Pathogenesis of Skin Diseases and Skin Appendage Diseases

Pathogenesis of Skin Diseases and Skin Appendage Diseases

I. Skin Diseases Caused by Microorganisms:

• Acne: Caused by the bacterium Propionibacterium acnes (P. acnes).

• Acute dermatitis: Often a manifestation of lesions caused by microorganisms.

II. Allergic Skin Diseases:

• Type I Allergy (Immediate Hypersensitivity):

• Includes conditions such as: eczema, urticaria.

• Mechanism:

• Upon first exposure to an antigen (Ag), helper T lymphocytes (Th2) are activated.

• Under the influence of interleukin 4 (IL4) and IL13, Th2:

• Differentiate B cells into plasma cells.

• Synthesize antigen-specific immunoglobulin E (IgE).

• IgE binds to mast cells through Fc.

• Upon second exposure to Ag:

• Fab of IgE binds to Ag, forming an Ag-IgE complex on the mast cell surface.

• Mast cells release chemical mediators (CMs), particularly histamine.

• Histamine causes:

• Increased vascular permeability, edema, and skin redness.

• Stimulation of sensory nerve endings in the skin, causing itching.

• Type IV Allergy (Delayed Hypersensitivity):

• Includes the condition: contact dermatitis.

• Mechanism:

• Antigens (nickel, gold, cobalt) are captured by antigen-presenting cells (APCs).

• APCs present the antigen to helper T lymphocytes (Th).

• Th activates cytotoxic T lymphocytes (Tc) and delayed hypersensitivity T lymphocytes (Tdth).

• First sensitization: Creates responsive cells, developing into numerous cell lines and memory cells.

• Second exposure: Tdth secretes chemotactic factors (MIF, MAF).

• Attracts APCs, which eliminate antigen directly through phagocytosis or by late inflammatory substances (after 48 hours): redness, blisters, sometimes ulcers and erosion, necrosis, itching.

III. Autoimmune Skin Diseases:

• Systemic Lupus Erythematosus: A typical autoimmune disease.

• Two main contributing factors:

• Genetics.

• Immune dysfunction.

• Mechanism of immune dysfunction:

• Uncontrolled activity of B lymphocytes by T lymphocytes.

• When cells in the body transform into autoantigens, uncontrolled B cells proliferate, producing large amounts of autoantibodies against autoantigens.

• Autoantibodies combine with autoantigens to form immune complexes (ICs) that deposit, causing pathology in organs and tissues.

IV. Skin Disorders in the Elderly:

• Manifestations: Dry skin, wrinkles, creases, dark brown or black patches of skin, multiple black moles.

• Mechanism:

• Ultraviolet radiation from the sun and cell aging cause immunosuppression and impairment of the blood vessel system that nourishes the skin.

Note:

• This article provides general information about the pathogenesis of some skin diseases.

• For accurate diagnosis and treatment of skin diseases, consult a healthcare professional.