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    • "LILRs [4], [5], [6] are also called Ig-like transcript (ILT) or leukocyte Ig-like receptor (LIR) or CD85 and are closely related to KIRs but expressed on the surface of a more broad range of cells (i.e., on lymphoid and/or myeloid cells). There are 13 members (two of them are believed to be pseudogenes) of either activating or inhibitory receptors in the LILR family [7]. LILR family members contain either two or four C2-type Ig-like domains in their extracellular portions (D1, D2, D3, and D4). "
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    ABSTRACT: Structurally, Group 1 LILR (Leukocyte Immunoglobulin (Ig)-Like Receptor, also known as Ig-like transcripts, ILT; Leukocyte Ig-like receptor, LIR; and CD85) members are very similar in terms of the HLAIs (human leukocyte antigen class I molecules) binding region and were hypothesized that they all bind to HLAIs. As one of the Group 1 LILRs, LILRA3 is the only secretory LILR and may greatly control the inhibitory immune response induced by LILRB1, LILRB2, and other HLA-binding LILR molecules like LILRA1. Nevertheless, little was known about the binding of LILRA3 to HLAIs. In this report, we present the crystal structure of the LILRA3 domain 1 (D1) and evaluate the D1 and D1D2 (domain 1 and domain 2) binding to classical and non-classical HLAIs using BIAcore® surface plasmon resonance analysis (SPR). We found that LILRA3 binds both classical HLA-A*0201 and non-classical HLA-G1 but with reduced affinities compared to either LILRB1 or LILRB2. The polymorphic amino acids and the LILRA3 D1 structure support this notion.
    Full-text · Article · Apr 2011 · PLoS ONE
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    • "L refers to inhibitory receptors that have a long cytoplasmic tail, and S refers to activating receptors that have a short cytoplasmic tail. KIR CD nomenclature from the VII International Workshop on Human Leukocyte Differentiation Antigens (Andre et al, 2001). Bold font refers to the activating receptors. "
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    ABSTRACT: Chronic natural killer (NK) lymphocytosis is a rare disorder characterized by an indolent clinical course. Despite high NK cell numbers, many patients present with only mild clinical symptoms, and are often asymptomatic. NK cells are equipped with a range of receptors that bind human leucocyte antigen (HLA)-class I molecules. The killer immunoglobulin-like receptors (KIR, CD158) bind groups of HLA alleles, the CD94/NKG2 receptors bind HLA-E, and the CD85j (ILT2, LIR-1) receptor binds to the relatively non-polymorphic alpha3 domain of HLA molecules. Inhibitory HLA class I receptors silence NK cells against cells expressing normal levels of HLA class I. Analysis of NK cells in six patients with chronic NK lymphocytosis revealed a high level of the inhibitory CD94/NKG2A receptor on all NK cells. In four patients, KIR were absent, in one patient a single KIR was expressed in the absence of self-ligand, and in one patient CD85j and multiple KIR were expressed. Cytotoxicity assays demonstrated that all HLA class I receptors were functional. The ability of monoclonal antibodies to block the receptors and allow killing of autologous target cells established that both receptor and ligand expression were adequate for inhibitory function. We propose that the silent behaviour of NK cells in patients with chronic NK lymphocytosis is due to effective inhibitory HLA class I receptors.
    Full-text · Article · Jul 2003 · British Journal of Haematology
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    • "We have characterized the KIR repertoire by RT- PCR, based on the three groups of alternative splicing. Depending on the length of cytoplasmic domain, long (L) or short (S), these three groups could be further classified into 12 subgroups, which were recently given CD designations, CD158a to CD158k plus CD158z (Andre et al, 2001 ). Based on immunohistochemistry , four groups reported KIR T-cell lymphomas . "
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    ABSTRACT: Most sinonasal lymphomas have a restricted killer immunoglobulin-like receptor (KIR) repertoire without a monoclonal T-cell receptor-gamma (TCR-gamma) rearrangement, implying an NK lineage. However, the lineage assignment of sinonasal lymphoma with a monoclonal TCR-gamma rearrangement is unclear because of its mixed NK/T phenotype. The possibility of a mixed NK/T lineage arises with the discovery of T cells with NK features, such as KIR(+) T cells or Valpha24(+) NKT cells. The former might transform into a T-cell lymphoma with both a monoclonal TCR-gamma rearrangement and a restricted KIR repertoire; the latter might give rise to a T-cell lymphoma with a monoclonal Valpha24 rearrangement and possibly a restricted KIR repertoire. To identify such mixed-lineage lymphomas, we undertook a survey of 15 consecutive sinonasal lymphomas and found six with both a restricted KIR repertoire and a monoclonal TCR-gamma rearrangement, consistent with KIR(+) T-cell lymphomas. Among these six cases, four female CD56(-)/CD44(-)/CD8(-)/CD45RO(+)/CD45RA(-) cases constituted a distinct group with a better prognosis than the rest of the male cases of sinonasal lymphomas. None of the six cases had a monoclonal Valpha24 repertoire, thus excluding a derivation from NKT cells. The predominance of KIR(+) T cells that normally function in chronic viral infections over Valpha24(+) NKT cells that typically recognize glycolipid antigens is consistent with the known association of Epstein-Barr virus infection with sinonasal lymphoma. The demonstration of mixed lineage in a mature lymphoid neoplasm is unusual and echoes the World Health Organization classification that placed NK-cell and T-cell lymphomas in a mixed group.
    Full-text · Article · Feb 2003 · Laboratory Investigation
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