B-1 cells constitute a unique B cell population with distinct ontogenic, phenotypic, and functional characteristics. Naïve, unmanipulated B-1 cells induce differentiation of CD4(+) T cells to become pro-inflammatory Th17 cells whereas naïve B-2 cells do not. We examined the role of distinctly expressed surface membrane molecules in providing B-1 cells with Th17-differentiating function. Neither Mac-1, CD25, PD-L2 nor CD73 appeared to contribute to B-1 cell induction of Th17 differentiation. In contrast, we found that CD44 and CD86 are involved on the basis of studies with neutralizing antibodies and knock-out mice. Activation imparted to naïve B-2 cells the ability to induce Th17 differentiation and this was similarly partially interrupted by interfering with CD44 and CD86. Our findings suggest that CD44-OPN and B7 family members play important roles in the induction of Th17 cell differentiation by B cells.
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 11 September 2012.
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