Chapter 13 :: Basic Principles of Immunologic Diseases in Skin (Pathophysiology of Immunologic/Inflammatory Skin Diseases) Flashcards
- Cytokine, Toll-like receptor and inflammasome-mediated activation of APCs
- No skin inflammation
Initial hapten exposure
Sensitization (Allergic contact dermatitis)
Cytokine, Toll-like receptor and in inflammasome-mediated activation of APCs
* Skin inflammation elicited by T cells
Subsequent exposure
Elicitation (Allergic contact dermatitis)
- Resident memory T cells poised for subsequent exposure
Postinflammation
Resolution (Allergic contact dermatitis)
Existence of clones of drug-reactive CD8+ resident memory T (TRM) cells that remain at sites of previous skin lesions where they are poised to respond if offending drugs are readministered
Fixed Drug Erupions : resident memory T cells
A disease with eczematous dermatitis as a prominent feature, is caused by mutations in the cell surface protease inhibitor SPINK5
Netherton syndrome
Loss of SPINK5 leads to increased activity of cell surface serine proteases that compromises the barrier function of the stratum corneum
Blocks IL-4 and IL-13 signaling
Dupilumab
Expressed in oral and esophageal mucosae, mucosal involvement is observed in PV but not in PF
Dsg3
Binds the cell surface protein CD20 that is expressed by B cells
Rituximab