Haq J A, Szewczuk M R
Department of Microbiology & Immunology, Queen's University, Kingston, Ontario, Canada.
Reg Immunol. 1993 Jan-Feb;5(1):60-7.
The capacity of exogenous interleukin-4 (IL-4) and IL-5 to augment the antigen-specific senescent Peyer's patch (PP), lamina propria (LP), and mesenteric lymph nodes (MLN) B cells was investigated in the present studies. CTx-primed lymphocytes in the PP, LP, and MLN were obtained from 4-and 24-month old C57BL/6J male mice, 14 days after oral immunization with cholera toxin (CTx). Cells were cultured optimally for 4 days either alone, with lipopolysaccharide (LPS), with LPS plus recombinant IL-4 or IL-5, or with LPS plus IL-4 or IL-5 plus monoclonal antibodies specific for the respective interleukin. Culture supernantants were tested for IgA and IgG anti-CTx antibodies by an ELISA assay. The data indicated impaired antibody responses of aged PP and MLN B cells by the lack of LPS plus IL-4 induced enhancement of anti-CTx IgG antibody production as compared with the young group. For anti-CTx IgA production, aged LP and MLN B cells did not respond equally as well to LPS plus IL-5 stimulation as the young group. In contrast, aged PP B cells responded equally as well by anti-CTx IgA production to LPS plus IL-5 stimulation as the young group. Both anti-IL-4 and anti-IL-5 Mabs blocked the respective IL-4 and IL-5-induced enhancement of antigen-specific IgG or IgA antibody production. The findings suggest a regional dichotomy of IL-5 induced enhancement of aged IgA-producing B cells specific for CTx in the Peyer's patches, mesenteric lymph nodes, and lamina propria.
在本研究中,我们调查了外源性白细胞介素-4(IL-4)和IL-5增强抗原特异性衰老派尔集合淋巴结(PP)、固有层(LP)和肠系膜淋巴结(MLN)B细胞的能力。PP、LP和MLN中经霍乱毒素(CTx)致敏的淋巴细胞取自4月龄和24月龄的C57BL/6J雄性小鼠,这些小鼠在口服CTx免疫14天后获取。细胞分别单独培养、与脂多糖(LPS)一起培养、与LPS加重组IL-4或IL-5一起培养,或与LPS加IL-4或IL-5加针对相应白细胞介素的单克隆抗体一起培养,最佳培养4天。通过酶联免疫吸附测定(ELISA)检测培养上清液中的抗CTx IgA和IgG抗体。数据表明,与年轻组相比,衰老的PP和MLN B细胞因缺乏LPS加IL-4诱导的抗CTx IgG抗体产生增强而导致抗体反应受损。对于抗CTx IgA的产生,衰老的LP和MLN B细胞对LPS加IL-5刺激的反应不如年轻组。相比之下,衰老的PP B细胞在抗CTx IgA产生方面对LPS加IL-5刺激的反应与年轻组相同。抗IL-4和抗IL-5单克隆抗体均阻断了各自IL-4和IL-5诱导的抗原特异性IgG或IgA抗体产生的增强。这些发现表明,在派尔集合淋巴结、肠系膜淋巴结和固有层中,IL-5诱导的针对CTx的衰老IgA产生B细胞的增强存在区域二分法。