Killer cell lectin-like receptors (KLRs) are C-type lectin-like glycoproteins encoded by genes clustered in the natural killer gene complex (NKC) located on the short arm of human chromosome 12. In addition to the NKG2 subfamily, the NKC includes a less characterized group of genes coding for NKRP1 receptors and their ligands of the C-type lectin (CLEC) subfamily. Among this group, the best recognized is the NKRP1A/LLT1 pair encoded respectively by the KLRB1 and CLEC2D genes. Both molecules are type II transmembrane-signaling glycoproteins with an extracellular C-type lectin domain. NKRP1A is predominantly expressed on NK cells, where it acts as an inhibitory receptor. However, it stimulates T cells, which results in release of IL-17 and inflammatory cytokines. Triggering LLT1 on NK cells stimulates IFN-γ production. Similarly, it stimulates activation of B cells. LLT1 is also expressed by osteoblasts and chondrocytes and inhibits bone degradation. Expression of LLT1 by tumor cells may facilitate their escape from NK cell surveillance. On the other hand, NKRP1A may be involved in activation of T and B lymphocytes in the course of inflammatory reactions and pathogenesis of autoimmune disorders. Thus, the NKRP1A/LLT1 receptor/ligand system appears to be a new therapeutic target that may be useful in the treatment of cancer as well as some autoinflammatory disorders.

中文翻译：

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人NKRP1A / LLT1受体/配体相互作用的生物学和临床意义。

杀伤细胞凝集素样受体（KLR）是C型凝集素样糖蛋白，由位于人类12号染色体短臂上的自然杀伤基因复合体（NKC）中簇集的基因编码。除NKG2亚家族外，NKC还包括编码NKRP1受体及其C型凝集素（CLEC）亚家族的配体的基因较少。在这一组中，最能识别的是分别由KLRB1和CLEC2D基因编码的NKRP1A / LLT1对。这两个分子都是具有细胞外C型凝集素结构域的II型跨膜信号糖蛋白。NKRP1A主要在NK细胞上表达，在那里它起抑制受体的作用。但是，它刺激T细胞，导致IL-17和炎性细胞因子释放。在NK细胞上触发LLT1会刺激IFN-γ的产生。同样，它刺激B细胞的活化。LLT1也由成骨细胞和软骨细胞表达，并抑制骨降解。肿瘤细胞表达LLT1可能有助于其逃避NK细胞监视。另一方面，在自身免疫性疾病的炎症反应和发病过程中，NKRP1A可能参与T和B淋巴细胞的活化。因此，NKRP1A / LLT1受体/配体系统似乎是一种新的治疗靶标，可用于治疗癌症以及某些自身炎症性疾病。在炎症反应和自身免疫性疾病的发病过程中，NKRP1A可能参与T和B淋巴细胞的活化。因此，NKRP1A / LLT1受体/配体系统似乎是一种新的治疗靶标，可用于治疗癌症以及某些自身炎症性疾病。在炎症反应和自身免疫性疾病的发病过程中，NKRP1A可能参与T和B淋巴细胞的活化。因此，NKRP1A / LLT1受体/配体系统似乎是一种新的治疗靶标，可用于治疗癌症以及某些自身炎症性疾病。