Innate Immune B Cell Activation by Leishmania donovani Exacerbates Disease and Mediates Hypergammaglobulinemia

Silva-Barrios, Sasha; Smans, Mélina; Duerr, Claudia; Qureshi, Salman; Fritz, Jorg; Descoteaux, Albert ORCID: https://orcid.org/0000-0002-0633-5309 et Stäger, Simona (2016). Innate Immune B Cell Activation by Leishmania donovani Exacerbates Disease and Mediates Hypergammaglobulinemia Cell Reports , vol. 15 , nº 11. pp. 2427-2437. DOI: 10.1016/j.celrep.2016.05.028.

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La transcription des symboles et des caractères spéciaux utilisés dans la version originale de ce résumé n’a pas été possible en raison de limitations techniques. La version correcte de ce résumé peut être lue en PDF. The symbols and special characters used in the original abstract could not be transcribed due to technical problems. Please use the PDF version to read the abstract. Participation of B cells in the immune response by various antibody-independent mechanisms has recently been uncovered. B cells producing cytokines have been described for several infections and appear to regulate the adaptive immune response. B cell activation by Leishmania donovani results in disease exacerbation. How Leishmania activates B cells is still unknown. We show that L. donovani amastigotes activate B cells by triggering endosomal TLRs; this activation leads to the induction of various cytokines. Cytokine expression is completely abrogated in B cells from Ifnar(-/-) mice upon exposure to L. donovani, suggesting an involvement of IFN-I in a positive feedback loop. IFN-I also appears to enhance the expression of endosomal TLRs following exposure to L. donovani. Cell-specific ablation of endosomal TLR signaling in B cells revealed that innate B cell activation by L. donovani is responsible for disease exacerbation through IL-10 and IFN-I production and for the promotion of hypergammaglobulinemia.

Type de document:	Article
Informations complémentaires:	Résumé avec symboles
Mots-clés libres:	-
Centre:	Centre INRS-Institut Armand Frappier
Date de dépôt:	24 août 2016 18:17
Dernière modification:	08 juin 2023 18:53
URI:	https://espace.inrs.ca/id/eprint/4536

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