Cutaneous Immunology Flashcards
Physical defenses of the skin:
keratinocyte with desmosomal adhesions, impermeable stratum corneum, keratinocyte turnover, antimicrobial peptises and secretion of free FA’s in sebum. All can be modified in an immune response.
Describe innate immunity, what is involved, and what stimulates it.
The initial, non-specific immune response where phagocytic cells (neutrophils and macrophages), cells that release inflammatory mediators (mast cells, eosinophils), and NK cells cause local tissue destruction and inflammation from release of cytokines (IL-1, TNF-alpha, IFN-gamma) and mediators of blood flow, fluid accumulation, and recruit other immune cells.
Describe adaptive immunity, its actions, and main cells.
An acquired response after a few days to specific antigens. Leads to long-term memory formation to future infection from similar antigens. Cells are B- and T-lymphocytes and the antigen presenting cells stimulate the response.
Specialized dendritic cells that reside in the epidermis that phagocytose and process antigens
Langerhans cells
Specialized dendritic cells that reside in the dermis that phagocytose and process antigens
Dermal dendritic cells
How long after Langerhans or DDC encounter an antigen does it take to migrate and mount an immune response?
7-14 days. Shorter time with subsequent exposure to similar antigens.
What do T-cells stimulated by Langerhans cells and dermal dendritic cells express to allow them to migrate into inflammed skin?
Cutaneous lymphocyte antigen
What are the cytokines released, immune response type, and pathogens cleared by TH1 cells?
IFN-gamma and TNF direct the cell-mediated immunity to clear viruses, tumors, and intracellular pathogens.
TH1 are responsible for what type of allergic reaction seen in allergic contact dermatitis and psoriasis?
Delayed type (Type 4) hypersensitivity
What are TH2 cytokines, immune response type, and pathogens cleared?
IL-4, IL-5, IL-10 for humoral immunity via plasma cells and IgE production to clear parasites and extracellular microbes. Seen in atopic dermatitis, urticaria, and other allergic disease.
Diseases from autoimmunity in newly discovered TH17 cells?
Crohn’s, ulcerative colitis, and psoriasis.
Clinical expression of allergic contact dermatitis
Itchy, red papules and vesicles 24-48 hours after exposure and can worsen up to 4-7 days later. Varies from mild erythema to vesicles and bullae if severe or scale and lichenification if chronic. Shape and distribution give clue to inciting allergen. (Ex: poison ivy= linear rash, nickel jewelry geometric rash)
Common skin allergens?
poison ivy, poison oak, nickel, fragrances, preservatives, topical antibiotics.
Describe how to do a patch test.
Place suspected allergen on patch, apply to skin for 48 hours, observe for redness and blistering.
Molecules that are too small to be recognized independently but capable of stimulating the immune system by binding to native proteins
haptens
Pathology of atopic dermatitis
Imbalance in immune system, with TH2 predominance rather than a hypersensitivity. Combination of genetic predisposition (filaggrin mutation), environmental irritants and allergens, and colonization w/ Staph aureus. Associated with atopic triad.
Clinical expression of atopic dermatitis
generalized itchy scale and ill-defined erythematous papules and plaques with scale, and crust. Lichenification. Common on face, scalp, and extensors in infants, flexural areas and face in adults.
Irritating or scratching skin in areas with psoriasis leading to more psoriasis in otherwise normal skin
Koebner’s phenomenon
Clinical expression and pathology of guttate psoriasis
small, round papules and plaques precipitated by a strep infection.
Pathology of psoriasis
mediated by TH1 lymphocytes and cytotoxic T cells and others. Histo shows presence of neutrophils in epidermis and lymphocytes signal rapid proliferation leading to thick plaque formation. Control outbreaks by targeting T cell activation or blocking TNF-alpha receptor.
Clinical expression of urticaria (hives)
Itchy, annular, edematous, pink papules or plaques known as wheals. Can also present as linear wheals in areas where skin is stroked or scratched (dermatographism). In deep dermis, called angioedema, causing painful swelling in lips or face. Resolves in 24 hours.
Pathology of urticaria
Mast cell degranulation and histamine release. Result of Type 1 hypersensitivity reactions. Mast cells coated in IgE respond to antigen, activate, and release histamine, leukotrienes, and prostaglandins.
Mast cell stimulators
IgE, nonimmune activators like drugs, or physical stimuli like heat, cold, pressure, vibration, and sunlight.
Most common drugs causing drug eruptions
antibiotics, anticonvulsants, and NSAIDS
