Allergen

Allergens can be classified according to different aspects:

• IgE-reactive allergens: Allergens against which a misdirected immune response is directed in type I allergies. These allergens are ubiquitous. Contact occurs via inhalation, ingestion or touch.
• Allergen source: e.g. animal hair allergens, pollen allergens (see below pollen, pollinosis), mould allergens (see below mould diseases), insect venom allergy.
• Type of contact with allergens: e.g. inhalation allergens (see below inhalation allergies, occupational; see below contact allergens).
• Pathomechanisms via which allergens trigger an allergic reaction: see below. allergy.
• Membership of certain protein families (e.g. lipocalins, structural proteins [e.g. profilins], storage proteins, proteases [e.g. cysteine proteases and serine proteases]).

• Due to the physicochemical properties of the allergenic substance, a sensitization to the substance or to the substance bound to a carrier occurs when the substance is disposed of accordingly.
• T-helper cells play a key role in the immune system. Depending on the type of contact with the allergen, they differentiate into two different types:
  • If macrophages present the antigen, TH1 cells are formed which cause the production of class G immunoglobulins.
  • If B lymphocytes or dendritic cells present the allergen, TH2 cells are formed in the case of a genetically determined allergic predisposition, which ensure the production of IgE. The specific IgE attaches itself to the mast cells concentrated in the skin and mucous membranes and stimulates them to release mediators, i.e. pro-inflammatory substances such as histamine, when the allergen is encountered again. At the same time the allergen activates the specific TH2 cells. The stimulated TH2 cells additionally intensify the allergic symptoms by sensitising the mast cells via cytokines, activating eosinophils, stimulating the expression of adhesion molecules and suppressing the formation of TH1 cells.
• Allergens have different epitopes for IgE and TH cells.
• The IgE-forming B lymphocytes and TH cells react with different regions of the allergenic molecules, the B and T cell epitopes. B-lymphocytes bind with their immunoglobulin receptors preferably to surface structures of the native allergen molecules. These B-cell epitopes are determined by the characteristic spatial structure of the native allergens and are often composed of unconnected peptide segments. Such B-cell epitopes are discontinuous and conformation dependent. However, in order for a B lymphocyte activated by B cell epitopes to produce IgE antibodies, it needs further signals from an allergen-specific TH2 cell. The TH cells do not react with the intact allergen, but with allergenic fragments, which in addition must be bound to the body's own MHC molecules of class II of antigen-presenting cells (APC). To do this, the allergens would have to be taken up by the APC and degraded to peptides of 10-35 amino acids. These T-cell epitopes depend on the sequence of the amino acids and not on the conformation of the native allergen.
• The switch of the B-lymphocyte to the synthesis of IgE antibodies is controlled by the cytokines IL-4 and IL-13 of the activated TH2 cell and by direct contact of certain cell membrane molecules.