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10.1080/2162402X.2017.1353856

http://scihub22266oqcxt.onion/10.1080/2162402X.2017.1353856
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C5665082!5665082!29123965
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suck abstract from ncbi


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pmid29123965      Oncoimmunology 2017 ; 6 (10): ä
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  • Ig-like transcript 2 (ILT2) suppresses T cell function in chronic lymphocytic leukemia #MMPMID29123965
  • Villa-Álvarez M; Lorenzo-Herrero S; Gonzalez-Rodriguez AP; López-Soto A; Payer AR; Gonzalez-Garcia E; Huergo-Zapico L; Gonzalez S
  • Oncoimmunology 2017[]; 6 (10): ä PMID29123965show ga
  • Chronic lymphocytic leukemia (CLL) is associated with a profound dysregulation of the immune system. Loss of T cell function is frequently caused in cancer by sustained signaling of inhibitory receptors. Here, we analyzed the role of the novel inhibitory receptor Ig-like transcript 2 (ILT2) in the pathogenesis of CLL. We observed that ILT2 expression was markedly reduced on leukemic cells, whereas it was increased on CD8 and CD4 T cells from CLL patients, particularly in those patients harboring chromosome 11q deletion, which includes the ATM gene. A deep dysregulation of ILT2 ligands expression in leukemia cells was also observed. ILT2 impaired the activation and proliferation of CD4 and CD8 T cells in CLL patients, but it had no effect in leukemic cells. ILT2 downregulated the production of IL-2 by CD4 T cells of CLL patients and induced the expression of cytokines that promote the survival of leukemic cells, such as IFN-?, by T cells. Importantly, ILT2 blockade restored the activation, proliferation and cytokine production of T cells. In conclusion, we describe a novel immune inhibitory pathway that is upregulated in CLL and delineate a new potential target to be explored in this disease.
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