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Abstract：
BACKGROUND: The role of the scavenger receptor CD36 in cell metabolism and the immune response has been investigated mainly in macrophages, dendritic cells, and T cells. However, its involvement in B cells has not been comprehensively examined.
METHODS: To investigate the function of CD36 in B cells, we exposed Cd36fl/flMB1cre mice, which lack CD36 specifically in B cells, to apoptotic cells to trigger an autoimmune response. To validate the proteins that interact with CD36 in primary B cells, we conducted mass spectrometry analysis following anti-CD36 immunoprecipitation. Immunofluorescence and co-immunoprecipitation were used to confirm the protein interactions.
RESULTS: The data revealed that mice lacking CD36 in B cells exhibited a reduction in germinal center B cells and anti-DNA antibodies in vivo. Mass spectrometry analysis identified 30 potential candidates that potentially interact with CD36. Furthermore, the interaction between CD36 and the inhibitory Fc receptor FcγRIIb was first discovered by mass spectrometry and confirmed through immunofluorescence and co-immunoprecipitation techniques. Finally, deletion of FcγRIIb in mice led to decreased expression of CD36 in marginal zone B cells, germinal center B cells, and plasma cells.
CONCLUSIONS: Our data indicate that CD36 in B cells is a critical regulator of autoimmunity. The interaction of CD36-FcγRIIb has the potential to serve as a therapeutic target for the treatment of autoimmune disorders.
METHODS: To investigate the function of CD36 in B cells, we exposed Cd36fl/flMB1cre mice, which lack CD36 specifically in B cells, to apoptotic cells to trigger an autoimmune response. To validate the proteins that interact with CD36 in primary B cells, we conducted mass spectrometry analysis following anti-CD36 immunoprecipitation. Immunofluorescence and co-immunoprecipitation were used to confirm the protein interactions.
RESULTS: The data revealed that mice lacking CD36 in B cells exhibited a reduction in germinal center B cells and anti-DNA antibodies in vivo. Mass spectrometry analysis identified 30 potential candidates that potentially interact with CD36. Furthermore, the interaction between CD36 and the inhibitory Fc receptor FcγRIIb was first discovered by mass spectrometry and confirmed through immunofluorescence and co-immunoprecipitation techniques. Finally, deletion of FcγRIIb in mice led to decreased expression of CD36 in marginal zone B cells, germinal center B cells, and plasma cells.
CONCLUSIONS: Our data indicate that CD36 in B cells is a critical regulator of autoimmunity. The interaction of CD36-FcγRIIb has the potential to serve as a therapeutic target for the treatment of autoimmune disorders.
摘要：
背景：主要在巨噬细胞中研究了清道夫受体CD36在细胞代谢和免疫反应中的作用，树突状细胞,和T细胞。然而,它在B细胞中的参与尚未得到全面检查。
方法：为了研究CD36在B细胞中的功能，我们暴露了Cd36fl/flMB1cre小鼠，在B细胞中特别缺乏CD36，凋亡细胞引发自身免疫反应。为了验证在原代B细胞中与CD36相互作用的蛋白质，我们在抗CD36免疫沉淀后进行了质谱分析。免疫荧光和免疫共沉淀用于确认蛋白质相互作用。
结果：数据显示，B细胞中缺乏CD36的小鼠在体内表现出生发中心B细胞和抗DNA抗体的减少。质谱分析鉴定了30种可能与CD36相互作用的潜在候选物。此外，CD36与抑制性Fc受体FcγRIIb之间的相互作用首先是通过质谱发现的，并通过免疫荧光和免疫共沉淀技术证实。最后,小鼠FcγRIIb缺失导致边缘区B细胞CD36表达降低,生发中心B细胞，和浆细胞。
结论：我们的数据表明B细胞中的CD36是自身免疫的关键调节因子。CD36-FcγRIIb的相互作用具有作为治疗自身免疫性疾病的治疗靶标的潜力。
方法：为了研究CD36在B细胞中的功能，我们暴露了Cd36fl/flMB1cre小鼠，在B细胞中特别缺乏CD36，凋亡细胞引发自身免疫反应。为了验证在原代B细胞中与CD36相互作用的蛋白质，我们在抗CD36免疫沉淀后进行了质谱分析。免疫荧光和免疫共沉淀用于确认蛋白质相互作用。
结果：数据显示，B细胞中缺乏CD36的小鼠在体内表现出生发中心B细胞和抗DNA抗体的减少。质谱分析鉴定了30种可能与CD36相互作用的潜在候选物。此外，CD36与抑制性Fc受体FcγRIIb之间的相互作用首先是通过质谱发现的，并通过免疫荧光和免疫共沉淀技术证实。最后,小鼠FcγRIIb缺失导致边缘区B细胞CD36表达降低,生发中心B细胞，和浆细胞。
结论：我们的数据表明B细胞中的CD36是自身免疫的关键调节因子。CD36-FcγRIIb的相互作用具有作为治疗自身免疫性疾病的治疗靶标的潜力。
