The Skin's Immune System

The body's own defence against microorganisms begins directly on the skin surface. Special fatty acids from the sebaceous glands and the secretions of certain bacteria belonging to the physiological skin flora inhibit the growth of fungi and bacteria. Certain enzymes present in sweat (lysozymes) can destroy the cell walls of invading bacteria. If a foreign body passes this first line of defence - for example due to skin damage - the skin's immune system reacts. Many cells take part in the defence against foreign bodies. Among these are the Langerhans' cells which are specific to the skin's immune system.

Origin and physiology of the Langerhans' cells
The dendritic Langerhans' cells originate in the bone marrow. They migrate to the epidermis where they form a regularly ordered network reaching a density of some 700 to 800 cells per square millimetre. They are the furthest "outposts" of the immune system and together with macrophages and granulocytes belong to the myeloid cells.

Easily recognised in the electron microscope image are the characteristic intracellular, cytoplasmic organelles resembling a tennis racket, the "Langerhans-granula". They play an important role in receptor-specific endocytosis processes.

Macrophages - a form of phagocyte - are the first to react to invaders. They take various forms in the skin: in the epidermis as Langerhans' cells, in the dermis as tissue macrophages.

Functions of the Langerhans' cells
The Langerhans' cells specifically activate dormant T-helper cells and thus initiate a primary T-cell dependent immune response. They play an important role in contact allergies, the reflection of skin transplants and other immunological processes of the skin.

After contact with the corresponding antigens (viruses, contact allergens, skin transplants) the Langerhans' cell leaves the epidermis and reaches a lymph node via the lymphatic system. On its journey the cell undergoes a maturation process leading to the presentation of the antigen on the cell surface. The migrating cells are replaced by a corresponding number of new Langerhans' cells from the bone marrow.

In the lymph nodes the mature Langerhans' cells activate the T-helper cells that have the matching antigen-specific receptors on their surfaces. In this way they steer the reaction of the immune system.

T-helper cells belong to the group of T-lymphocytes. They are divided into suppressor and helper cells, those that control the immune response and those that are responsible for the eliminating of antigens.

External influences on the skin's immune system
Factors influencing the activity of the Langerhans' cells in the epidermis include:

• cellular messenger substances (cytokines) such as interleukin-10
• UV radiation
• photochemotherapy
• immunosuppressive drugs (for example corticoids)

After intensive UV exposure, Langerhans' cells retract their dendritic cell protuberances and leave the epidermis. Interleukin-10 (IL-10) that is set free in the skin cells by UV radiation, impairs the function of the entire immune system, even in the non-irradiated areas. Immunosuppressed areas in the skin are formed that give the UV-damaged skin cells the chance to repair their damage and not be eliminated by a premature immune response.

Genetically altered cells are hard to identify. After years of chronic sun exposure, basal cell carcinomas and prickle cell carcinomas that have developed from mutated keratinocytes may appear.

Additionally, immunosuppression makes it impossible to effectively combat microorganisms like herpes viruses. This can explain the reactivation of herpes simplex infections with UV exposure.

Reduced count of epidermal Langerhans' cells (dark spots) in a suction blister biopsy, two days after exposure to artificial sunlight