivity type
A
  • molecular target: gangliosides (GM1 & GM1b) in myelin
  • organ target: PNS
  • hypersensitivity type IV
98
Q

what is a major complication of Sjogren’s syndrome?

A

non-hodgkins lymphoma

99
Q

GBS - mechanism

A
  • type IV hypersensitivity
    • molecular mimicry induced - by either viral infection or previous vaccination
      • viral infection: campylobacter -m/c
        • also VZV/EBV/CMV
    • causes CD4+ mediated immune response against myelin gangliosides (GM1 & GMb1) in PNS → abnormal nerve conduction
100
Q

GBS - presentation

A
  • PNS dysfunction → muscle weakness
    • dysphagia, dysarthria (trouble speaking)
    • diminished reflexes
    • ataxia
    • facial droop / double vision
101
Q

GBS - Dx

A
  • anti-ganglioside antibodies
  • abnormal nerve conduction tests
  • nerve root enhancement on MRI
102
Q

multiple sclerosis

  • organ target
  • molecular target
  • hyperesensitivity type
A
  • organ target: CNS
  • molecular target: myelin basic protein
  • type IV hypersensitivity
103
Q

MS - mechanism

A
  • type IV hypersensitivity
    • likely induced by molecular mimicry d/t
      • EBV
      • HTLV-1
    • TH1/Th17 beat out Treg
      • produce cytokines that induce killing of oligodrocytes → destruction of myelin sheath in white matter of CNS
104
Q

MS - presentation

A
  • unilateral
    • paresthesia
      • trunk
      • one side of face
    • visual disturbances
  • charcot triad
    • dysarthria
    • ataxia
    • tremor
  • poor bladder control
105
Q

MS - dx

A
  • plaques of demyelination on MRI
  • oligoclonal IgG bands on agarose electrophoresis
  • +/- myelin basic protein demyelination
106
Q

MS - tx

A
  • corticosteroids (methylprednisolone), unlike GB
  • ABC therapy

IMMUNO (4 decks)

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