Identification of CD72 as a lymphocyte receptor for the class IV semaphorin CD100: A novel mechanism for regulating B cell signaling
Identification of CD72 as a lymphocyte receptor for the class IV semaphorin CD100: A novel mechanism for regulating B cell signaling
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DOI：
10.1016/s1074-7613(00)00062-5
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发表时间：
2000-11-01
期刊：
影响因子：
32.4
通讯作者：
Kikutani, H
中科院分区：
文献类型：
--
作者：
Kumanogoh, A;Watanabe, C;Kikutani, H
我们通过差减cDNA克隆鉴定了淋巴细胞信号素CD100/Sema4D是CD40诱导的分子。CD100刺激可显著增强CD40对B细胞反应的影响。注射可溶性CD100可显著加速体内抗原特异性抗体反应。在肾小管上皮细胞(K-d=类似于1×10(-9)M)和淋巴细胞(K-d=类似于3×10(-7)M)上检测到不同结合亲和力的CD100受体克隆表明，淋巴细胞上的CD100受体是CD72，它是B细胞反应性的负调节因子。因此，CD72代表了一类新的信号素受体。CD100刺激诱导CD72酪氨酸去磷酸化和SHP-1从CD72解离。我们的发现表明，CD100通过CD72关闭负信号的新机制在免疫反应中发挥关键作用。
We have identified the lymphocyte semaphorin CD100/Sema4D as a CD40-inducible molecule by subtractive cDNA cloning. CD100 stimulation significantly enhanced the effects of CD40 on B cell responses. Administration of soluble CD100 markedly accelerated in vivo antigen-specific antibody responses. CD100 receptors with different binding affinities were detected on renal tubular cells (K-d = similar to1 X 10(-9) M) and lymphocytes (K-d = similar to3 x 10(-7) M) Expression cloning revealed that the CD100 receptor on lymphocytes is CD72, a negative regulator of B cell responsiveness. CD72 thus represents a novel class of semaphorin receptors. CD100 stimulation induced tyrosine dephosphorylation of CD72 and dissociation of SHP-1 from CD72. Our findings indicate that CD100 plays a critical role in immune responses by the novel mechanism of turning off negative signaling by CD72.