Differential Regulation of Type 2 Immunity by Glucocorticoids.

Abstract

Glucocorticoids (GCs) are steroid hormones that are commonly utilized in clinical practice due to their immunosuppressive properties. While GCs are commonly understood to diminish various aspects of the immune response, there is evidence suggesting that they may, under certain conditions, enhance immune responses, particularly within the realm of type 2 immunity. In this mini review, we delineate the current understanding of how GCs differentially affect immune responses related to type 2 immunity, including both in vivo and in vitro-such as Th2 (T helper type 2) cell differentiation, regulatory T cell functions, immunoglobulin E production by B cells, and the roles of myeloid cells like dendritic cells, mast cells, eosinophils, and basophils. Furthermore, we probe the molecular mechanisms by which GCs selectively influence these cell types, and discuss how these insights enhance our basic understanding of GC-driven immune regulation. Unraveling these intricate, context-dependent effects could inform the development of more precise and efficacious GC-based treatments, while reducing adverse outcomes associated with Th1/Th2 imbalance, including heightened infection risks and exacerbation of allergic responses.