Allergy is an acquired
specific alteration in the capacity of the host to react with an antigen .
It is an immunological reaction depending on antigen-antibody complexes.
The allergic reaction may
be immediate that occurs after exposure to the antigen or delayed taking
few hours or even days or weeks to appear.
Allergic skin diseases
constitute the main and bulk of skin dermatoses in children and adults .
Immune
function of the skin
The skin is an
environmental barrier which initiates an immune response to the penetrating
foreign antigens.
This will lead to:
Destruction of infective
organisms.
Neutralization and
removal of the potential toxins and the damaged tissue.
The skin contains many
elements of the immune system, which have been designated, the
skin-associated lymphoid tissue (SALT) or the skin immune system (SIS).
Human epidermis contains
Langerhans cells, and Keratinocytes which when stimulated will synthesize
several types of Cytokines that activate and induce proliferation of
lymphocytes and macrophages, which contribute, induce and enhance
sensitization.
The immune system
functions in the skin as in other body organs are either a non-specific,
(innate) or specific type, (adaptive).
A. The
non-specific immune system
The non-specific immune
mechanism is the first line of the body defense when it is exposed to an
antigen which it includes:
-
Physical defense
performed by the skin.
-
Body Secretions
(the mucous, celia in the respiratory tract, sebaceous gland
secretions).
-
Cellular: this is
performed by the phagocytes or the natural killer cells (NK).
B. The
specific immune system
This type has its role
when the non-specific immune system failes to take care of the offending
antigen.
The specific immune
system includes the cellular and humoral components that
characteristically have an immunological mirror memory, where it can
enhance an immunological response on repeated exposure to the same
antigen.
Functions
of the specific immune system
The specific immune
system produces the immuno-competent cells, which are the T cells
and B-cells .
T- cells modulate both
the cellular and humoral immune responses .
B - cells produce the
different antibody immunoglobulin groups; IgG, IgE, IgM, IgA and IgD .
Allergic reaction may be
related to an endogenous or exogenous factors .
Antigen: is a foreign
substance that can stimulate an immunological response.
This will lead to:
Formation of antibodies.
Alters the reactivity of
lymphocytes, which is known as cell mediated response.
Chemical
characteristics of antigens
Antigens may have high or
low molecular weight.
-
High
molecular weight antigens
are composed of amino acids and peptides that can stimulate the
formation of antibodies.
-
Low
molecular weight antigens
cannot stimulate the formation of antibodies unless combined with a
protein. These are known as haptens. These can stimulate humoral
antibodies or delayed-type (cell-mediated) sensitivity, which is
specific for the haptens.
Antigens that commonly
sensitize persons to anaphylactic or to delayed-type hypersensitivity and
these are known as allergens.
Antibody: is a
serum immunoglobulin that is formed in response to antigen stimulation.
Immunoglobulins are synthesized by plasma cells and are composed of
polypeptide chains.
The basic antibody unit
is the immunoglobulin molecule (Ig). There are different immunoglobulins
mainly IgG that constitutes around 75 per cent of the immunoglobulins.
Different
Immunoglobulins: IgG, IgE, IgA, IgD are found in varying amounts in the
external secretions, e.g. respiratory, intestinal tract.
Failure of any part of
the immune system may predispose to allergy, infection or malignancy.
Different
immunological reactions
Antigen-antibody reaction
is either an immediat which appears after exposure to a certain antigen or
may be delayed type.
Immediate
allergic reactions (Type (1, 11,
111) : these reactions represent a humoral response, stimulating
B-lymphocytes, plasma cells that produce and activate different
immunoglobulins.
Delayed
allergic reaction (Type 1V): The
allergic reaction may take few hours, days or even weeks to appear from
the time of exposure to the antigen. This type is cell mediated by
sensitizing T-lymphocytes.
The different
hypersensitivity reactions according to Gell and Coombs classification
are:
1. The
immediate, anaphylactic type (Type I)
The antigens in this type
may be foodstuff, pollens, drugs, dust, feathers or others.
The antibodies are
immunoglobulins IgE.
The antigen -antibody
reaction causes degranulation of mast cells which release different
mediators mainly histamine, serotenin, bradykinin and slow reacting
substances (SRS-A).
The
physiopathological changes are:
-
Vasodilatation of
blood vessels.
-
Increase of the
vascular permeability.
-
Contraction of
the smooth muscles.
The clinical
manifestations of Type I reactions are: Urticaria, angioedema,
anaphylactic shock, bronchial asthma and allergic rhinitis.
