sigmodontis infection did not display the anti-inflammatory capac

sigmodontis infection did not display the anti-inflammatory capacity of IL-10-producing regulatory B cells [26, 27], which have been shown to ameliorate allergic airway inflammation and protect against fatal sepsis during Schistosoma mansoni infection [28, 29]. Although both B cells and T cells produced IL-10 during L. sigmodontis infection, complete IL-10 deficiency clearly resembled the phenotype of T-cell-specific IL-10 deficiency. We recognize that other leukocytes such as alternatively activated macrophages [30] are also potent producers of IL-10 during L. sigmodontis infection and recently macrophage-specific IL-10 overexpression was shown to

revert the resistant phenotype of FVB mice to patency [31]. Afatinib nmr Thus, further studies with cell type-specific IL-10−/− mice will be necessary to elucidate the divergent functions of IL-10 during the immune response to L. sigmodontis. All in vivo experiments were carried out at the animal facility of the Bernhard Nocht Institute for Tropical Medicine (BNI) with permission of the Federal Health Authorities of the State of Hamburg, Germany. Animals were kept in individually ventilated cages. IL-10-eGFP reporter mice [22], a kind gift from Matthias Haury and Dinis Calado, C57BL/6 mice, IL-10−/− mice, IL-10FL/FL CD4-Cre+ [24], IL-10FL/FL

CD19-Cre+ [23], and IL-10FL/FL Cre− mice were bred at the BNI. The life cycle of L. sigmodontis was maintained, and infection of mice performed as described [20]. SCH727965 concentration Mice were sacrificed at indicated time points, spleen cells harvested for stimulation and flow cytometry, and L4, adults, or granulomatae were counted after flushing the thoracic cavity with 10 mL cold

PBS. In detail parasite burden in IL-10−/− and C57BL/6 mice was compared in three independent experiments with n = 4 (exp. 1), n = 6 (exp. 2), and n = 5 (exp. 3) Racecadotril mice per group. Cytokine production in IL-10−/− and C57BL/6 mice was compared in two independent experiments with n = 4 (exp. 1) and n = 5 (exp. 2) mice per group. Cytokine production in noninfected IL-10FL/FL Cre−, IL-10FL/FL CD4-Cre+, and IL-10FL/FL CD19-Cre+ was compared in two independent experiments using n = 5 (exp. 1) and n = 3 (exp. 2) mice per group. Parasite burden for day 17 p.i. in IL-10FL/FL Cre− and IL-10FL/FL CD4-Cre+ was compared in three independent experiments using n = 3 (exp. 1), n = 5 (exp. 2), and n = 3 (exp. 3) mice per group. Cytokine production for day 17 p.i. in IL-10FL/FL Cre− and IL-10FL/FL CD4-Cre+ was compared in two independent experiments using n = 3 (exp. 1) and n = 5 (exp. 2) mice per group. Parasite burden and cytokine production for day 17 p.i. in IL-10FL/FL Cre− and IL-10FL/FL CD19-Cre+ was compared in three independent experiments using n = 4 (exp. 1), n = 4 (exp. 2), and n = 3 (exp. 3) mice per group. For day 30 p.i., cytokine production and parasite burden in IL-10FL/FL Cre−, IL-10FL/FL CD4-Cre+, and IL-10FL/FL CD19-Cre+ were compared in three independent experiments using n = 3 (exp.

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