IL-17-deficient allogeneic bone marrow transplantation prevents the induction of collagen-induced arthritis in DBA/1J mice
IL-17-producing CD4 + T cells (Th17) play important functions in autoimmune diseases and allograft rejection of solid organs. We examined the effects of IL 17 and its mechanism of action on arthritis in a murine collagen-induced arthritis (CIA) model using bone marrow transplantation (BMT) system. D...
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| Published in: | Experimental & molecular medicine Vol. 44; no. 11; pp. 694 - 705 |
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| Main Authors: | , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
London
Nature Publishing Group UK
2012
Springer Nature B.V Korean Society for Biochemistry and Molecular Biology 생화학분자생물학회 |
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| Abstract | IL-17-producing CD4
+
T cells (Th17) play important functions in autoimmune diseases and allograft rejection of solid organs. We examined the effects of IL 17 and its mechanism of action on arthritis in a murine collagen-induced arthritis (CIA) model using bone marrow transplantation (BMT) system. DBA/1J mice were administered a lethal radiation dose and then rescued with bone marrow derived from either wild-type (WT) or IL-17
-/-
mice on C57BL/6 background mice. CIA was induced after the bone marrow transplant, and disease progression was characterized. DBA/1J mice with CIA that received IL-17
-/-
donor bone marrow showed potently inhibited development and severity of clinical arthritis as compared with CIA mice that received WT bone marrow. Reduced secretion of the pro-inflammatory cytokines tumor necrosis factor-α, IL-1β, and IL-6, and collagen-specific T cell responses were observed in mice that received IL-17
-/-
bone marrow. IL-17 blockade also inhibited effector T cell proliferation by reciprocally regulating the Treg/Th17 ratio. IL-17 blockade prevented joint destruction in mice with CIA. These findings suggest that CIA with BMT is a viable method of immunological manipulation and that IL-17 deficiency suppresses severe joint destruction and inflammation in CIA mice. There may be clinical benefits in blocking IL-17 and BMT in the treatment of rheumatoid arthritis. |
|---|---|
| AbstractList | IL-17-producing CD4+ T cells (Th17) play important functions in autoimmune diseases and allograft rejection of solid organs. We examined the effects of IL 17 and its mechanism of action on arthritis in a murine collagen-induced arthritis (CIA) model using bone marrow transplantation (BMT) system. DBA/1J mice were administered a lethal radiation dose and then rescued with bone marrow derived from either wild-type (WT) or IL-17-/- mice on C57BL/6 background mice. CIA was induced after the bone marrow transplant, and disease progression was characterized. DBA/1J mice with CIA that received IL-17-/- donor bone marrow showed potently inhibited development and severity of clinical arthritis as compared with CIA mice that received WT bone marrow. Reduced secretion of the pro-inflammatory cytokines tumor necrosis factor-α,IL-1β, and IL-6, and collagen-specific T cell responses were observed in mice that received IL-17-/- bone marrow. IL-17 blockade also inhibited effector T cell proliferation by reciprocally regulating the Treg/Th17ratio. IL-17 blockade prevented joint destruction in mice with CIA. These findings suggest that CIA with BMT is a viable method of immunological manipulation and that IL-17 deficiency suppresses severe joint destruction and inflammation in CIA mice. There may be clinical benefits in blocking IL-17 and BMT in the treatment of rheumatoid arthritis. KCI Citation Count: 22 IL-17-producing CD4+ T cells (Th17) play important functions in autoimmune diseases and allograft rejection of solid organs. We examined the effects of IL 17 and its mechanism of action on arthritis in a murine collagen-induced arthritis (CIA) model using bone marrow transplantation (BMT) system. DBA/1J mice were administered a lethal radiation dose and then rescued with bone marrow derived from either wild-type (WT) or IL-17 -/- mice on C57BL/6 background mice. CIA was induced after the bone marrow transplant, and disease progression was characterized. DBA/1J mice with CIA that received IL-17-/- donor bone marrow showed potently inhibited development and severity of clinical arthritis as compared with CIA mice that received WT bone marrow. Reduced secretion of the pro-inflammatory cytokines tumor necrosis factor-α, IL-1β, and IL-6, and collagen-specific T cell responses were observed in mice that received IL-17 -/- bone