Inflammation & Immune Responses
The skin is the "front line defense against the invasion"1 of microorganisms and the insult of toxic or foreign substances from the external environment. The skin also protects itself from harmful internal agents, such as disruption by tumor cells.
Inflammation and the immune response are two interrelated processes the skin deploys to defend itself and the body it encloses.
Inflammation
Infection, immune reactions, burns, trauma, and exposure to chemicals can all evoke inflammation - a complex series of vascular and cellular changes that helps repair damaged tissue.Dilation of capillaries causes redness (erythema), and leakage of plasma into the skin causes swelling (edema) and heat.
The Immune Response
The immune response is orchestrated by the immune systems, an intricate mix of cellular, molecular, and antibody components that protects the body against invaders.An invader that the immune system recognizes as harmful is called an antigen. When the immune system recognizes a foreign antigen it responds by producing one or both of two types of defenders. The antibody, a molecule produced by B cells that circulates in the bloodstream and neutralizes antigens. The other type of defender is the T cell. T cells assault antigens directly by producing substances called lymphokines.
The immune system is like a security guard that constantly seeks out, recognizes, and destroys harmful antigens. Lymphocytes are able to recognize foreign antigens because they have a sort of memory - they remember an invader from a previous encounter and are programmed to destroy those cells.
The immune system, of course, doesn’t identify every foreign substance that enters the body as an enemy. If it did, we couldn’t eat, drink, or take medications without setting off immune responses. Sometimes, however, the immune system does mistake a harmless substance, such as pollen or wool, for a harmful antigen, such as bacteria. The subsequent immune response is called allergic reaction.
There are four type of immune responses that cause tissue damage. The two types that cause commonly seen skin problems are immediate hypersensitivity reactions and delayed hypersensitivity reactions.
Urticaria, or hives, is the classic immediate hypersensitivity reaction. Immediate hypersensitivity reactions are produced when the reaction between an antigen and an antibody provokes the release of histamine, heparin, prostaglandins and leukotrienes from dermal mast cells and circulating white blood cells. The resulting inflammatory response dilates blood vessels and causes plasma to leak into the dermis, causing it to swell. This is seen as a wheal, the characteristic lesion of hives. The wheal is a raised, red, flat-topped lesion with a white center. There is usually intense itching and stinging.
Immediate hypersensitivity reactions, which are provoked by insect bites, foods, and drugs, occur within minutes after exposure to the antigen and last for 8-12 hours.
Poison ivy is an example of a delayed hypersensitivity reaction. In delayed hypersensitivity reactions, skin exposure to an allergen sensitizes lymphocytes which eventually migrate to the epidermis, where they release lymphokines. Lymphokines attract neutrophils and macrophages, which release inflammatory mediators that provoke the blister-like lesions that are characteristic of poison ivy.
In a delayed hypersensitivity reaction, there is a 5-21 day incubation period (called the sensitization phase) after the first exposure to the antigen. When the skin is exposed to the antigen again, the elicitation phase begins, and 12-48 hours later inflammation and skin lesions appear.
Inflammation and the immune response interact to protect and defend the skin. But these defenders also produce common skin problems which send patients to dermatologists for medication to treat erythema, swelling, lesions, itching, and other symptoms.
1. Odland GF. The Skin: Introduction to the Biology and Pathophysiology of the Skin. ASUW Publishing. Seattle: University of Washington; 1992: 79.
© Copyright 1996 - 2004 GALDERMA L.P. Legal Disclaimer