HLA-G and its KIR ligands in cancer--another enigma yet to be solved?
Alterations of antigen-presenting human leukocyte antigen (HLA) molecules often occur in cancer and represent one of the mechanisms by which tumours evade host immunosurveillance. One such molecule, HLA-G, was recently implicated in the same context. HLA-G is thought to mediate the tolerance of the semi-allogeneic fetus during pregnancy, by inhibiting maternal immune response through interaction with different HLA-G-recognizing killer-cell inhibitory receptors (KIRs). A report in this issue of the journal demonstrates for the first time the expression of HLA-G and its KIR ligand, ILT-2 in human breast cancer. Apart from the up-regulation on tumour cells, the authors describe HLA-G induction on the macrophages and T cells infiltrating the breast cancer lesions. Moreover, a subset of infiltrating cells also expressed HLA-G-recognizing KIR, ILT-2. This editorial discusses the induction of HLA-G and related KIR molecules as another mechanism for tumours to escape immune recognition.
Urosevic
Mirjana
M
Trojan
Andreas
A
Dummer
Reinhard
R
D001943:Breast Neoplasms / Q000276:immunology*; D005260:Female; D006680:HLA Antigens / Q000276:immunology*; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000276:immunology*; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology; D011971:Receptors, Immunologic / Q000276:immunology*; D054340:Receptors, KIR; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D019139:Tumor Escape
D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D011971:Receptors, Immunologic; D054340:Receptors, KIR