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WVSOM - Immunity
Skin Immune System & Dermatologic Diseases
Question | Answer |
---|---|
Role of langerhans cells in the skins defenses | Antigen presenting cells (APCs) |
What specific molecules allow Langerhans cells to act as APCs? | MHC-I, MHC-II, CD40 (co-stimulatory molecule), CAMs (adhesion molecule), B7 |
How do keratinocytes partake in the immune response? | Induced to express MHC-I, MHC-II, CAM (adhesion molecule), cytokine production (IL-1,6,8, TNF = pro-inflammatory), produce prostaglandins |
What is allergic contact dermatitis? | Inflammatory skin disease caused by cell-mediated hypersensitivity to external agents that contact skin (ex: poison ivy) |
Term used to describe antigen that contacts skin and become immnunogenic | Hapten |
Role of LC in allergic contact dermatitis | LC transports antigen via vascular to lymph, presents antigen to T cells |
Process whereby T cells are activated and memory T cells are formed when first encountering antigen | Sensitization |
Cause of erythema in allergic contact dermatitis | Mast cell degranulation due to sensitized antigen activating memory T cells, cytokines |
Treatment for allergic contact dermatitis | Topical steroids, education (avoid contact allergin) - skin testing (patch testing) = type IV |
Sensitization takes _____ days | 10-14 |
Types of immunobullous diseases | Bullous pemphigoid, pemphigus, dermatitis herpetiformis |
Which immunobullous disease is most serious? | Pemphigus |
Histaological location of bullous pemphigoid | Junction btw dermis and epidermis |
Etiology of bullous pemphigoid | Ab against keratinocyte Ag |
Immunobullous disease most common in > 60 years old | Bullous pemphigoid |
Bullous pemphigoid treatment | Corticosteroids |
Clinical presentation of bullous pemphigoid | Large tense blisters |
Immune response to bullous pemphigoid | IgG and complement |
Types of pemphigus | Pemphigus vulgaris (more common) and pemphigus foliaceus (usually just skin) |
Pemphigus is characterized by widespread blistering of ______ and _______ membranes | skin, mucous |
Pemphigus treatment | Corticosteroids, azathioprine |
Pemphigus has a strong association with which allele? | HLA-DR allele (MHC-II) |
Pemphigus etiology | Auto-Ab against keratinocyte Ag |
Histalogical location of pemphigus | Intraepidermal acantholysis; located in desmosomes; lack of adhesion btw keratinocytes |
Clinical presentation of dermatitis herpetiformis | Intensely pruritic vesicles |
Clinical location of dermatitis herpetiformis lesions | Elbows, knees, back, neck, buttocks |
Dermatitis herpetiformis is associated with | Gluten-sensitive enteropathy (Celiac disease) and certain HLA alleles |
Histalogical location of dermatitis herpetiformis | Btw epidermis and dermis |
Immune response associated with dermatitis herpetiformis | IgA - starts inflammatory response; LOTS of PMNs |
Psoriasis features | Sharply demarcated with clear-cut borders, non-coherent silvery scales, glossy homogeneous erythema, positive Auspitz sign (scratch off scale = drop of blood immediately forms) |
Koebner phenomenon | Skin lesion appears along lines of trauma |
Psoriatic arthritis | Negative for RA factor |
Keratinocyte maturation in psoriasis | 3-4 days |
What causes accelerated keratinocyte maturation in psoriasis? | T cells (cytokines increase process) |
Treatment of psoriasis | Monoclonal Ab that bind Il-12 (assists Th1 helper cell differentiation = pro-inflammatory), IL-23 (produce Th17 helper T cells = recruit PMNs) |