Receptor for CLEC2D/OCIL. Ligand-binding contributes to inhibition of cytotoxic natural killer (NK) cells. May mediate MHC class I-independent 'missing-self' recognition of allografts, tumor cells and virus-infected cells. Homodimer; disulfide-linked. Interacts with tyrosine kinase LCK. Binds PTPN6/SHP-1 in a phosphorylation-dependent manner. Expressed in a subset of natural killer cells. Contains 1 copy of a cytoplasmic motif that is referred to as the immunoreceptor tyrosine-based inhibitor motif (ITIM). The phosphorylated ITIM motif can bind the SH2 domain of several SH2-containing phosphatases leading to down-regulation of cell activation (By similarity). Alleles A, B and C are highly divergent forms of Klrb1b. Alleles A and B differ in their susceptibility to evasion of innate immunity by the rat cytomegalovirus (CMV). In contrast to allele B, allele A shows very low binding of a viral protein mimicking the Klrb1b ligand CLEC2D as well as low susceptibility to this MHC class I-independent viral evasion mechanism.