Abstract
Lymphotoxin‐β receptor (LTβR) signaling is essential for IgA production in the intestinal lamina propria (LP) and it has been proposed that LTβR‐signaling is needed for the accumulation of IgA‐secreting B‐1 cells in the LP. Yet, in spite of diminished numbers of B‐1 cells in the LP of LTβR−/− mice, a residual population of B‐1 cells remain and B‐2 cell numbers in the LP are normal. To further explore the mechanism for LTβR‐dependent IgA production in the gut, we hypothesized that LTβR signaling may regulate accessory cells in the LP that influence IgA production by LP‐resident B cells. The LP harbors a recently described subset of iNOS+ dendritic cells (DC) that are required for IgA responses. We characterized this DC population in the LP of WT mice as CD11c+ CD11blo Thy1+ CD8α − B220− and, interestingly, we found that these cells were essentially undetectable in LTβR−/ − mice. In mixed bone marrow chimeras, the presence of iNOS+ DC in the LP depended primarily on the expression of LTβR by radio‐resistant cells, whereas the expression of LTβR on DC themselves was not essential. We conclude that the presence of IgA‐promoting iNOS+ DCs in the LP requires intact LTβR signaling on the LP stroma, and these data provide a mechanism for defective IgA production in LTβR−/ − mice. This work was supported by the Canadian Institutes of Health Research.
Published Version
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