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
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.
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.