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SBL Final > Immuno > Flashcards

Immuno Flashcards

1
Q
  • A group of rare autoimmune diseases characterized by blistering of the skin and mucous membranes
  • Fatal w/out immunosuppressive therapy
  • Auto-abs against desmosomal proteins (desmoglein) causes cell separation
A

Pemphigus

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2
Q

What are the 4 classifications of pemphigus?

A

I. Pemphigus Vulgaris
II. Bullous Pemphigoid
III. Mucous Membrane Pemphigoid
IV. IgA pemphigus

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3
Q
  • Autoimmune blistering
  • intra-epidermal bullae and superficial vesicles
  • Jewish and Mediterranean predisposition
  • HLA-D4 and HLA-D6
  • Both males and females affected
  • Blisters in both superficial and deep epidermis

Which desmoglein are affected?

A

Desmoglein 3 and 1

Pemphigus Vulgaris

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4
Q

What layer of the skin is desmoglein 1 more associated with? Desmoglein 3?

A 
Dsg1 = stratum corneum (superificial epidermis)
Dsg3 = basal layer or basement membrane (deep epidermis)
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5
Q

What type of hypersensitivity rxn is pemphigus?

A

Type II: Abs directed against desmogleins in the tissue!

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6
Q

What is the immune mechanism of pemphigus vulgaris?

Ab-dep activation of complement-->
Damage to epidermal cells-->
Release of inflammatory mediators-->
Inflammation and recruitment of \_\_\_\_\_\_ \_\_ \_\_\_\_-->
Separation of epidermal cells
A

activated T cells

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7
Q

How do we diagnose pemphigus vulgaris? (2 ways)

A
  • ELISA: detection of circulating anti-desmoglein 3 auto-ab (IgG)
  • Skin biopsy: direct immunofluorescence of IgG deposit by anti-IgG labeled Ab
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8
Q

How do we treat pemphigus vulgaris? (2 ways)

A
  • Corticosteroids

- Anti-CD20 mAb (removes mature B cells)

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9
Q

What is the mechanism of anti-CD20 immunotherapy?

A

Anti-CD20 mAbs cross link on CD20 B cells and induce apoptosis through ADCC (antibody-dependent cell mediated cytotoxicity) and CDC (complement dependent cytotoxicity)

(note: we use CD20 and not CD19 because CD19 is also on dendritic cells)

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10
Q
  • Autoimmune, subepidermal blistering skin dz
  • IgG auto-Abs against hemidesmosomal BP Ags: BPAg1 and BPAg2** (BP=base protein) on the basement membrane

What is described?

A

Bullous pemphigoid

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11
Q

What is MOA of bullous pemphioid?

IgG auto-Abs bind to skin basement membrane–>
Complement activation–>
Inflammatory mediators and proteases–>
Degradation of ____________ _____–>
Blister formation (may contain eosinophils!)

A

hemidesmosomal proteins

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12
Q

What type of hypersensitivity reaction is bullous pemphigoid?

A

hypersensitivity type II

ALL pemphigus are

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13
Q

How do we treat bullous pemphigoid? (2)

A
  • Corticosteroids

- Anti-CD20 mAbs

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14
Q
  • Autoimmune blistering of the conjunctiva and skin (occasionally)
  • Leads to decreased vision and blindness
  • Cutaneous form gets blisters on head, neck, or trauma sites
  • Auto-Ab against epidermal-dermal jx
  • No specific auto-Ag identified
A

Mucous Membrane Pemphigoid

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15
Q
  • Autoimmune blistering cause by gluten-sensitive enteropathy (GSE/Celiacs)
  • Tx: GLUTEN FREE DIET
  • Located on elbows, knees, butt, back
  • Dx requires direct immuno-fluorescence of skin biopsy showing IgA deposition (use anti-IgA)
  • IgA deposition–>complement/neutrophils–>MBL (mannose binding lectin protein)

What are the IgA antibodies directed against?

A

Transglutaminase 3 (TGase3)

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16
Q
  • Progressive disorder of skin and mucous membranes
  • Melanocytes destroyed&raquo_space; Hypopigmented macules or patches
  • 0.5-2% of world population affected
  • Age of onset 20 yo
  • Multifactorial polygenic disorder
A

Vitiligo

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17
Q

What type of disease is vitiligo? What is the MOA?

A
  • B/T-cell mediated disease
  • Alterations in both humoral and cellular immunity&raquo_space; destruction of melanocytes
  • Circulating auto-abs found
  • Activated CD8+ T cells also found
18
Q

What other autoimmune diseases are assoc with vitiligo? (2)

A
  • Hashimoto thyroiditis

- Graves dz

19
Q
  • Recurrent non-scarring type of hair loss
  • Primarily an autoimmune T-cell mediated dz
  • Auto-Abs directed to hair follicle
  • CD4 and CD8 T cells play a role
  • Animal studies: depletion of T cells–>partial or complete hair growth (evidence-based education impt!!!)
A

Alopecia Areata

20
Q

What cytokines in alopecia areata inhibit hair growth? (2)

A

IL-1 and TNF

21
Q
  • Pruritus, erythema, thickened epidermis, mononuclear infiltrate
  • Cutaneous immune response to environmental Ags
  • Humoral Th2-type of response generates IgE
  • What type of hypersensitivity is it?
A

Hypersensitivity type I

atopic dermatitis

22
Q

What Ags are common atopic dermatitis and how do they cause inflammation?

