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Abstract
Allergen immunotherapy is effective in patients with IgE-dependent allergic rhinitis
and asthma. When immunotherapy is given continuously for 3 years, there is persistent
clinical benefit for several years after its discontinuation. This disease-modifying
effect is both antigen-specific and antigen-driven. Clinical improvement is accompanied
by decreases in numbers of effector cells in target organs, including mast cells,
basophils, eosinophils, and type 2 innate lymphoid cells. Immunotherapy results in
the production of blocking IgG/IgG4 antibodies that can inhibit IgE-dependent activation
mediated through both high-affinity IgE receptors (FcεRI) on mast cells and basophils
and low-affinity IgE receptors (FcεRII) on B cells. Suppression of TH2 immunity can
occur as a consequence of either deletion or anergy of antigen-specific T cells; induction
of antigen-specific regulatory T cells; or immune deviation in favor of TH1 responses.
It is not clear whether the altered long-term memory resides within the T-cell or
the B-cell compartment. Recent data highlight the role of IL-10-producing regulatory
B cells and "protective" antibodies that likely contribute to long-term tolerance.
Understanding mechanisms underlying induction and persistence of tolerance should
identify predictive biomarkers of clinical response and discover novel and more effective
strategies for immunotherapy.