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B-1 lymphocytes are able to produce IL-10, but is not pathogenic during Leishmania (Leishmania) amazonensis infection.
Immunobiology ( IF 2.8 ) Pub Date : 2019-10-24 , DOI: 10.1016/j.imbio.2019.10.006
Luan Firmino-Cruz 1 , Tadeu Diniz Ramos 1 , Alessandra Marcia da Fonseca-Martins 1 , Diogo Oliveira-Maciel 1 , Gabriel Oliveira-Silva 1 , Júlio Souza Dos Santos 1 , Cecília Cavazzoni 1 , Alexandre Morrot 2 , Daniel Claudio Oliveira Gomes 3 , André Macedo Vale 1 , Debora Decoté-Ricardo 4 , Celio G Freire-de-Lima 1 , Herbert Leonel de Matos Guedes 5
Affiliation  

Over the years research has found an association between B lymphocytes and pathogenesis during Leishmania sp. infections. Recently we demonstrated that B-2 lymphocytes are the main producers of IL-10 during L. amazonensis infection, and that the disease severity in BALB/c mice was attributed to these IL-10-producing B-2 lymphocytes. Here, we aim to understand the role of peritoneal B-1 lymphocytes in the pathogenesis of L. amazonensis infection. We found that infection resulted in a decrease in the number of B-1a lymphocytes and increase in B-1b lymphocytes in the peritoneal cavity of WT BALB/c mice but not in B lymphocyte deficient mice (BALB/Xid) mice. In vitro interaction between B-1 lymphocytes and L. amazonensis showed that the amastigote form of the parasite was able to induce higher levels of IL-10 in B-1 lymphocytes derived from infected BALB/c mice than the promastigote. Moreover, B-1 lymphocytes derived from infected mice produced more IL-10 than B-1 lymphocytes derived from naïve mice under amastigote interaction. However, the repopulation of BALB/Xid mice with B-1 lymphocytes from WT BALB/c mice did not affect the lesion development. Together, these results suggest that although B-1 lymphocytes are able to produce IL-10 during in vitro interaction with L. amazonensis, they are not directly related to pathogenesis in vivo.

中文翻译:

B-1淋巴细胞能够产生IL-10,但在亚马逊利什曼原虫(Leishmania)感染期间没有致病性。

多年来的研究发现利什曼原虫(Leishmania sp。)期间B淋巴细胞与发病机制之间存在关联。感染。最近,我们证明了B-2淋巴细胞是亚马逊河杆菌感染期间IL-10的主要产生者,而BALB / c小鼠的疾病严重程度归因于这些产生IL-10的B-2​​淋巴细胞。在这里,我们旨在了解腹膜B-1淋巴细胞在亚马逊乳杆菌感染的发病机理中的作用。我们发现感染导致WT BALB / c小鼠腹膜腔中B-1a淋巴细胞数量减少和B-1b淋巴细胞数量增加,但在B淋巴细胞缺乏小鼠(BALB / Xid)小鼠中却没有。B-1淋巴细胞与L之间的体外相互作用。亚马逊表明,这种寄生虫的鞭毛体形式比原鞭毛体能够诱导来自感染的BALB / c小鼠的B-1淋巴细胞中更高水平的IL-10。此外,在鞭毛相互作用下,感染小鼠的B-1淋巴细胞比幼稚小鼠的B-1淋巴细胞产生更多的IL-10。但是,用来自WT BALB / c小鼠的B-1淋巴细胞重新填充BALB / Xid小鼠并不影响病变的发展。在一起,这些结果表明,尽管B-1淋巴细胞在与亚马逊乳杆菌的体外相互作用过程中能够产生IL-10,但它们与体内发病机理没有直接关系。WT BALB / c小鼠的B-1淋巴细胞使BALB / Xid小鼠重新繁殖并没有影响病变的发展。在一起,这些结果表明,尽管B-1淋巴细胞在体外与亚马孙乳杆菌相互作用期间能够产生IL-10,但它们与体内发病机理没有直接关系。WT BALB / c小鼠的B-1淋巴细胞使BALB / Xid小鼠重新繁殖并没有影响病变的发展。在一起,这些结果表明,尽管B-1淋巴细胞在与亚马逊乳杆菌的体外相互作用过程中能够产生IL-10,但它们与体内发病机理没有直接关系。
更新日期:2020-04-21
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