2.
Cytotoxic antibody (Type II)
The antigen in Type II
allergic reaction is haptens, which deposits on the cell wall or cell
membrane fragments, which can act as an antigen.
The antibodies are
cytotoxic antibodies of the classes IgG, IgA and IgM.
The allergic reaction
occurs as a result of reaction of the circulating antibodies or the
cellular antibodies with the circulating antigens, which lead to
attachment of complements with the antigen-antibody complex leading to
lyses of the target cells.
The effect of such
reaction is cytolysis.
The clinical
manifestations of the cytotoxic reactions are: Thrombocytopenia, hemolytic
anemia, agranulocytosis and autoimmune diseases.
3.
Antigen - antibody immune complex (Type
III), Arthus reaction.
The antigens in this type
may be drugs, foreign serum and other different antigens such as from
streptococci and tumors.
The antibodies of Type
III reaction are immunoglobulins IgG and complements.
The allergic reaction occurs as a result
of complex mechanism.
Physico-chemical
changes:
-
Deposition of
antigen-antibody complexes in the capillary walls.
-
Activation of
the complement system.
-
Leucotaxis and
phagocytosis of the immune complex by leukocytes.
-
Lyses of the
phagocytosing cells.
-
Destruction of
the cell walls by the lysosomal enzymes.
The effects of these
complex reactions are inflammation and necrosis of tissues.
The
clinical manifestations of type III allergic reactions are:
-
Arthus
reactions, arthus phenomenon, serum sickness.
-
Drug rash.
-
Toxic epidermal
necrolysis
-
Erythema
multiforme and erythema nodosum.
4. Delayed type cell
mediated (Type IV). The antigens are different types of chemicals and
other substances.
The antibody is the
T-lymphocytes.
The allergic reaction is
due to lymphocyte-antigen reaction due to humoral factors released
(lymphokines).The effects of these reactions are: vasodilatation, edema,
and monolymphocytic infiltration.
The clinical
manifestations are: allergic contact dermatitis, allergic photodermatitis,
allergic exanthemas, id eruptions, and transplacental rejection.
The manifestation of the
allergic reaction may be localized only to the skin , internal organs or
both.
The immediate and delayed
type of hypersensitivity reactions are the most important in dermatitis
-eczema mechanism.
The
immediate reaction
Occurs as a result of
degranulation of mast cells due to an antigen stimulation leading to
release of mediators as histamine, leukotrienes, platelet activating
factor, proteases and others. This reaction may elicit skin disorders such
as in early stages of atopic eczema, urticaria and angioedema.
Investigation of this
type includes: skin prick test, serum IgE and (RAST) test.
The
delayed reaction
Repeated contact of a
specific antigen with a previously sensitized T-cells leads to stimulation
and the release of lymphokines. Lymphokines induce inflammatory reactions
and activate macrophages to release mediators.
This type of reaction
corresponds to the delayed type of contact dermatitis, photo-allergic
dermatitis and late stages of atopic dermatitis.
Cell mediated immune
reactions are common in the defense against fungal, viral, granulomatous
infections of the skin and mediating reactions to insect bite.
Patch tests and
lymphocyte transformation may help to detect the sensitizing allergen.
Skin tests may be of
value in detecting the sensitizing antigen.
ECZEMA
Eczema is an inflammatory
skin reaction in response to an antigen stimulation. Eczema is Greek word
, which means "to boil out" or "to effervesce".
Baer describes eczema as
a pruritic papulovesicular reaction, which is associated in its acute
phase with erythema and edema, and in its chronic phase by thickening,
lichenifecation, scaling, and retaining some of its papulovesicular
features.
Dermatitis constitutes
more than thirty per cent of clinical dermatology.
Classification
of Eczema
There are different
classifications of eczema, which are sometimes confusing and therefore
most authors prefer the word ‘dermatitis‘.
In spite that all cases
of eczema is dermatitis, not all cases of dermatitis is considered as
eczema since dermatitis means skin inflammation.
Classification of eczema
is sometimes arbitrary depending on the causative triggering factors.
Eczema may be classified
into: endogenous, which is due to processes originating within the body or
exogenous eczema that is, mediated by exogenous factors.
-
Endogenous Eczema
The term endogenous
eczema implies that the eczematous condition is not due to exogenous or
external environmental factors, but is mediated by processes originating
within the body.
In some conditions,
however, there are both external and internal precipitating factors.