marrow. IL-17 blockade also inhibited effector T cell proliferation by reciprocally regulating the Treg/Th17 ratio. IL-17 blockade prevented joint destruction in mice with CIA. These findings suggest that CIA with BMT is a viable method of immunological manipulation and that IL-17 deficiency suppresses severe joint destruction and inflammation in CIA mice. There may be clinical benefits in blocking IL-17 and BMT in the treatment of rheumatoid arthritis. IL-17-producing CD4 + T cells (Th17) play important functions in autoimmune diseases and allograft rejection of solid organs. We examined the effects of IL 17 and its mechanism of action on arthritis in a murine collagen-induced arthritis (CIA) model using bone marrow transplantation (BMT) system. DBA/1J mice were administered a lethal radiation dose and then rescued with bone marrow derived from either wild-type (WT) or IL-17 -/- mice on C57BL/6 background mice. CIA was induced after the bone marrow transplant, and disease progression was characterized. DBA/1J mice with CIA that received IL-17 -/- donor bone marrow showed potently inhibited development and severity of clinical arthritis as compared with CIA mice that received WT bone marrow. Reduced secretion of the pro-inflammatory cytokines tumor necrosis factor-α, IL-1β, and IL-6, and collagen-specific T cell responses were observed in mice that received IL-17 -/- bone marrow. IL-17 blockade also inhibited effector T cell proliferation by reciprocally regulating the Treg/Th17 ratio. IL-17 blockade prevented joint destruction in mice with CIA. These findings suggest that CIA with BMT is a viable method of immunological manipulation and that IL-17 deficiency suppresses severe joint destruction and inflammation in CIA mice. There may be clinical benefits in blocking IL-17 and BMT in the treatment of rheumatoid arthritis. IL-17-producing CD4 super(+) T cells (Th17) play important functions in autoimmune diseases and allograft rejection of solid organs. We examined the effects of IL 17 and its mechanism of action on arthritis in a murine collagen-induced arthritis (CIA) model using bone marrow transplantation (BMT) system. DBA/1J mice were administered a lethal radiation dose and then rescued with bone marrow derived from either wild-type (WT) or IL-17 super(-/-) mice on C57BL/6 background mice. CIA was induced after the bone marrow transplant, and disease progression was characterized. DBA/1J mice with CIA that received IL-17 super(-/-) donor bone marrow showed potently inhibited development and severity of clinical arthritis as compared with CIA mice that received WT bone marrow. Reduced secretion of the pro-inflammatory cytokines tumor necrosis factor- alpha , IL-1 beta , and IL-6, and collagen-specific T cell responses were observed in mice that received IL-17 super(-/-) bone marrow. IL-17 blockade also inhibited effector T cell proliferation by reciprocally regulating the Treg/Th17 ratio. IL-17 blockade prevented joint destruction in mice with CIA. These findings suggest that CIA with BMT is a viable method of immunological manipulation and that IL-17 deficiency suppresses severe joint destruction and inflammation in CIA mice. There may be clinical benefits in blocking IL-17 and BMT in the treatment of rheumatoid arthritis. |
| Author | Cho, Seok-Goo Park, Min-Jung Park, Hyun-Sil Oh, Hye-Joa Kim, Ho-Youn Yoon, Bo-Young Cho, Mi-La Lim, Jung-Yeon |
| AuthorAffiliation | 2 Immune Tolerance Research Center, Convergent Research Consortium for Immunologic Disease (CRCID), The Catholic University of Korea College of Medicine, Seoul 137-701, Korea 1 Rheumatism Research Center, Catholic Research Institutes of Medical Science, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea 4 Department of Internal Medicine, Inje University Ilsan Paik Hospital, Seoul 411-706, Korea 3 Catholic Blood and Marrow Transplantation Center, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea |
| AuthorAffiliation_xml | – name: 3 Catholic Blood and Marrow Transplantation Center, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea – name: 1 Rheumatism Research Center, Catholic Research Institutes of Medical Science, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea – name: 2 Immune Tolerance Research Center, Convergent Research Consortium for Immunologic Disease (CRCID), The Catholic University of Korea College of Medicine, Seoul 137-701, Korea – name: 4 Department of Internal Medicine, Inje University Ilsan Paik Hospital, Seoul 411-706, Korea |
