Regulation of T‐cell immunity by leucocyte immunoglobulin‐like receptors: innate immune receptors for self on antigen‐presenting cells

Abstract

Summary Following recognition of microbial patterns, innate immune receptors provide a rapid innate response and trigger antigen‐presenting cell maturation to instruct adaptive immune responses. Here we discuss a family of innate immune receptors for self – the leucocyte immunoglobulin‐like receptors (LILRs). These LILRs exert powerful inhibitory effects on antigen‐presenting cell phenotype and subsequent T‐cell responses, and may act to constrain the effects of Toll‐like receptor signalling. Despite their broad ligand specificity, differing affinities of LILRs for individual complexes of peptide–major histocompatiblity complex can determine the nature of their effect on downstream immune responses. Expression and function of LILRs may be skewed in certain conditions such as cancer or human immunodeficiency virus infection, particularly by ectopic expression of human leucocyte antigen‐G, a high‐affinity LILR ligand. We discuss the relevance of LILR‐mediated immune regulation across a range of scenarios from autoimmunity to transplant medicine, infection and cancer.

Amelioration of 2,4,6-trinitrobenzene sulfonic acid-induced colitis in mice by immunoregulatory dendritic cells

“…Thus, LILRs with inhibitory and stimulatory activity can also influence the antigen-presenting properties of macrophages and dendritic cells and may thus play a role in T cell tolerance. The wide-ranging effects of LILR signaling on immune cell activity imply that these receptors are likely to play an important role in a range of clinical situations, including autoimmune diseases, infectious diseases, transplantation, and cancer [33,34]. Actually, it has been reported that triggering of LILRs through their interaction with self proteins can modulate the DC activation status, antigen-presenting functions, and the capacity to elicit T cell responses [34].…”

Comparative transcriptome analysis of muscular dystrophy models Largemyd, Dmdmdx/Largemyd and Dmdmdx: what makes them different?

“…It is believed that this receptor controls inflammatory responses and cytoxicity, limiting auto reactivity. 46 There is no information in the literature that helps to correlate Lilrb3 upregulation with the double-mutant phenotype.…”

The importance of HLA-G expression in embryos, trophoblast cells, and embryonic stem cells

“…It is known that HLA-G mRNA transcription is up-regulated by hormones (i.e., progesterone) [48] and interferons (IFNs) [49]. Interleukin-10 up-regulates both HLA-G [50,51] and its receptors LILRB1 and LILRB2 [52]. Hypoxia induces the expression of all HLA-G transcripts in term CTBs [53]; epidermal growth factor (EGF), a trophoblast growth and syncytialization factor, enhances protein expression of HLA-G5 [41].…”