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Changes in 1,25-(OH)₂D₃ Synthesis and Its Receptor Expression in Spleen Cell Subpopulations of Mice Infected with LPBM5 Retrovirus

CNRS (T.M.N., J.P., H.G., O.W.-D., M.G.), URA 583, Université Paris V, Hôpital Saint-Vincent de Paul, 75014 Paris, France; INSERM U345 (M.P., C.P.), Institut Necker, 75015 Paris, France

Address all correspondence and requests for reprints to: T. M. Nguyen, CNRS URA 583, Hôpital Saint-Vincent de Paul, 82 avenue Denfert-Rochereau, 75014 Paris, France.

This study examines the influence of chronic retroviral infection of mice with a LPBM5 virus mixture on the paracrine system involving immune cells and 1,25-(OH)₂D₃ in the spleen. Plasma ionized calcium, 25-(OH)D and 1,25-(OH)₂D of infected mice were unchanged. In contrast, the specific binding of 1,25-(OH)₂D₃ to spleen cytosol and the number of monocyte/macrophages expressing 1,25-(OH)₂D₃ receptors (VDR) were markedly increased. The retroviral infection also influenced the local production of 1,25-(OH)₂D₃ in the spleen. It did not alter this production in monocyte/macrophages but increased that in isolated T cells. Isolated B cells in control mice did not produce 1,25-(OH)₂D₃, but they increased the ability of isolated T cells to produce this metabolite during coculture incubations. Infection altered this cell interaction as 1,25-(OH)₂D₃ production in infected T cells decreased when these cells were cocultured with infected B cells.

Thus, chronic retroviral infection alters both the local vitamin D metabolism and VDR expression by immune cells in mice. These findings suggest close local interactions between 1,25-(OH)₂D₃ and immune system activation during retroviral infection.

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