C-Kit Ligand Promotes Mast Cell Infection by Toxoplasma gondii

M. Bidri, M. Conti, N. Hanoun, R. L. Kuen, F. Féger, Z. Taoufiq, M. Arock, D. Mazier, I. Vouldoukis
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引用次数: 1

Abstract

Biological functions of mast cells include a functional role in innate immunity against parasitic infections. Here, we demonstrated that mast cells could also play a role in the anti-microbial defenses regulation and might partici- pate as a parasite reservoir. We observed that Toxoplasma gondii infected massively in vitro mouse bone marrow derived mast cells (BMMC), a mucosal mast cell (MMC) phenotype, followed by substantial cell lysis. This induced release of  - hexosaminidase, but not of preformed or neosynthesized TNF- . Culturing MMC in the presence of recombinant mouse stem cell factor (c-kit ligand) led to their maturation into connective tissue-like mast cells (CTMC), which T. gondii was able to adhere on and to infect more. T. gondii infection did not induce release of  -hexosaminidase and serotonin from BMMC. These results demonstrated that mast cells interact with T. gondii and are massively infected, especially after their maturation by c-kit ligand.
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C-Kit配体促进弓形虫感染肥大细胞
肥大细胞的生物学功能包括在抵抗寄生虫感染的先天免疫中的功能作用。在这里,我们证明肥大细胞也可能在抗微生物防御调节中发挥作用,并可能作为寄生虫储存库参与。我们观察到刚地弓形虫在体外大量感染小鼠骨髓源性肥大细胞(BMMC),这是一种粘膜肥大细胞(MMC)表型,随后发生大量细胞裂解。这诱导了-己糖氨酸酶的释放,但不诱导预形成或新合成的TNF-的释放。在重组小鼠干细胞因子(c-kit配体)的存在下培养MMC,使其成熟为结缔组织样肥大细胞(CTMC),弓形虫能够附着并感染更多的细胞。弓形虫感染不诱导BMMC释放-己糖氨酸酶和血清素。这些结果表明肥大细胞与弓形虫相互作用并被大量感染,特别是在它们被c-kit配体成熟后。
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