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Antagonism between MyD88‐ and TRIF‐dependent signals in B7RP‐1 up‐regulation

Type I interferons (IFN) play a critical role in the Toll‐like receptor (TLR)‐mediated expression of B7 costimulatory family members. For example, LPS‐induced up‐regulation of CD80 (B7.1) and CD86 (B7.2) is abrogated in antigen‐presenting cells (APC) deficient in TRIF or TRAM, two adaptors that are responsible for TLR4‐mediated production of Type I IFN. In this report, we demonstrate that LPS‐induced up‐regulation of B7‐related protein 1 (B7RP‐1), a ligand for ICOS, is dependent primarily upon the MyD88‐dependent signaling pathway. Signaling via the TRIF pathway sharply limits MyD88‐dependent B7RP‐1 up‐regulation. Hence, LPS induces significantly higher B7RP‐1 expression on TRIF‐ or TRAM‐deficient mouse peritoneal macrophages and on TRIF‐deficient mouse splenic B cells as compared to wild‐type cells. Further studies reveal that Type I IFN are general suppressors of TLR‐mediated up‐regulation of B7RP‐1. These data indicate that Type I IFN play a dual role in the TLR‐mediated expression of B7 costimulatory family members and suggest that they may act to limit B7RP‐1 expression and thus limit signals derived from B7RP‐1‐ICOS interaction.