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H. Lee Moffitt Cancer Center, University of South Florida, Tampa;
Department of Cell Biology and Cancer Center, Albert Einstein College of Medicine, Bronx, New York;
Department of Surgery, University of Pittsburgh, Pennsylvania; and
Department of Medicine and Cancer Center, Vanderbilt University, Nashville, Tennessee
Correspondence: Dmitry Gabrilovich, M.D., Ph.D., H. Lee Moffitt Cancer Center, University of South Florida, MRC-2E, Room 2067, 12902 Magnolia Dr., Tampa, FL 33612. E-mail: dgabril{at}moffitt.usf.edu
Dendritic cells (DC) play a central role in antitumor immune responses. Abnormal differentiation of DC and their inability to stimulate T cells are important factors in tumor escape from immune-system control. However, the mechanisms of this process remain elusive. Here, we have described one possible molecular mechanism that involves replacement linker histone H1°. A close association between expression of H1° and DC differentiation in vitro has been found. DC production in H1°-deficient mice was decreased significantly, whereas generation and function of macrophages, granulocytes, and lymphocytes appear to be normal. However, these mice had a significantly reduced response to vaccination with antigens. Tumor-derived factors considerably reduced h1° expression in hematopoietic progenitor cells. We have demonstrated that transcription factor NF-
B is involved actively in regulation of h1°. Thus, H1° histone may be an important factor in normal DC differentiation. Tumor-derived factors may inhibit DC differentiation by affecting H1° expression.
Key Words: monocytes/macrophages • cellular differentiation • tumor immunity
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