Allergic diseases are highly prevalent disorders that exact a heavy toll of morbidity. Whereas a fine balance is normally struck between immune effector and tolerogenic mechanisms to ensure effective but self-contained and minimally damaging immune responses, this balance fails in those disorders. Of particular interest is the role in these disorders of regulatory T (Treg) cells, which act to maintain immune homeostasis and ward off exuberant or tissue damaging immune responses. In this review, we explore how chronic allergic inflammation can destabilize Treg cells and promote their acquisition of pathogenic T helper cell phenotypes that aggravate disease. We describe cellular and molecular mechanisms involved in such re-programming of Treg cells and therapeutic opportunities by which reprogramming can be reversed to reestablish enduring tolerance.
Download Citation: Endnote/Zotero/Mendeley (RIS) RIS File
Download Citation: BibTeX BibTeX File