Nurse-like cells control the activity of chronic lymphocytic leukemia B cells via galectin-1

CROCI DIEGO; MORANDE PABLO; DERGAN-DYLON SEBASTIÁN; BORGE MERCEDES; TOSCANO MARTA; STUPIRSKI JC; BEZARES FERNANDO; ÁVALOS JS; NARBAITZ M; GAMBERALE ROMINA; RAVINOVICH GABRIEL; GIORDANO MIRTA

LEUKEMIA

NATURE PUBLISHING GROUP

Lugar: Londres; Año: 2013 vol. 27 p. 1413 - 1416

0887-6924

Chronic lymphocytic leukemia (CLL) cells are preferentially activated in so-called proliferation centers frequently found in lymph nodes and bone marrow from CLL patients.1 In these ?privileged? sites leukemic cells establish close contact with a variety of cell types that provide long-term support for their survival and progression. In addition, CLL cells favor the establishment of immunosuppressive microenvironments by altering the cytokine milieu. Galectin 1 (Gal1), an endogenous β-galactoside-binding lectin found at sites of inflammation and tumor growth, displays pro-survival activity on malignant cells as demonstrated for CD45RA(−) primary myeloma cells. Moreover, it controls tumor cell proliferation and invasiveness and has key roles in tumor-immune escape by dampening T-cell-mediated immunity. In Hodgkin lymphoma, Gal1 is overexpressed in Reed?Sternberg cells, which is a predictive biomarker of disease progression and is responsible for creating the Th2/regulatory T-cell-skewed microenvironment typical of this lymphoproliferative disease. These unique characteristics of Gal1 prompted us to investigate its potential role in CLL biology.