Surface localization of high-mobility group nucleosome-binding protein 2 (HMGN2) on leukemic B cells from chronic lymphocytic leukemia patients is related to secondary autoimmune hemolytic anemia.

MORANDE PABLO; BORGE MERCEDES; ABREU CECILIA; GALLETTI JEREMÍAS; ZANETTI SAMANTA ROMINA; NANNINI PAULA ROMINA; BEZARES RAIMUNDO FERNANDO; PANTANO S; DIGHIERO GUILLERMO; OPPEZZO PABLO; GAMBERALE ROMINA; GIORDANO MIRTA

LEUKEMIA AND LYMPHOMA

TAYLOR & FRANCIS LTD

Lugar: Londres; Año: 2015 vol. 56 p. 1115 - 1122

1042-8194

Chronic lymphocytic leukemia (CLL) is the main cause ofautoimmune hemolytic anemia (AHA). However, the cellularbasis underlying this strong association remains unclear. Wepreviously demonstrated that leukemic B cells from patientswith CLL recognize the erythrocyte protein Band 3, a prevalentautoantigen in AHA. Here we show that the major binding siteof Band 3 on leukemic cells is an extrinsic protein identifi ed ashigh-mobility group nucleosome binding protein 2 (HMGN2), anucleosome-interacting factor which has not been previouslyreported at the cell surface. T lymphocytes do not expressHMGN2 or bind Band 3. Removal of HMGN2 from the cellmembrane abrogated the capacity of Band 3-pulsed CLL cellsto induce CD4 T cell proliferation. We conclude that surfaceHMGN2 in leukemic B cells is involved in Band 3 binding, uptakeand presentation to CD4 T lymphocytes, and as such may favorthe initiation of AHA secondary to CLL.