dermatitis facts
dermatitis facts Home  |  Contact us 
  Atopic eczema, irritant dermatitis and contact dermatitis


Atopic dermatitis or eczema is a common skin disease marked by an inflammatory, itchy, chronic and relapsing condition. Though the pathogenesis of this challenging disease is still being researched, its primary causes are associated with genetic factors, environmental interactions, skin barrier disorders or immunological reactions.

Since, immunological reactions are a major trigger of eczema, immunology or the scientific study of the immune system in an atopic dermatitis patient is very important. This apart, certain body parts, organs or systems fail to function normally or develop a medical abnormality when our body is affected by a disease. This dysfunction also occurs in atopic dermatitis and is of two types in eczema; neurologic and pharmacologic.

However, before we go into the details of immunology and dysfunction, here are few points that we need to know. Firstly, the diagnosis of atopic dermatitis is based on the three standard stages of the disease - infantile, childhood and adult - often with dormant phases in between. Then again, each may be diagnosed as acute, subacute, and/or chronic. Furthermore, the disease must be categorized as either intrinsic or extrinsic. The former is the non-allergic kind while the latter is generally associated with a medical history (either personal or hereditary) of respiratory allergy.

Seventy to eighty per cent of patients with eczema generally go on to develop allergic rhinitis or asthma later in childhood, while there is a simultaneous improvement in atopic dermatitis. However, herein atopic dermatitis actually becomes latent and often recurs later in life in up to 40% of patients.


The study of immunology in atopic dermatitis can be divided into medical disorders related to immunology, the associated pathology of biology (immunopathology) and regulation at the cellular level (immunoregulation).

Medical disorders related to immunology

Allergic disorders and infections are a predominant occurrence in atopic dermatitis. They are:

Respiratory allergy: It occurs in 70% of adult patients. The common triggers or allergens are dust mites, pollen, animal fur and molds.

Food allergy: This is common among infants and children with moderate to acute atopic dermatitis. It occurs in about 40% of patients. The common triggers are cow’s milk, eggs, peanuts and soy.

Microbial allergy: Staphylococcus aureus is the most common microbial offender in atopic dermatitis. Microbial agents generally affect over 90% skin lesions in atopic dermatitis patients. Proteins, carbohydrates and glycolipids present in these microbes work as foreign antigens and their exotoxins as super-antigens to aggravate an atopic dermatitis attack.

Autoallergy: It has been presumed that IgE autoantibodies create a connecting link in autoallergens (proteins) present in the human skin. This is over and above the outside sources of allergens involved in instantaneous hypersensitivity in acute and chronic atopic dermatitis cases. Moreover, it is disease action that has a connection with the occurrence of IgE autoimmunity (caused by the response of an antibody to naturally present matter in the human body) in atopic dermatitis.

Viral and fungal infections: On the contrary, eczema patients (mainly those with high IgE levels) are vulnerable to viral (herpes simplex, molluscum contagiosum and verrucae) and fungal (trichophyton rubrum and pityrosporum ovate) attacks. This is often linked to weak and slow hypersensitivity.


The biology of the above immunologic disorders are traced to the deficit and malfunction of circulating CD8+ suppressor/cytotoxic T cells and reduced activity of natural killer cells. The immunopathology is also associated with hypersensitivity and hyposensitivity reactions.

The immunopathologic features of atopic dermatitis are based on the two-phases of acute and chronic atopic dermatitis. The features of the acute phase are determined by skin patch tests with allergens administered to body sites. The chronic phase is studied by the chronic atopic dermatitis plaques.

The patch test performed with house dust mite allergens have reported that IL-4-positive cells were completely CD4+ T cells in the initial phase. Moreover, IL-4 synthesis by T cells was larger than IFN-gamma synthesis. On the contrary, in the delayed and chronic phases, IFN-gamma synthesis held primacy over IL-4.

Cell-mediated immunoregulation

The dysregulation of atopic dermatitis involves major cells like the Langerhans cells (LC), monocytes/macrophages, lymphocytes, eosinophils, mast cells/basophils and keratinocytes. The details of cell-mediated immunoregulation are a complex process beyond the scope of this article.

Neurologic and pharmacologic dysfunction

Neurologic dysfunction involves Neuropeptides (NPs), which are constituted by a few amino acid residues. They are found in the central nervous system and the peripheral nervous system consisting of the skin. They act as neurotransmitters and neuromodulators. There is an assumption that the itchiness (pruritis) and the immunopathogenesis of atopic dermatitis is caused by a greater presence of NPs in atopic dermatitis lesions, combined with the misplaced susceptibility of the mast cells and blood vessels of these peptides.

Pharmacologic dysfunction in atopic dermatitis is associated with a molecule called the cyclic AMP-phosphodiesterase (cAMP-PDE). This is related to a faulty cAMP response. Since cAMP generally has an effect on immune and inflammatory reaction, a reduction in cAMP count in atopic dermatitis lesions causes hyperreactivity of the skin.