Palanivel V, Posey C, Horauf A M, Solbach W, Piessens W F, Harn D A
Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
Exp Parasitol. 1996 Nov;84(2):168-77. doi: 10.1006/expr.1996.0102.
In many parasitic infections, dominant T helper cell (Th) type-2 CD4+ T cell responses exacerbate the disease. We have previously demonstrated that lacto-N-fucopentaose-III (LNFPIII), a sugar found on soluble egg antigens (SEA) of Schistosoma mansoni, stimulates splenic B cells from parasite-infected mice to proliferate and produce IL-10, a cytokine that promotes the generation of Th2 immune responses. In the present study, we extend our observations on ligand-specific activation of IL-10 producing B cells to leishmaniasis and lymphatic filariasis. We report here that infection with Leishmania major increases the splenic B220+ B cell subset in BALB/c mice, but not BALB/c. xid (lacking B-1 cells and carrying defective B-2 cells). In addition, these B cells secrete large amounts of IL-10 in vitro in response to stimulation with soluble leishmanial extract (LSE), LNFPIII, or SO4-Lewis(x). We also observed that injection of LSE increased the level of peritoneal exudate (PeC) B-1 cells (CD5+B220+) in BALB/c mice, but not C57BL/6, as compared to buffer-injected controls. Further, LSE elicited PeC B cells secreted IL-10 in response to LSE as well as to the sugars tested. A similar differential secretion of IL-10 by splenic B cells from BALB/c and BALB/c.xid was seen after S. mansoni infection. Likewise, injection of soluble microfilarial extract (MFX) resulted in an increase in percentage of PeC B-1 cells in BALB/c mice, but not C57BL/6, and these cells secreted IL-10 in response to stimulation with MFX or phosphorylcholine (PC). Collectively, these results suggest a correlation between expansion of ligand-specific IL-10 producing B and B-1 cells with dominance of Th2-type T cells in mice with the susceptible phenotype for these diseases.
在许多寄生虫感染中，占主导地位的2型辅助性T细胞（Th）CD4 + T细胞反应会加剧疾病。我们之前已经证明，乳糖-N-岩藻五糖-III（LNFPIII）是一种在曼氏血吸虫可溶性虫卵抗原（SEA）上发现的糖类，它能刺激来自寄生虫感染小鼠的脾脏B细胞增殖并产生白细胞介素-10（IL-10），这种细胞因子可促进Th2免疫反应的产生。在本研究中，我们将对产生IL-10的B细胞的配体特异性激活的观察扩展到利什曼病和淋巴丝虫病。我们在此报告，感染硕大利什曼原虫会增加BALB / c小鼠脾脏中的B220 + B细胞亚群，但不会增加BALB / c.xid小鼠（缺乏B-1细胞且携带缺陷B-2细胞）的该亚群。此外，这些B细胞在体外对可溶性利什曼原虫提取物（LSE）、LNFPIII或SO4-岩藻糖基化路易斯x（SO4-Lewis(x)）刺激产生反应时会分泌大量IL-10。我们还观察到，与注射缓冲液的对照组相比，注射LSE会增加BALB / c小鼠腹腔渗出液（PeC）B-1细胞（CD5 + B220 +）的水平，但不会增加C57BL / 6小鼠的该水平。此外，LSE诱导PeC B细胞在对LSE以及所测试的糖类产生反应时分泌IL-10。在曼氏血吸虫感染后，观察到来自BALB / c和BALB / c.xid的脾脏B细胞也有类似的IL-10差异分泌。同样，注射可溶性微丝蚴提取物（MFX）会导致BALB / c小鼠腹腔渗出液B-1细胞百分比增加，但不会增加C57BL / 6小鼠的该百分比，并且这些细胞在对MFX或磷酸胆碱（PC）刺激产生反应时会分泌IL-10。总体而言，这些结果表明，在对这些疾病具有易感表型的小鼠中，产生配体特异性IL-10的B细胞和B-1细胞的扩增与Th2型T细胞的主导地位之间存在相关性。
