Recent evidence from different experimental systems has demonstrated that autocrine activation of antigen-presenting cells (APCs) may be important at the initiation of an immune response, and that a specific set of cytokines may meet the dual needs of activating APCs and priming and/or maintaining the antigen-specific T-cell response. Composite factors with p40, including IL-12 (p40/p35) and IL-23 (p40/p19), may be two such immunoregulatory cytokines, their effects encompassing actions on both myeloid APCs and T cells. However, although both cytokines enhance the Th1 costimulatory functions of APCs, and IL-23 does induce IL-12 from APCs, their effects, which in part overlap, can be differentiated from one another. This review summarizes recent data on the actions of IL-12 and IL-23 on dendritic cells and macrophages at the interface between innate and adaptive immunity.
Effects of IL-12 and IL-23 on antigen-presenting cells at the interface between innate and adaptive immunity.
PUCCETTI, Paolo;BELLADONNA, Maria Laura;GROHMANN, Ursula
2002
Abstract
Recent evidence from different experimental systems has demonstrated that autocrine activation of antigen-presenting cells (APCs) may be important at the initiation of an immune response, and that a specific set of cytokines may meet the dual needs of activating APCs and priming and/or maintaining the antigen-specific T-cell response. Composite factors with p40, including IL-12 (p40/p35) and IL-23 (p40/p19), may be two such immunoregulatory cytokines, their effects encompassing actions on both myeloid APCs and T cells. However, although both cytokines enhance the Th1 costimulatory functions of APCs, and IL-23 does induce IL-12 from APCs, their effects, which in part overlap, can be differentiated from one another. This review summarizes recent data on the actions of IL-12 and IL-23 on dendritic cells and macrophages at the interface between innate and adaptive immunity.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.