 |
|
|
|
|
|
| |
The skin is the largest organ in area. With the
Langerhans' cells in the lowest epidermal layers, it is equipped with
specialized immunologically competent cells. The Langerhans' cells
play a central role in the skin's immune system and an integral part
of the body's total defence 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 that belong 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 cells - like the Langerhans' cells - that are specific to the
skin's immune system.
|
|
Various fatty acids
in sebum are found only on the skin surface
|
|
| |
|
|
|
|
| |
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 recognized 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. |
|
Distribution of epidermal Langerhans' cells (dark
spots) in a suction blister biopsy
|
|
| |
|
|
|
|
| |
Functions
of the Langerhans' cells
The Langerhans' cells specifically activate dormant T-helper cells
and thus initiate a primary T-cell dependent immune response. Therefore
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. |
|
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. |
|
| |
|
|
|
|
| |
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.
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 it was observed that the 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. In this manner, immunosuppressed areas in the skin are formed
that, on the one hand give the UV-damaged skin cells the chance to
repair their damage and not be eliminated by a premature immune response.
|
|
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.
|
|
| |
|
|
|
|
| |
On the other hand, genetically
altered cells are hard to identify. So after years of chronic sun
exposure, basal cell carcinomas and prickle cell carcinomas may appear
that have developed from mutated keratinocytes.
Additionally, the immunosuppression make 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
|
|
| |
|
|
|
|
| |
|
|
more
 |
|
