Dendritic cells play an important role in allergy illness by regulating immunological responses to innate stimuli and encouraging the development of T helper 2 (TH2) effector versus T-regulatory cells. This study will discuss recent developments in the knowledge of how current types of immunotherapy influence dendritic cell responses in this paper. Sublingual immunotherapy (SLIT) and oral immunotherapy (OIT) for peanut allergy change the expression of costimulatory molecules on dendritic cells, resulting in decreased antigen-nonspecific production of TH2 effector cytokines. SLIT and OIT also influence dendritic cell innate immunological responses to Toll-like receptor agonists, including increased interferon production and decreased expression of proinflammatory cytokines, which may aid in the establishment of tolerance. Following OIT, dendritic cells isolated from patients induced hypomethylation of the FOXP3 gene in effector T cells. Reduced methylation of the FOXP3 gene has been linked to longer-lasting clinical desensitization after OIT. Recent research has also revealed that B cells have a role in the induction of tolerogenic dendritic cell populations and T-regulatory cells during immunotherapy. Epicutaneous immunotherapy may also induce immunosuppressive populations of cutaneous dendritic cells, however, antigen exposure through the skin might cause sensitization in some circumstances. Finally, efforts have been directed toward discovering pharmacologic and/or antigen-independent methods for modifying dendritic cell activity in order to improve the immunosuppressive effects of immunotherapy.
Immunotherapy relies heavily on dendritic cells. The immunosuppressive effects of this therapy are most likely due to changes in both adaptive and innate immunity.