Durkin H G, Auci D L, Chice S M, Smith M C, Murali M R, Bazin H, Tarcsay L, Dukor P
Department of Pathology, State University of New York Health Science Center, Brooklyn 11203.
Clin Immunol Immunopathol. 1989 Jan;50(1 Pt 2):S52-72. doi: 10.1016/0090-1229(89)90113-x.
Peyer's patches (PP) in germ-free rats (GF) and in the hyper-IgE syndrome patient (HIES) differ from their conventional rat (C) and healthy human (HH) counterparts in that GF rats contained fewer (two-fold) PP and none was detected in HIES. Existing PP in GF rats had reduced cellularity (three-fold) and different B and T cell subsets: high numbers of IgE-bearing (sIgE+) B cells (approximately 15% of total cells), one-half of which also expressed sIgA, were present in GF rat PP while none was detected in C rat PP (less than 1%). GF rat PP also contained elevated numbers of sIgA+ cells and decreased sIgM+ cells, with elevated numbers of sThy 1+ RT 7.1+ Ig- T cells (suppressor phenotype) and reduced sThy 1- RT 7.1+ Ig- T cells (helper phenotype). The cellular composition of GF rat PP was converted to that resembling a C rat within 18 hr after (a) use of standard (unautoclaved) chow; (b) feeding with certain bacteria or "working" bacterial cell wall components (BCWC) and synthetic derivatives, murein, MTP-PE, and norMDP, but not with LPS, core lipid A, or lipoprotein; BCWC had no effect if injected intravenously; or (c) thymectomy. Each procedure resulted in (i) elimination of sIgE+ B cells and normalization of the other isotypes, and (ii) loss of T suppressor cells and normalization of T helper cells. After treatments, no sIgE+ cells were detected in bone marrow (BM), thymus, other lymphoid organs, or blood. PP were not detected in HIES, although they were present in HH (approximately 10/individual). P blood contained two distinct sIgE+ B cell subpopulations, the apparent source of which was mesenteric lymph node (MLN), the only organ in which high numbers of these cells (35%) (five nodes examined) were detected; far fewer IgE+ cells were found in spleen (less than 5%), and none was detected in BM, thymus, other LN, or appendix, which was virtually acellular. Virtually no IgE secreting plasma cells were detected in MLN, spleen, appendix, other lymphoid organs, or in gut lamina propria. IgE+ B cells in MLN were not detected in follicles (classical B cell areas); instead, they were found in high numbers in the thymus-dependent area and in medulla. Most follicles (greater than 98%) in MLN and spleen contained intercellular IgE complexed to bacterial antigen and/or CD23 (IgE-binding factor? antigen?), but contained no germinal centers.(ABSTRACT TRUNCATED AT 400 WORDS)
无菌大鼠(GF)和高IgE综合征患者(HIES)的派尔集合淋巴结(PP)与其正常大鼠(C)和健康人类(HH)的对应物不同,无菌大鼠的PP数量较少(减少两倍),而在HIES中未检测到PP。无菌大鼠现有的PP细胞数量减少(减少三倍),且B细胞和T细胞亚群不同:无菌大鼠的PP中存在大量携带IgE的(sIgE+)B细胞(约占总细胞的15%),其中一半还表达sIgA,而正常大鼠的PP中未检测到(不到1%)。无菌大鼠的PP中sIgA+细胞数量增加,sIgM+细胞数量减少,sThy 1+ RT 7.1+ Ig- T细胞(抑制表型)数量增加,sThy 1- RT 7.1+ Ig- T细胞(辅助表型)数量减少。在使用标准(未高压灭菌)食物后18小时内,无菌大鼠PP的细胞组成转变为类似于正常大鼠的组成;喂食某些细菌或“活性”细菌细胞壁成分(BCWC)以及合成衍生物、胞壁质、MTP-PE和去甲MDP,但不包括LPS、核心脂多糖或脂蛋白;静脉注射BCWC则无效果;或进行胸腺切除术后,无菌大鼠PP的细胞组成也会发生转变。每种处理方法都会导致:(i)sIgE+ B细胞消失,其他同种型恢复正常;(ii)T抑制细胞减少,T辅助细胞恢复正常。处理后,在骨髓(BM)、胸腺、其他淋巴器官或血液中未检测到sIgE+细胞。高IgE综合征患者未检测到PP,尽管健康人存在PP(约每人10个)。高IgE综合征患者的血液中含有两个不同的sIgE+ B细胞亚群,其明显来源是肠系膜淋巴结(MLN),这是唯一检测到大量此类细胞(35%)(检查了五个淋巴结)的器官;脾脏中发现的IgE+细胞要少得多(不到5%),在骨髓、胸腺、其他淋巴结或阑尾中未检测到,阑尾实际上无细胞。在MLN、脾脏、阑尾、其他淋巴器官或肠道固有层中几乎未检测到分泌IgE的浆细胞。MLN中的IgE+ B细胞在滤泡(经典B细胞区域)中未检测到;相反,在胸腺依赖区域和髓质中大量存在。MLN和脾脏中大多数滤泡(超过98%)含有与细菌抗原和/或CD23(IgE结合因子?抗原?)复合的细胞间IgE,但没有生发中心。(摘要截断于400字)