A

Ag = house-dust mites

Proteases secreted by mites–>
Epidermal injury–>
Release of inflammatory cytokines–>
Inflammation

23
Q

Reminder: atopic dermatitis is a hypersensitivity type I reaction. What is the MOA?

First exposure to allergen-->
Allergen presented to T-cell by APC-->
T-cell releases \_\_\_\_\_ onto B-cell-->
B-cell matures and releases \_\_\_-->
IgE binds to mast cells FceRI

Subsequent allergen binds to IgE on mast cell–>
Cross-linking of the FceRI on mast cell–>
Mast cell degranulation

A

IL-4
IgE

First exposure to allergen-->
Allergen presented to T-cell by APC-->
T-cell releases IL-4 onto B-cell-->
B-cell matures and releases IgE-->
IgE binds to mast cells FceRI

Subsequent allergen binds to IgE on mast cell–>
Mast cell degranulation

24
Q

What is released by mast cells that causes tissue damage in atopic dermatitis?

A
  • Histamine
  • Proteolytic enzymes
  • Cytokines (IL-4, IL-5, TNF-a)
  • Leukotrienes
  • Chemokines
25
Q
  • Atopic dermatitis involves Ag-specific T cells that produce Th2 type 2 cytokines.
  • These cytokines (IL-4, IL-13) promote a switch from IgM to IgE while IL-5 promotes eosinophils, leading to scratching of the skin and entrance of microbes.

This leaves the skin susceptible to infx and pathogens can enter and cause perpetual inflammation.

What does this do to the Th1/Th2 balance?

A

The Th1/Th2 balance is shifted to a Th1-type of immune response (CHRONIC AD=T-cell mediated immune disease!)

(acute=B-cell mediated, Th2)

26
Q

Allergic contact dermatitis involves which type of hypersensitivity?

A

Type IV hypersensitivity

27
Q

Type IV hypersensitivity in allergic contact dermatitis is also called delayed hypersensitivity. What is the MOA?

A

First exposure to Ag makes memory T cells–>
Subsequent exposure to Ag–>
Ag-specific T cells are activated in the skin–>
Cytokines–>
Injury to keratinocytes

CD4 T cells respond to Ag presented by MHC class II and develop Th1 type of response (IFN-g and TNF-a)

28
Q

What is a common culprit of allergic contact dermatitis?

A

Poison ivy!

(Pentadeca catechol molecules combined with skin proteins makes a neoantigen. No dermatitis upon primary contact but dermatitis on secondary contact! This is delayed hypersensitivity (IV).)

29
Q
  • A chronic, persistent, lifelong disease characterized by scaly, red cutaneous patches on the elbows, knees, and sites of repetitive trauma
  • Assoc. with innate immune sys: bacterial and fungal infections of the skin can cause flare ups
  • Polygenic inheritance

What type of hypersensitivity?

A

Type IV hypersensitivity!!

Psoriasis

30
Q

-Psoriasis is characterized by ____ T cells (IFN-gamma, lymphotoxin, and TNF-B)

Trauma of epidermis–>
Keratinocytes release ____–>
Inflammation–>
T cells recruited (Th1-type cytokines)

A

CD8

IL-1

31
Q

How can we treat psoriasis?

A

Cyclosporine (blocks IL-2)

32
Q

What type of hypersensitivity are cutaneous drug reactions? What cell type dominates the inflammation?

A

Hypersensitivity type III

Neutrophil dominated inflammation

33
Q
  • Strong assoc with anti-Ro (SSA) auto-abs against ribonucleoprotein complexes
  • UV may cause modulation of auto-Ags, epidermal cytokines, adhesion molecules, keratinocyte apop
  • More common in whites and females
  • Later in life (43 yo)
A

Cutaneous Lupus Erythematosus

34
Q
  • Strong assoc with anti-Ro (SSA) auto-abs against ribonucleoprotein complexes
  • UV may cause modulation of auto-Ags, epidermal cytokines, adhesion molecules, and keratinocyte apop
  • More common in whites and females
  • Later in life (43 yo)
A

Cutaneous Lupus Erythematosus

35
Q

What are the 3 types of cryoglobulinemia?

A

Type I is monoclonal Ig (IgM)
Type II is monoclonal Ig or IgM RF
Type III is polyclonal Ig + IgM RF

36
Q

What type of hypersensitivity is cryoglobulinemia?

A

Type III hypersensitivity

RF IgM complex in circulation

37
Q

What type of hypersensitivity is cryoglobulinemia? What are the two factors involved?

A

Type III hypersensitivity: (RF IgM complex in circulation)

Solubility and protein conformation

38
Q
  • Autoimmune dz caused by auto-Abs (IgG)
  • Overlaps with SLE and RA
  • Th2 cells modulate fibroblasts and endothelial cells
  • Leads to abnormal ECM deposition, pathologic fibrosis, and vasculopathy
A

Systemic Sclerosis

39
Q

What is the MOA of systemic sclerosis?

Th2 cells release ____ and ____ on fibroblasts.
Fibroblasts release ____, which is pro-angiogenic

A

IL-4 and IL-13; IL-8

40
Q

Th1 blocks systemic sclerosis by releasing _____ on fibroblasts.
Fibroblasts release ____, which is anti-angiogenic

A

IFN-gamma, IL-10

SBL Final (4 decks)

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