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      Trypanosoma cruzi trans-sialidase initiates an ROR-γt–AHR-independent program leading to IL-17 production by activated B cells

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          Abstract

          We identified B cells as a major source for rapid, innate-like interleukin 17 (IL-17) production in vivo in response to Trypanosoma cruzi infection. IL-17 + B cells exhibited a plasmablast phenotype, outnumbered T H17 cells and were required for optimal response to this pathogen. Using both murine and human primary B cells, we demonstrate that exposure to parasite-derived trans-sialidase in vitro was sufficient to trigger modification of the cell surface mucin, CD45, leading to Btk-dependent signaling and IL-17A or IL-17F production via an ROR-γt and AHR-independent transcriptional program. Our combined data suggest that generation of IL-17 + B cells may be an unappreciated feature of innate immune responses required for pathogen control or IL-17-mediated autoimmunity.

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          IL-17 produced by neutrophils regulates IFN-gamma-mediated neutrophil migration in mouse kidney ischemia-reperfusion injury.

          Li Li, Liping Huang, Amy Vergis … (2010)
          The IL-23/IL-17 and IL-12/IFN-gamma cytokine pathways have a role in chronic autoimmunity, which is considered mainly a dysfunction of adaptive immunity. The extent to which they contribute to innate immunity is, however, unknown. We used a mouse model of acute kidney ischemia-reperfusion injury (IRI) to test the hypothesis that early production of IL-23 and IL-12 following IRI activates downstream IL-17 and IFN-gamma signaling pathways and promotes kidney inflammation. Deficiency in IL-23, IL-17A, or IL-17 receptor (IL-17R) and mAb neutralization of CXCR2, the p19 subunit of IL-23, or IL-17A attenuated neutrophil infiltration in acute kidney IRI in mice. We further demonstrate that IL-17A produced by GR-1+ neutrophils was critical for kidney IRI in mice. Activation of the IL-12/IFN-gamma pathway and NKT cells by administering alpha-galactosylceramide-primed bone marrow-derived DCs increased IFN-gamma production following moderate IRI in WT mice but did not exacerbate injury or enhance IFN-gamma production in either Il17a-/- or Il17r-/- mice, which suggested that IL-17 signaling was proximal to IFN-gamma signaling. This was confirmed by the finding that IFN-gamma administration reversed the protection seen in Il17a-/- mice subjected to IRI, whereas IL-17A failed to reverse protection in Ifng-/- mice. These results demonstrate that the innate immune component of kidney IRI requires dual activation of the IL-12/IFN-gamma and IL-23/IL-17 signaling pathways and that neutrophil production of IL-17A is upstream of IL-12/IFN-gamma. These mechanisms might contribute to reperfusion injury in other organs.
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            Thymic origin of intestinal alphabeta T cells revealed by fate mapping of RORgammat+ cells.

            Gerard Eberl, Dan R. Littman (2004)
            Intestinal intraepithelial T lymphocytes (IELs) are likely to play a key role in host mucosal immunity and, unlike other T cells, have been proposed to differentiate from local precursors rather than from thymocytes. We show here that IELs expressing the alphabeta T cell receptor are derived from precursors that express RORgammat, an orphan nuclear hormone receptor detected only in immature CD4+CD8+ thymocytes, fetal lymphoid tissue-inducer (LTi) cells, and LTi-like cells in cryptopatches within the adult intestinal lamina propria. Using cell fate mapping, we found that all intestinal alphabeta T cells are progeny of CD4+CD8+ thymocytes, indicating that the adult intestine is not a significant site for alphabeta T cell development. Our results suggest that intestinal RORgammat+ cells are local organizers of mucosal lymphoid tissue.
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              The aryl hydrocarbon receptor in immunity.

              Charlotte Esser, Agneta Rannug, Brigitta Stockinger (2009)
              Low-molecular-weight chemicals or xenobiotics might contribute to the increasing prevalence of allergies and autoimmunity. Certain chemicals can alter immune responses via their action on the cytosolic transcription factor aryl hydrocarbon receptor (AhR). AhR recognizes numerous small xenobiotic and natural molecules, such as dioxin and the tryptophan photoproduct 6-formylindolo[3,2-b]carbazole. Although AhR is best known for mediating dioxin toxicity, knockout studies have indicated that AhR also plays a role in normal physiology, including certain immune responses. In particular, Th17 cells and dendritic cells express high levels of AhR. We review here current evidence for the physiological role of AhR in the immune system, focussing in particular on T-cell biology.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 100941354
                Journal ID (pubmed-jr-id): 21750
                Journal ID (nlm-ta): Nat Immunol
                Journal ID (iso-abbrev): Nat. Immunol.
                Title: Nature immunology
                ISSN (Print): 1529-2908
                ISSN (Electronic): 1529-2916
                Publication date Nihms-submitted: 4 March 2013
                Publication date (Electronic): 07 April 2013
                Publication date (Print): May 2013
                Publication date PMC-release: 07 October 2013
                Volume: 14
                Issue: 5
                Pages: 514-522
                Affiliations
                [1 ]Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI-CONICET). Facultad de Ciencias Químicas. Universidad Nacional de Córdoba. Córdoba. Argentina
                [2 ]Department of Pediatrics, University of Washington School of Medicine, Seattle, WA 98195
                [3 ]Department of Immunology, University of Washington School of Medicine, Seattle, WA 98195
                [4 ]Seattle Children's Research Institute, Seattle, WA 98101
                [5 ]Instituto de Investigaciones Biotecnológicas, Universidad Nacional de San Martín, B1650WGA San Martín, Argentina
                [6 ]Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA 98195
                Author notes
                Correspondence should be addressed to D.J.R. ( drawling@ 123456u.washington.edu ) or A. G. ( agruppi@ 123456fcq.unc.edu.ar ), David J. Rawlings, M.D., Center for Immunity and Immunotherapies, Seattle Children’s Research Institute, 1900 Ninth Avenue, Seattle, WA 98101, Tel. (206) 987-7450, Fax (206) 987-7310, Adriana Gruppi, PhD., Inmunología. Departamento de Bioquímica Clínica. Facultad de Ciencias Químicas. Universidad Nacional de Córdoba. Haya de la Torre y Medina Allende. Ciudad Universitaria. Córdoba (5000). Argentina., Tel.: +54 351-4344973., Fax: +54 351-4333048
                [7]

                A.G. and D.J.R. contributed equally to this work.

                Article
                Manuscript ID: NIHMS445334
                DOI: 10.1038/ni.2569
                PMC ID: 3631452
                PubMed ID: 23563688
                SO-VID: 86492878-701f-486a-94c6-0e36644fbe27
                License:

                Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Funding
                Funded by: National Institute of Arthritis and Musculoskeletal and Skin Diseases : NIAMS
                Award ID: T32 AR007108 || AR
                Funded by: National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID
                Award ID: R56 AI084457 || AI
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Award ID: R01 HL075453 || HL
                Funded by: National Institute of Child Health & Human Development : NICHD
                Award ID: R01 HD037091 || HD
                Funded by: National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID
                Award ID: R01 AI075589 || AI
                Funded by: National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID
                Award ID: R01 AI071163 || AI
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                Subject: Article

                ScienceOpen disciplines: Immunology
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                ScienceOpen disciplines: Immunology

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