دورية أكاديمية
Neutrophils releasing IL-17A into NETs are essential to plasma cell differentiation in inflamed tissue dependent on IL-1R.
| العنوان: | Neutrophils releasing IL-17A into NETs are essential to plasma cell differentiation in inflamed tissue dependent on IL-1R. |
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| المؤلفون: | Grund LZ; a Immunoregulation Unit of the Special Laboratory of Applied Toxinology (CEPID/FAPESP), Butantan Institute , São Paulo , Brazil., Novaski I; b Cell Cycle Unit of the Special Laboratory of Applied Toxinology (CEPID/FAPESP), Butantan Institute , São Paulo , Brazil , and., Quesniaux VF; c Allergy and Lung Inflammation Unit of the Molecular and Experimental Immunology and Neurogenetics (CNRS) , Orléans , France., Ryffel B; c Allergy and Lung Inflammation Unit of the Molecular and Experimental Immunology and Neurogenetics (CNRS) , Orléans , France., Lopes-Ferreira M; a Immunoregulation Unit of the Special Laboratory of Applied Toxinology (CEPID/FAPESP), Butantan Institute , São Paulo , Brazil., Lima C; a Immunoregulation Unit of the Special Laboratory of Applied Toxinology (CEPID/FAPESP), Butantan Institute , São Paulo , Brazil. |
| المصدر: | Autoimmunity [Autoimmunity] 2017 Mar; Vol. 50 (2), pp. 86-101. Date of Electronic Publication: 2016 Dec 23. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Taylor & Francis Country of Publication: England NLM ID: 8900070 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1607-842X (Electronic) Linking ISSN: 08916934 NLM ISO Abbreviation: Autoimmunity Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2015- : Abingdon, Oxford : Taylor & Francis Original Publication: Chur ; New York : Harwood, c1988- |
| مواضيع طبية MeSH: | Cell Differentiation/*immunology , Extracellular Traps/*metabolism , Interleukin-17/*metabolism , Neutrophils/*immunology , Neutrophils/*metabolism , Plasma Cells/*immunology , Plasma Cells/*metabolism , Receptors, Interleukin-1 Type I/*metabolism, Animals ; Cyclooxygenase 2/metabolism ; Enzyme-Linked Immunosorbent Assay ; Extracellular Traps/immunology ; Fish Venoms/immunology ; Immunoglobulin G/blood ; Immunoglobulin G/immunology ; Immunologic Memory ; Lymphocyte Activation ; Male ; Mice ; Mice, Knockout ; Passive Cutaneous Anaphylaxis/immunology ; Plasma Cells/cytology |
| مستخلص: | Interleukin (IL) 17A in chronic inflammation is also produced by innate immune cells as neutrophils. Mice with chronic humoral response induced by venom of Thalassophryne nattereri (VTn) proved to be a good tool for evaluating the impact of IL-17A on the development of long-lived plasma cells in the inflamed peritoneal cavity. Here, we report that VTn induces IL-17A production by neutrophils accumulating in the peritoneal cavity and triggers the extrusion of IL-17A along with neutrophil extracellular traps (NETs). Neutrophil depletion reduced the number of IL17A-producing cells in VTn-immunized mice and blocked the differentiation of long-lived plasma cells. Specific antibody production and survival of long-lived plasma cells was ablated in VTn-immunized mice deficient in CD4, while CD28 signaling had the opposite effect on differentiation of long-lived plasma cells. Further, maturation of long-lived plasma cells in inflamed peritoneal cavity was IL-1R1 and COX-2 dependent. Finally, when both the Raf-MEK-ERK pathway and the IL-17A or IL-1R1 activities were blocked, neutrophils were unable to promote the differentiation of memory B cells into long-lived plasma cells, confirming the essential role of neutrophils and IL-17A along with NETs in an IL-1/IL-1R-dependent manner as the novel helping partner for plasma cell differentiation in chronically inflamed tissues. |
| فهرسة مساهمة: | Keywords: Fish venom; IL-17A; IL-1R; NETs; neutrophils; plasma cells |
| المشرفين على المادة: | 0 (Fish Venoms) 0 (Immunoglobulin G) 0 (Interleukin-17) 0 (Receptors, Interleukin-1 Type I) EC 1.14.99.1 (Cyclooxygenase 2) |
| تواريخ الأحداث: | Date Created: 20161225 Date Completed: 20171222 Latest Revision: 20220409 |
| رمز التحديث: | 20221213 |
| DOI: | 10.1080/08916934.2016.1261834 |
| PMID: | 28010135 |
| قاعدة البيانات: | MEDLINE |
PDF full text from Publisher | تدمد: | 1607-842X |
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| DOI: | 10.1080/08916934.2016.1261834 |