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Título : Ig-like transcript 2 (ILT2) suppresses T cell function in chronic lymphocytic leukemia.
Autor : Villa, Mónica
Lorenzo-Herrero, Seila
González Rodríguez, Ana Pilar
López-Soto, Alejandro
Rodríguez Payer, Ángel
González-García, Esther
González, Segundo
Palabras clave : B cells
Chronic Lymphocytic Leukemia
IFN-γT cells
T cells
inhibitory receptors
Fecha de publicación : 20-jul-2017
Editorial : Taylor&Francis
Citación : Mónica Villa-Álvarez, Seila Lorenzo-Herrero, Ana P. Gonzalez-Rodriguez, Alejandro López-Soto, Angel R. Payer, Esther Gonzalez-Garcia, Leticia Huergo-Zapico & Segundo Gonzalez (2017) Ig-like transcript 2 (ILT2) suppresses T cell function in chronic lymphocytic leukemia, OncoImmunology, 6:10, DOI: 10.1080/2162402X.2017.1353856
Resumen : 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-γ, 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.
URI : https://ria.asturias.es/RIA/handle/123456789/10946
ISSN : 2162-402X
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