T-Cell-Independent Immune Responses Do Not Require Cxc Ligand 13-Mediated B1 Cell Migration
T-Cell-Independent Immune Responses Do Not Require Cxc Ligand 13-Mediated B1 Cell Migration
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DOI：
10.1128/iai.00371-10
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发表时间：
2010-09-01
影响因子：
3.1
通讯作者：
Alugupalli, Kishore R.
中科院分区：
文献类型：
--
作者：
Colombo, Matthew J.;Sun, Guizhi;Alugupalli, Kishore R.
B细胞的动态运动增加了遇到特定抗原的可能性，并促进了快速抗体反应所需的细胞间相互作用。B1a和B1b细胞在体腔中富集，有助于t细胞非依赖性（TI）抗体反应，并在抗原暴露时数量增加。B1细胞的运动主要由Cxc配体13 （Cxcl13）控制，缺乏这种趋化因子的小鼠腹膜B1细胞严重减少。在这项研究中，我们检测了依赖于cxcl13的B细胞通过赫氏疏疏杆菌感染或肺炎球菌多糖或4-羟基-3-硝基苯基乙酰(NP)-Ficoll腹腔免疫的迁移作用，所有这些都能诱导B1b细胞产生强大的抗体反应。令人惊讶的是，我们发现野生型和Cxcl13（-/-）小鼠对hermsii或FhbA （B1b细胞的抗原靶点）的抗体反应和菌血症的解决在野生型和Cxcl13（-/-）小鼠之间没有区别。重要的是，我们没有观察到Cxcl13（-/-）小鼠腹膜B1b细胞数量的增加。尽管如此，已经解决感染的小鼠对再次感染具有抵抗力，这表明腹膜B1b细胞储存库不是控制hermsii所需的。此外，尽管腹膜B1b隔室减少，肺炎球菌多糖疫苗免疫在野生型和Cxcl13（-/-）小鼠中产生了相当的抗原特异性抗体反应，并赋予了对肺炎链球菌的保护。同样，NP-Ficoll免疫在野生型和Cxcl13（-/-）小鼠中引起类似的抗体反应。这些数据表明，B1细胞归巢进入体腔并不是产生保护性TI抗体反应的必要条件，即使抗原最初定位于该解剖腔。
The dynamic movement of B cells increases the probability of encountering specific antigen and facilitates cell-cell interactions required for mounting a rapid antibody response. B1a and B1b cells are enriched in the coelomic cavity, contribute to T-cell-independent (TI) antibody responses, and increase in number upon antigen exposure. B1 cell movement is largely governed by Cxc ligand 13 (Cxcl13), and mice deficient in this chemokine have a severe reduction in peritoneal B1 cells. In this study, we examined the role of Cxcl13-dependent B cell migration using Borrelia hermsii infection or intraperitoneal immunization with pneumococcal polysaccharide or 4-hydroxy-3-nitrophenyl-acetyl (NP)-Ficoll, all of which induce robust antibody responses from B1b cells. Surprisingly, we found that antibody responses to B. hermsii or to FhbA, an antigenic target of B1b cells, and the resolution of bacteremia were indistinguishable between wild-type and Cxcl13(-/-) mice. Importantly, we did not observe an expansion of peritoneal B1b cell numbers in Cxcl13(-/-) mice. Nonetheless, mice that had resolved infection were resistant to reinfection, indicating that the peritoneal B1b cell reservoir is not required for controlling B. hermsii. Furthermore, despite a reduced peritoneal B1b compartment, immunization with pneumococcal polysaccharide vaccine yielded comparable antigen-specific antibody responses in wild-type and Cxcl13(-/-) mice and conferred protection against Streptococcus pneumoniae. Likewise, immunization with NP-Ficoll elicited similar antibody responses in wild-type and Cxcl13(-/-) mice. These data demonstrate that homing of B1 cells into the coelomic cavity is not a requirement for generating protective TI antibody responses, even when antigen is initially localized to this anatomical compartment.