| Author_xml | – sequence: 1 givenname: Min-Jung surname: Park fullname: Park, Min-Jung organization: Rheumatism Research Center, Catholic Research Institutes of Medical Science, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea., Immune Tolerance Research Center, Convergent Research Consortium for Immunologic Disease (CRCID), The Catholic University of Korea College of Medicine, Seoul 137-701, Korea – sequence: 2 givenname: Hyun-Sil surname: Park fullname: Park, Hyun-Sil organization: Rheumatism Research Center, Catholic Research Institutes of Medical Science, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea., Immune Tolerance Research Center, Convergent Research Consortium for Immunologic Disease (CRCID), The Catholic University of Korea College of Medicine, Seoul 137-701, Korea – sequence: 3 givenname: Hye-Joa surname: Oh fullname: Oh, Hye-Joa organization: Rheumatism Research Center, Catholic Research Institutes of Medical Science, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea., Immune Tolerance Research Center, Convergent Research Consortium for Immunologic Disease (CRCID), The Catholic University of Korea College of Medicine, Seoul 137-701, Korea – sequence: 4 givenname: Jung-Yeon surname: Lim fullname: Lim, Jung-Yeon organization: Rheumatism Research Center, Catholic Research Institutes of Medical Science, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea., Immune Tolerance Research Center, Convergent Research Consortium for Immunologic Disease (CRCID), The Catholic University of Korea College of Medicine, Seoul 137-701, Korea – sequence: 5 givenname: Bo-Young surname: Yoon fullname: Yoon, Bo-Young organization: Department of Internal Medicine, Inje University Ilsan Paik Hospital, Seoul 411-706, Korea – sequence: 6 givenname: Ho-Youn surname: Kim fullname: Kim, Ho-Youn organization: Rheumatism Research Center, Catholic Research Institutes of Medical Science, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea – sequence: 7 givenname: Mi-La surname: Cho fullname: Cho, Mi-La email: iammila@catholic.ac.kr organization: Rheumatism Research Center, Catholic Research Institutes of Medical Science, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea., Immune Tolerance Research Center, Convergent Research Consortium for Immunologic Disease (CRCID), The Catholic University of Korea College of Medicine, Seoul 137-701, Korea – sequence: 8 givenname: Seok-Goo surname: Cho fullname: Cho, Seok-Goo email: chosg@catholic.ac.kr organization: Immune Tolerance Research Center, Convergent Research Consortium for Immunologic Disease (CRCID), The Catholic University of Korea College of Medicine, Seoul 137-701, Korea., Catholic Blood and Marrow Transplantation Center, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea |
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| Keywords | T-lymphocytes, regulatory interleukin-17 arthritis, experimental bone marrow transplantation Th17 cells transplantation, homologous |
| Language | English |
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| Snippet | IL-17-producing CD4
+
T cells (Th17) play important functions in autoimmune diseases and allograft rejection of solid organs. We examined the effects of IL 17... IL-17-producing CD4+ T cells (Th17) play important functions in autoimmune diseases and allograft rejection of solid organs. We examined the effects of IL 17... IL-17-producing CD4 super(+) T cells (Th17) play important functions in autoimmune diseases and allograft rejection of solid organs. We examined the effects of... |
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| SubjectTerms | Animals Antigens, Differentiation - metabolism Arthritis, Experimental - pathology Arthritis, Experimental - prevention & control Biomedical and Life Sciences Biomedicine Bone Marrow Transplantation Cell Differentiation Cell Proliferation Cells, Cultured Collagen Type II Cytokines - metabolism Humans Interleukin-17 - deficiency Interleukin-17 - genetics Joints - pathology Male Medical Biochemistry Mice Mice, Inbred C57BL Mice, Inbred DBA Mice, Knockout Molecular Medicine Original Osteoclasts - metabolism Osteoclasts - physiology Signal Transduction Stem Cells T-Lymphocytes - metabolism T-Lymphocytes - physiology Transplantation, Homologous 생화학 |
| Title | IL-17-deficient allogeneic bone marrow transplantation prevents the induction of collagen-induced arthritis in DBA/1J mice |
| URI | https://link.springer.com/article/10.3858/emm.2012.44.11.078 https://www.ncbi.nlm.nih.gov/pubmed/23114425 https://www.proquest.com/docview/1800145670 https://search.proquest.com/docview/1808627081 https://pubmed.ncbi.nlm.nih.gov/PMC3509186 https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART001712892 |
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