Skin Disorders Overview Quiz

Skin Disorders Overview

• The subcutaneous layer consists of fat cells organized into lobules by fibrous walls of collagen and large blood vessels.
• Clinical manifestations of skin dysfunction include various types of lesions such as nodules, tumors, vesicles, bullae, pustules, cysts, telangiectasia, scales, lichenification, keloid scars, excoriations, fissures, erosions, ulcers, and atrophy.
• Inflammatory skin disorders encompass dermatitis, which is a general term for skin inflammation characterized by pruritus, lesions with indistinct borders, and epidermal changes, and includes types such as atopic dermatitis, allergic contact dermatitis, non-allergic contact dermatitis, irritant contact dermatitis, stasis dermatitis, and seborrheic dermatitis.
• Hypersensitivity reactions, including allergic contact dermatitis, are mediated by immune mechanisms and result in manifestations such as erythema, swelling, pruritus, and vesicular lesions.
• Urticaria, or hives, is caused by type I hypersensitivity reactions to allergens, leading to endothelial cell contraction and fluid leakage from vessels, typically treated with antihistamines and steroids.
• Papulosquamous disorders involve the development of papules, scales, plaques, and erythema, including conditions such as psoriasis, pityriasis rosea, lichen planus, acne vulgaris, acne rosacea, and lupus erythematosus.
• Psoriasis is a chronic, non-contagious, autoimmune skin disorder characterized by T cell immune-mediated thick, silvery, elevated lesions, with evidence of dermal and epidermal thickening and altered skin cell growth and differentiation.
• In psoriasis, dendritic cells in the skin play a role in the immune response, presenting antigens to T cells, leading to the release of cytokines and chemokines, recruitment of neutrophils, and hyperplasia of keratinocytes.
• TNF-a is produced in excess amounts by activated T cells in people with psoriasis and psoriatic arthritis, leading to rapid skin cell growth and joint symptoms, with biologic medications targeting TNF-a and T cells.
• Acne vulgaris encompasses noninflammatory acne, caused by factors such as follicular plugging, excessive sebum production, and colonization of Propionibacterium acnes, as well as inflammatory acne, resulting from follicular wall rupture and deeper inflammation, which may cause scarring.
• Acne vulgaris is influenced by physiologic factors such as plugging of folliculosebaceous units, follicular hyperkeratinization, excessive sebum production, and inflammation secondary to the action of inflammatory products produced by P. acnes.
• The manifestations of acne vulgaris include noninflammatory and inflammatory lesions, such as blackheads, whiteheads, and cystic nodules.

T Cell Subsets and Their Roles in Psoriasis

• Different subsets of helper cells contribute to the pathogenesis of psoriasis, with the IL-23/Th17 axis playing a central role in amplifying inflammation and cutaneous manifestations.
• Th1 cells likely participate in the early stages of psoriasis pathogenesis by inducing CCL20 and IL-23 production by myeloid dendritic cells.
• Tissue resident Th22 and CD8 Tc17 cells are proposed as repositories of disease memory in sites of recurrent psoriasis, linked to prominent histological features of the disease due to the action of IL-22 on keratinocytes.
• IL-9-producing Th9 cells have been found to play significant roles in the pathogenesis of psoriasis.
• CD4 T cells recirculating between the skin and blood have an emerging role in the clinical manifestations of psoriasis and associated comorbidities.
• CCR4+ CD4 and CD8 T cells may amplify skin and systemic inflammation in psoriasis, respectively.
• Further investigations are needed to elucidate the connection between T cell responses in the skin and the comorbidities associated with psoriasis.
• The authors declare no competing interests in the research.
• The IL-23/T17 pathogenic axis in psoriasis is amplified by keratinocyte responses.
• Th17 and Th22 cells have been identified in psoriatic arthritis and psoriasis.
• A novel proinflammatory human skin-homing V𝛾9V𝛿2 T cell subset has been identified with a potential role in psoriasis.
• Laser capture microdissection and cDNA microarray analysis have identified locally expressed disease-related genes in focal regions of psoriasis vulgaris skin lesions.