Department of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, California, USA.
Nat Immunol. 2010 Dec;11(12):1110-8. doi: 10.1038/ni.1954. Epub 2010 Oct 31.
B lymphocytes differentiate into antibody-secreting cells under the antigen-specific control of follicular helper T cells (T(FH) cells). Here we demonstrate that isotype-switched plasma cells expressed major histocompatibility complex (MHC) class II, the costimulatory molecules CD80 and CD86, and the intracellular machinery required for antigen presentation. Antigen-specific plasma cells accessed, processed and presented sufficient antigen in vivo to induce multiple helper T cell functions. Notably, antigen-primed plasma cells failed to induce interleukin 21 (IL-21) or the transcriptional repressor Bcl-6 in naive helper T cells and actively decreased these key molecules in antigen-activated T(FH) cells. Mice lacking plasma cells showed altered T(FH) cell activity, which provided evidence of this negative feedback loop. Hence, antigen presentation by plasma cells defines a previously unknown layer of cognate regulation that limits the antigen-specific T(FH) cell program that controls ongoing B cell immunity.
B 淋巴细胞在滤泡辅助 T 细胞（T(FH) 细胞）的抗原特异性控制下分化为分泌抗体的细胞。在这里，我们证明了同种型转换的浆细胞表达主要组织相容性复合体（MHC）II 类、共刺激分子 CD80 和 CD86 以及用于抗原呈递的细胞内机制。抗原特异性浆细胞在体内获取、加工和呈递足够的抗原，以诱导多种辅助 T 细胞功能。值得注意的是，抗原激活的浆细胞未能在幼稚辅助 T 细胞中诱导白细胞介素 21（IL-21）或转录抑制因子 Bcl-6，并且在抗原激活的 T(FH)细胞中积极降低这些关键分子。缺乏浆细胞的小鼠表现出改变的 T(FH)细胞活性，这为这种负反馈环提供了证据。因此，浆细胞的抗原呈递定义了以前未知的同源调节层，该层限制了控制持续 B 细胞免疫的抗原特异性 T(FH)细胞程序。
