David B. Rosen

TL;DR: Treatment with the IFN-α/β inducer polyinosine polycytidylic acid inhibited egress by a mechanism that was partly lymphocyte-intrinsic, and observations indicate that CD69 forms a complex with and negatively regulates S1P1 and that it functions downstream ofIFN- α/β, and possibly other activating stimuli, to promote lymphocyte retention in lymphoid organs.

TL;DR: Readily induced by IFN and other proinflammatory cytokines, BST2 may modulate the human pDC’s IFN responses through ILT7 in a negative feedback fashion.

TL;DR: In this article, the lectin-like transcript-1 (LLT1) is shown to be a physiologic ligand for NKR-P1A, and LLT1-containing liposomes bind to NKRp1A + cells, and binding is inhibited by anti-NKR-p1a mAb.

TL;DR: It is demonstrated that the lectin-like transcript-1 (LLT1) is a physiologic ligand for NKR-P1A, a C-type lectin receptors present on NK cells and subsets of T cells.

TL;DR: It is demonstrated here that ILT7 protein associates with the signal adapter protein FcɛRIγ to form a receptor complex that negatively regulates the innate immune functions of human pDCs.