Abstract

Understanding the Ly49 gene family can be challenging in terms of nomenclature and genetic organization. The Ly49 gene family has two major gene nomenclature systems, Ly49 and Killer Cell Lectin-like Receptor subfamily A (klra). Mice from different strains have varying numbers of these genes with strain specific allelic variants, duplications, deletions, and pseudogene sequences. Some members activate NK lymphocytes, invariant NKT (iNKT) lymphocytes and γδ T lymphocytes while others inhibit killing activity. One family member, Ly49Q, is expressed only on myeloid cells and is not found on NK, iNKT, or γδ T cells. There is growing evidence that these receptors may regulate not just the immune response to viruses, but other intracellular pathogens as well. Thus, this review’s primary goal is to provide a guide for researchers first encountering the Ly49 gene family and a foundation for future studies on the role that these gene products play in the immune response, particularly the response to intracellular viral and bacterial pathogens.

Highlights

  • The highly polymorphic Ly49 genes serve as a reminder that nature and evolution occasionally conspire to resist systematic classification schemes

  • The first identified function of the Ly49 genes was as an inhibitor of Natural Killer (NK) lymphocyte killing of tumor cell lines that express MHC Class I

  • It was subsequently found that some Ly49 genes inhibited killing but others activated killing, both via interactions with MHC Class I molecules and other molecules like murine cytomegalovirus m157 on the surface of target cells (Makrigiannis and Anderson, 2000)

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Summary

Introduction

The highly polymorphic Ly49 genes serve as a reminder that nature and evolution occasionally conspire to resist systematic classification schemes. The first identified function of the Ly49 genes was as an inhibitor of NK lymphocyte killing of tumor cell lines that express MHC Class I. It was subsequently found that some Ly49 genes inhibited killing but others activated killing, both via interactions with MHC Class I molecules and other molecules like murine cytomegalovirus m157 on the surface of target cells (Makrigiannis and Anderson, 2000).

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