Functional Consequences of Interactions between Human NKR-P1A and Its Ligand LLT1 Expressed on Activated Dendritic Cells and B Cells
作者： David B. Rosen , Wei Cao , Danielle T. Avery , Stuart G. Tangye , Yong-Jun Liu
DOI: 10.4049/JIMMUNOL.180.10.6508
关键词:
摘要: Lectin-like transcript-1 (LLT1) (also named osteoclast inhibitory lectin or CLEC2D) is a ligand for the human NKR-P1A (CD161) receptor, present on NK cells and T cells. To further understand physiological relevance of this interaction, we developed mAbs against LLT1, characterized expression pattern explored functional consequence LLT1 engagement receptor expressed TLR-activated plasmacytoid dendritic, monocyte-derived dendritic cells, B stimulated through TLR9, surface Ig, CD40. Interactions between target inhibit cell-mediated cytotoxicity cytokine production can TNF-α by TCR-activated NKR-P1A+ CD8+ In contrast, failed to augment TCR-dependent activation NKR-P1A-bearing CD4+ Expression activated suggests that it might regulate cross-talk APCs.
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