Richard A. Kroczek

TL;DR: ICOS signaling is required for inhibition of the transcription factor Klf2, which controls expression of genes expressed by follicular T helper (Tfh) cells, resulting in disruption of the germinal center response.

TL;DR: A biological role is proposed for ICOS as a costimulatory, agonistic molecule for a variety of effector T cells with differing and partly opposing functional roles to reconcile a number of past in vivo studies with seemingly contradictory results on ICOS function.

TL;DR: Results show that mLC spontaneously undergo apoptosis in culture and that the progression of mLC to apoptosis is inhibited by TRAP and TNF‐α, but accelerated by IL‐10.

TL;DR: The data suggest an important physiological role of ICOS-L in the reactivation of effector/memory T cells on the endothelium controlling the entry of immune cells into inflamed tissue.

TL;DR: It is demonstrated that primed CD8+ T cells reorganize the intranodal dendritic cell network to optimize pDC and XCR1+ DC cooperativity and thereby enhance CD8- T cell immunity.