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Blood, 15 February 2005, Vol. 105, No. 4, pp. 1694-1698.
Prepublished online as a Blood First Edition Paper on October 5, 2004; DOI 10.1182/blood-2004-08-3335.
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NEOPLASIA
HLA-G expression is associated with an unfavorable outcome and immunodeficiency in chronic lymphocytic leukemia
Holger Nückel,
Vera Rebmann,
Jan Dürig,
Ulrich Dührsen, and
Hans Grosse-Wilde
From the Department of Hematology, Medical Faculty, University of Duisburg-Essen, Germany; and the Institute of Immunology, Medical Faculty, University of Duisburg-Essen, Germany.
The human leukocyte antigen G (HLA-G) molecule exhibits limited tissue distribution and exerts multiple immunoregulatory functions. Recent studies indicate an ectopic up-regulation in tumor cells that may favor their escape from antitumor immune responses. The role of HLA-G in B-cell chronic lymphocytic leukemia (B-CLL) has not been defined. HLA-G expression was studied retrospectively in circulating B-CLL cells from 47 patients by flow cytometry using the anti-HLA-E specific monoclonal antibody MEM/G9. The proportion of leukemic cells expressing HLA-G varied from 1% to 54%. Patients with 23% or fewer HLA-G-positive cells (according to receiver operating characteristics [ROC] analysis; designated as HLA-G-negative group) had a significantly longer progression-free survival (PFS) time than patients with more than 23% positive cells (median PFS: 120 versus 23 months; P = .0001). In multivariate analysis, HLA-G expression (hazard ratio: 4.8; P = .002) was an even better independent prognostic factor than the zeta-associated protein 70 (ZAP-70) or CD38 status. Humoral and cellular immunosuppression were significantly more prominent in the HLA-G-positive compared with the HLA-G-negative patient group. In B-CLL, the level of HLA-G expression is correlated with the degree of immunosuppression and prognosis. HLA-G may contribute to the impairment of immune responses against tumor cells and infections. Thus, these findings need to be confirmed in a prospective study. (Blood. 2005;105:1694-1698)
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