Expression of Ig-Like Transcript 4 Inhibitory Receptor in Human Non-small Cell Lung Cancer

Inhibitory leukocyte immunoglobulin-like receptors in cancer development

“…LILRB2 is expressed in breast cancer cell lines and in 60.7% of primary ductal and lobular breast cancer tissues but is absent from normal breast tissues [33]. The receptor is also expressed on human non-small cell lung cancer cells [34,[39][40][41] and supports the their survival and cancer development [39].…”

“…While our in silico analyses indicate that expression of a number of ITIM inhibitory receptors negatively correlates with AML patient survival, it is possible that some of these receptors may also play positive roles in development of other types of cancer. Indeed, LILRB1, 2, and 4 are expressed in solid cancer cells such as gastric cancer, breast cancer, and lung cancer cells [30,33,34,[39][40][41]. Because there are numerous types of ITIM-containing receptors, different receptors may have different expression patterns in different types or subtypes of cancers.…”

“…Moreover, several LILRBs, PirB, and LAIR1 (a close related ITIM-containing receptor) [22][23][24][25] are expressed by primitive and differentiated acute leukemia cells that support leukemia development [21,26]. A number of reports also showed that LILRBs are expressed in hematopoietic and solid cancer cells and in most cases exert tumor-promoting functions [27][28][29][30][31][32][33][34][35][36][37][38][39][40][41]. Ligands and signaling pathways mediated through LILRBs have also been identified [21,26,38,39,[41][42][43][44].…”

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

“…72 LILRB2 has also been observed in tumour tissue samples derived from lung cancer patients. 73 These findings indicate that inhibitory LILR expression may be a frequent feature of tumorigenesis and, given the ability of LILRs to prevent T-cell priming, may enable tumours to evade a protective immune response. As such, LILRs could serve in the future as targets for intervention in cancer immunotherapy.…”

“…LILRA2 engagement Involved in HLA-G-mediated allograft tolerance 49,94 Peripheral blood mononuclear cells from patients with systemic lupus erythematosus exhibit poor LILRB1 function and diminished expression of this receptor on B cells 58 Coexpressed with HLA-G in multiple sclerosis lesions 60 Up-regulated during HIV infection (see text for details) 63,64,95,96 Proportion of LILRB1 + B cells correlates with severity of malaria 70 Involved in HLA-G-mediated tumour immune evasion 38,[75][76][77]79 LILRB2 Up-regulated on DCs and ECs in the T-cell suppression cascade which generates allograft tolerance 13,23,41 Involved in HLA-G-mediated allograft tolerance 48,94 Up-regulated in rheumatoid arthritis, suggested role in spondyloarthritis 51,53 Up-regulated by interleukin-10 in HIV patients 27 Higher affinity for HIV-1 viral escape mutant 15 Expressed on B cells in leukaemia patients and tumour cells in lung cancer patients 72,73 Involved in HLA-G-mediated tumour immune evasion 38,[75][76][77]79 LILRB4 Up-regulated on DCs and ECs in the T-cell suppression cascade which generates allograft tolerance 13,23,41 Suppresses pancreatic islet allograft rejection in humanized NOD/SCID mice 17 Role in tumour cell evasion of host immune system 18,71 Expressed on B cells in leukaemia patients 72 DCs, dendritic cells; ECs, endothelial cells; HCMV, human cytomegalovirus; HIV, human immunodeficiency virus; HLA, human leucocy...…”