CD27 is acquired by primed B cells at the centroblast stage and promotes germinal center formation
CD27 is acquired by primed B cells at the centroblast stage and promotes germinal center formation
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DOI：
10.4049/jimmunol.172.12.7432
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发表时间：
2004-06-15
影响因子：
4.4
通讯作者：
Borst, J
中科院分区：
文献类型：
--
作者：
Xiao, YL;Hendriks, J;Borst, J
对人B细胞的研究表明，CD 27是B细胞应答的标志物和介体。我们研究了小鼠B细胞上的CD 27表达和功能。我们发现B细胞在中心母细胞阶段获得CD 27，并在进一步分化时逐渐丧失。它不是体细胞突变的B细胞的标志物，并且以非常低的频率存在于记忆B细胞上。中心母细胞中CD 27的富集及其配体CD 70在生殖中心（GC）内或附近的T和B细胞上的偶见存在表明CD 27/CD 70相互作用在克隆B细胞扩增中的作用。因此，响应于流感病毒感染的GC形成在CD 27敲除小鼠中延迟。CD 27缺乏并不影响体细胞超突变或病毒特异性IgM，IgG和伊加的血清水平在主要和回忆反应。将T和B细胞连续转移到CD 27/CD 28（-/-）小鼠中揭示了CD 27通过两种不同的机制促进GC形成和随后的IgG产生。CD 28（+）Th细胞刺激B细胞上的CD 27，加速GC的形成，这很可能是通过促进中心母细胞的扩增。此外，T细胞上的CD 27可以部分替代CD 28支持GC的形成。
Studies on human B cells have featured CD27 as a marker and mediator of the B cell response. We have studied CD27 expression and function on B cells in the mouse. We find that B cells acquire CD27 at the centroblast stage and lose it progressively upon further differentiation. It is not a marker for somatically mutated B cells and is present at very low frequency on memory B cells. Enrichment of CD27 among centroblasts and the presence of its ligand CD70 on occasional T and B cells in or near germinal centers (GCs) suggested a role for CD27/CD70 interactions in clonal B cell expansion. Accordingly, GC formation in response to influenza virus infection was delayed in CD27 knockout mice. CD27 deficiency did not affect somatic hypermutation or serum levels of virus-specific IgM, IgG, and IgA attained in primary and recall responses. Adoptive transfer of T and B cells into CD27/CD28(-/-) mice revealed that CD27 promotes GC formation and consequent IgG production by two distinct mechanisms. Stimulation of CD27 on B cells by CD28(+) Th cells accelerates GC formation, most likely by promoting centroblast expansion. In addition, CD27 on T cells can partially substitute for CD28 in supporting GC formation.