دورية أكاديمية
IL-33-mediated IL-13 secretion by ST2+ Tregs controls inflammation after lung injury.
| العنوان: | IL-33-mediated IL-13 secretion by ST2+ Tregs controls inflammation after lung injury. |
|---|---|
| المؤلفون: | Liu Q; Thomas E. Starzl Transplantation Institute.; Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.; Southern University of Science and Technology School of Medicine, Shenzhen, China., Dwyer GK; Thomas E. Starzl Transplantation Institute.; Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA., Zhao Y; Thomas E. Starzl Transplantation Institute.; Tsinghua University School of Medicine, Beijing, China., Li H; Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine., Mathews LR; Thomas E. Starzl Transplantation Institute., Chakka AB; Department of Biomedical Informatics, and., Chandran UR; Department of Biomedical Informatics, and., Demetris JA; Thomas E. Starzl Transplantation Institute.; Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA., Alcorn JF; Department of Pediatrics, University of Pittsburgh Medical Center Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, USA., Robinson KM; Department of Biomedical Informatics, and., Ortiz LA; Department of Environmental and Occupational Heath, University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania, USA., Pitt BR; Department of Environmental and Occupational Heath, University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania, USA., Thomson AW; Thomas E. Starzl Transplantation Institute.; Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.; Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA., Fan MH; Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine., Billiar TR; Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA., Turnquist HR; Thomas E. Starzl Transplantation Institute.; Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.; Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA. |
| المصدر: | JCI insight [JCI Insight] 2019 Mar 21; Vol. 4 (6). Date of Electronic Publication: 2019 Mar 21 (Print Publication: 2019). |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Society for Clinical Investigation Country of Publication: United States NLM ID: 101676073 Publication Model: eCollection Cited Medium: Internet ISSN: 2379-3708 (Electronic) Linking ISSN: 23793708 NLM ISO Abbreviation: JCI Insight Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Ann Arbor, Michigan : American Society for Clinical Investigation, [2016]- |
| مواضيع طبية MeSH: | Inflammation/*metabolism , Interleukin-1 Receptor-Like 1 Protein/*metabolism , Interleukin-13/*metabolism , Interleukin-33/*metabolism , T-Lymphocytes, Regulatory/*metabolism, Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Animals ; Bronchoalveolar Lavage Fluid ; Chemokine CCL2 ; Cytokines/metabolism ; Disease Models, Animal ; Forkhead Transcription Factors/genetics ; Granulocyte Colony-Stimulating Factor ; Humans ; Interleukin-1 Receptor-Like 1 Protein/genetics ; Interleukin-33/genetics ; Interleukin-6 ; Lung/metabolism ; Lung/pathology ; Macrophages/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Respiratory Distress Syndrome/metabolism ; Transcriptome |
| مستخلص: | Acute respiratory distress syndrome is an often fatal disease that develops after acute lung injury and trauma. How released tissue damage signals, or alarmins, orchestrate early inflammatory events is poorly understood. Herein we reveal that IL-33, an alarmin sequestered in the lung epithelium, is required to limit inflammation after injury due to an unappreciated capacity to mediate Foxp3+ Treg control of local cytokines and myeloid populations. Specifically, Il33-/- mice are more susceptible to lung damage-associated morbidity and mortality that is typified by augmented levels of the proinflammatory cytokines and Ly6Chi monocytes in the bronchoalveolar lavage fluid. Local delivery of IL-33 at the time of injury is protective but requires the presence of Treg cells. IL-33 stimulates both mouse and human Tregs to secrete IL-13. Using Foxp3Cre × Il4/Il13fl/fl mice, we show that Treg expression of IL-13 is required to prevent mortality after acute lung injury by controlling local levels of G-CSF, IL-6, and MCP-1 and inhibiting accumulation of Ly6Chi monocytes. Our study identifies a regulatory mechanism involving IL-33 and Treg secretion of IL-13 in response to tissue damage that is instrumental in limiting local inflammatory responses and may shape the myeloid compartment after lung injury. |
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| معلومات مُعتمدة: | T32 CA082084 United States CA NCI NIH HHS; R01 HL122489 United States HL NHLBI NIH HHS; R01 HL107380 United States HL NHLBI NIH HHS; U19 AI131453 United States AI NIAID NIH HHS; R21 AI121981 United States AI NIAID NIH HHS; P30 CA047904 United States CA NCI NIH HHS; S10 OD011925 United States OD NIH HHS |
| فهرسة مساهمة: | Keywords: Cytokines; Immunology; Macrophages; Pulmonology; T cells |
| المشرفين على المادة: | 0 (Ccl2 protein, mouse) 0 (Chemokine CCL2) 0 (Cytokines) 0 (Forkhead Transcription Factors) 0 (Foxp3 protein, mouse) 0 (Il1rl1 protein, mouse) 0 (Il33 protein, mouse) 0 (Interleukin-1 Receptor-Like 1 Protein) 0 (Interleukin-13) 0 (Interleukin-33) 0 (Interleukin-6) 143011-72-7 (Granulocyte Colony-Stimulating Factor) |
| تواريخ الأحداث: | Date Created: 20190220 Date Completed: 20200622 Latest Revision: 20201209 |
| رمز التحديث: | 20231215 |
| مُعرف محوري في PubMed: | PMC6482994 |
| DOI: | 10.1172/jci.insight.123919 |
| PMID: | 30779711 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 2379-3708 |
|---|---|
| DOI: | 10.1172/jci.insight.123919 |