Endogenous eczema
includes:
Atopic dermatitis
Seborrheic dermatitis
Nummular (Discoid)
Pompholyx (dyshidrotic)
Metabolic eczema or
eczema associated with systemic diseases.
Juvenile planter
dermatoses
Eczematous drug eruption
Stasis dermatitis
-
Exogenous eczema
This type of eczema is
due to different exogenous factors that include the following:
Primary irritant
dermatitis
Allergic contact
dermatitis
Photo allergic dermatitis
Polymorphous light
eruption.
Infective dermatitis
-
Unclassified types of eczema
Neurodermatitis (Lichen
simplex chronicus)
Nodular prurigo
Eczema can be also
classified according to the course and clinical picture in to:
Acute eczema
Sub acute eczema
Chronic eczema
REFERENCES
-
Longley J,
Braverman IM, Edelson RL. Immunology and the Skin: Ann NY Acad Sci
1988
-
Bos JD, Zonneveld
I, Das PK et al. The skin immune system (SIS): distribution and
immunophenotype of lymphocyte subpopulations in normal human skin. J
Invest Dermatol 1987; 88: 569-73.
-
Bruynzeel-Koomen
C. IgE on Langerhans cells: new insights into the pathogenesis of
atopic dermatitis. Dermatologica 1986; 172: 181-3.
-
Kim KM,
Mayumi M, Iwai Y. IgE receptor-bearing lymphocytes in allergic and
non-allergic children. Pediatr Res 1988; 24: 254-7.
-
Streilein JW.
Skin-associated lymphoid tissues (SALT): Origins and functions. J
Invest Dermatol 1983; 80: 12s-15s.
-
Zola H. The
surface antigens of human B-lymphocytes. Immunology Today 1987; 8:
308-15.
-
Chernielewski
J, Vaigot P, Prunieras M. Epidermal Langerhans cells - a cycling
cell population. J Invest Dermatol 1985; 84: 424-6.
-
Wolff K, Stingl G.
The Langerhans cell. J Invest Dermatol 1983; 80: 17s-21s.
-
Weaver CT, Unanue
ET. The costimulatory function of antigen-presenting cells.
Immunology Today 1990; 11: 49-55
-
Quinti I,
Brozek C, Wood N et al. Circulating IgG auto-antibodies to IgE in
atopic syndromes. J Allergy Clin Immunol 1986; 77: 586-94.
-
Cronin E.
Contact Dermatitis. Edinburgh: Churchill Livingstone, 1980.
-
Sampson HA.
Role of immediate food hypersensitivity in the pathogenesis of
atopic dermatitis. J Allergy Clin Immunol 1983; 71: 473-80.
-
Rudzki E,
Grzywa A. Immediate reactions to Balsam of Peru, cassia oil and
ethyl vanillin. Contact Derm 1976; 2: 360-1.
-
Cronin E.
Studies in contact dermatitis. 18. Dyes in clothing. Trans St John‘s
Hosp Derm Soc 1960; 54: 156-64.
-
Reynolds CW,
Ortaldo JR. Natural killer activity: the definition of a function
rather than a cell type.Immunology Today 1987; 8: 172-4.
-
Maibach HI,
Epstein WL. Plant dermatitis: fact and fancy. Postgrad Med 1964; 35:
571-4.
-
Mitchell JC,
Dupuis G, Geissman TA. Allergic contact dermatitis from
sesquiterpenoids of plants. Br J Dermatol 1972; 87: 235-40.
-
Mitchell JC,
Geissmann TA, Dupuis G et al. Allergic contact dermatitis caused by
Artemisia and Chrysanthemum species. J Invest Dermatol 1971; 56:
98-101.
-
Mitchell JC,
Rook AJ. Diagnosis of contact dermatitis from plants. Int J Dermatol
1977; 16: 257-66.
-
Rothenborg
HW, Menne T, St3/4lin K-E. Temperature dependent primary irritant
dermatitis from lemon perfume. Contact Derm 1977; 3: 37-48.
-
Powell SM,
Barrett DK. An outbreak of contact dermatitis from Rhus verniciflua
(Toxicondendron vernifluvum). Contact Derm 1986; 14: 288-9.
-
Dahlquist I,
Fregert S. Formaldehyde releasers. Contact Derm 1978; 4: 173.
-
Menne T,
Hjorth N. Routine patch testing with paraben esters. Contact Derm
1988; 19: 189-91.
Top
|