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Vitamin D-Mediated Gene Regulation in Phenotypically Defined Human B Cell Subpopulations¹

Section of Experimental Pathology, Department of Pathology, Roger Williams Hospital, Providence, Rhode Island 02908; and Boston University, Boston, Massachusetts 02118

Address all correspondence and requests for reprints to: Dr. John W. Morgan, Department of Pathology, Roger Williams Hospital, 825 Chalkstone Avenue, Providence, Rhode Island 02908. E-mail: john_morgan{at}brown.edu

Isolation of distinct subpopulations of density-fractionated normal human B lymphocytes reveals that the requirements for up-regulation of the vitamin D receptor (VDR) and initiation of 1,25-dihydroxyvitamin D₃ [1,25-(OH)₂D₃]-mediated genomic trans-activation are dependent upon the state of cellular activation. The kinetics of the response differ widely among these B cell subpopulations. However, these density-fractionated B cell subpopulations are phenotypically diverse and therefore are not representative of distinct stages of B cell maturation and differentiation. To examine the role of B cell differentiation on the induction and maintenance of biological receptivity to 1,25-(OH)₂D₃, we purified naive, germinal center, and memory B cells based on their expression of CD38 and CD44 surface antigens and surface Ig isotype. These phenotypically defined B cell subpopulations were all found to constitutively express VDR, and all exhibited similar activation requirements and kinetics for initiation of 1,25-(OH)₂D₃-mediated genomic trans-activation. Taken together, these results suggest that defined stages of differentiation in normal B cells are not significant predicators of VDR expression or receptivity to 1,25-(OH)₂D₃. Rather, the degree of cellular activation, regardless of maturation stage, determines whether the effects of this immunoregulatory hormone will influence a mature B lymphocyte.

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