Center for Oncology and Cell Biology, The Feinstein Institute for Medical Research Manhasset, NY, USA.
Front Immunol. 2012 Sep 11;3:281. doi: 10.3389/fimmu.2012.00281. eCollection 2012.
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.
B-1 细胞是一种具有独特的发生、表型和功能特征的 B 细胞群体。未成熟、未受调控的 B-1 细胞诱导 CD4(+)T 细胞分化为促炎 Th17 细胞，而未成熟的 B-2 细胞则不会。我们研究了表达独特的表面膜分子在赋予 B-1 细胞 Th17 分化功能中的作用。Mac-1、CD25、PD-L2 和 CD73 似乎都没有促进 B-1 细胞诱导 Th17 分化。相反，我们发现基于中和抗体和敲除小鼠的研究，CD44 和 CD86 参与其中。激活赋予初始 B-2 细胞诱导 Th17 分化的能力，而通过干扰 CD44 和 CD86，这种能力也被部分阻断。我们的研究结果表明，CD44-OPN 和 B7 家族成员在 B 细胞诱导 Th17 细胞分化中发挥重要作用。
