Purpose of review
It has been a long lasting question that although a similar peripheral allergen-specific immune response has been observed, why some patients show only atopic dermatitis, rhinitis and asthma alone or their combinations. The answer resides in the propensity of resident tissue cells and local antigen-presenting cells and T cells for developing an allergic inflammatory immune response. Antigen-presenting cells introduce processed allergens to T helper lymphocytes, where a decision of developing different types of T cell immunity is given under the influence of several cytokines, chemokines, costimulatory signals and regulatory T cells.
We focused in this review article on effector T cell subsets, which have been recently described such as Th9, Th17 cells and Th22 cells, which are characterized by their IL-9 and IL-10, IL-17 (or IL-17A) and IL-22 expression, respectively together with other proinflammatory cytokines, which coordinate local tissue inflammation. Both naturally occurring CD4+CD25+ regulatory T (Treg) cells and inducible populations of allergen-specific, IL-10-secreting Treg type 1 cells inhibit allergen-specific effector cells and have been shown to play a central role in the maintenance of peripheral homeostasis and the establishment of controlled immune responses in allergic inflammatory tissues.
Better understanding and characterization of newly described effector cell subsets and their interaction between antigen presenting cells and resident tissue cells will enlighten our knowledge on the mechanisms of allergic diseases.