CCL22-Producing Resident Macrophages Enhance T Cell Response in Sjögren's Syndrome
Macrophages (MΦs) are critical regulators of immune response and serve as a link between innate and acquired immunity. The precise mechanism of involvement of tissue-resident MΦs in the pathogenesis of autoimmune diseases is not clear. Here, using a murine model for Sjögren's syndrome (SS), we...
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| Published in | Frontiers in immunology Vol. 9; p. 2594 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
Frontiers Media S.A
08.11.2018
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| Online Access | Get full text |
| ISSN | 1664-3224 1664-3224 |
| DOI | 10.3389/fimmu.2018.02594 |
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| Abstract | Macrophages (MΦs) are critical regulators of immune response and serve as a link between innate and acquired immunity. The precise mechanism of involvement of tissue-resident MΦs in the pathogenesis of autoimmune diseases is not clear. Here, using a murine model for Sjögren's syndrome (SS), we investigated the role of tissue-resident MΦs in the onset and development of autoimmunity. Two unique populations of CD11b
and CD11b
resident MΦs were observed in the target tissue of the SS model. Comprehensive gene expression analysis of chemokines revealed effective production of CCL22 by the CD11b
MΦs. CCL22 upregulated the migratory activity of CD4
T cells by increasing CCR4, a receptor of CCL22, on T cells in the SS model. In addition, CCL22 enhanced IFN-γ production of T cells of the SS model, thereby suggesting that CCL22 may impair the local immune tolerance in the target organ of the SS model. Moreover, administration of anti-CCL22 antibody suppressed autoimmune lesions in the SS model. Finally, histopathological analysis revealed numerous CCL22-producing MΦs in the minor salivary gland tissue specimens of the SS patients. CCL22-producing tissue-resident MΦs may control autoimmune lesions by enhancing T cell response in the SS model. These results suggest that specific chemokines and their receptors may serve as novel therapeutic or diagnostic targets for SS. |
|---|---|
| AbstractList | Macrophages (MΦs) are critical regulators of immune response and serve as a link between innate and acquired immunity. The precise mechanism of involvement of tissue-resident MΦs in the pathogenesis of autoimmune diseases is not clear. Here, using a murine model for Sjögren's syndrome (SS), we investigated the role of tissue-resident MΦs in the onset and development of autoimmunity. Two unique populations of CD11bhigh and CD11blow resident MΦs were observed in the target tissue of the SS model. Comprehensive gene expression analysis of chemokines revealed effective production of CCL22 by the CD11bhigh MΦs. CCL22 upregulated the migratory activity of CD4+ T cells by increasing CCR4, a receptor of CCL22, on T cells in the SS model. In addition, CCL22 enhanced IFN-γ production of T cells of the SS model, thereby suggesting that CCL22 may impair the local immune tolerance in the target organ of the SS model. Moreover, administration of anti-CCL22 antibody suppressed autoimmune lesions in the SS model. Finally, histopathological analysis revealed numerous CCL22-producing MΦs in the minor salivary gland tissue specimens of the SS patients. CCL22-producing tissue-resident MΦs may control autoimmune lesions by enhancing T cell response in the SS model. These results suggest that specific chemokines and their receptors may serve as novel therapeutic or diagnostic targets for SS.Macrophages (MΦs) are critical regulators of immune response and serve as a link between innate and acquired immunity. The precise mechanism of involvement of tissue-resident MΦs in the pathogenesis of autoimmune diseases is not clear. Here, using a murine model for Sjögren's syndrome (SS), we investigated the role of tissue-resident MΦs in the onset and development of autoimmunity. Two unique populations of CD11bhigh and CD11blow resident MΦs were observed in the target tissue of the SS model. Comprehensive gene expression analysis of chemokines revealed effective production of CCL22 by the CD11bhigh MΦs. CCL22 upregulated the migratory activity of CD4+ T cells by increasing CCR4, a receptor of CCL22, on T cells in the SS model. In addition, CCL22 enhanced IFN-γ production of T cells of the SS model, thereby suggesting that CCL22 may impair the local immune tolerance in the target organ of the SS model. Moreover, administration of anti-CCL22 antibody suppressed autoimmune lesions in the SS model. Finally, histopathological analysis revealed numerous CCL22-producing MΦs in the minor salivary gland tissue specimens of the SS patients. CCL22-producing tissue-resident MΦs may control autoimmune lesions by enhancing T cell response in the SS model. These results suggest that specific chemokines and their receptors may serve as novel therapeutic or diagnostic targets for SS. Macrophages (MΦs) are critical regulators of immune response and serve as a link between innate and acquired immunity. The precise mechanism of involvement of tissue-resident MΦs in the pathogenesis of autoimmune diseases is not clear. Here, using a murine model for Sjögren's syndrome (SS), we investigated the role of tissue-resident MΦs in the onset and development of autoimmunity. Two unique populations of CD11b and CD11b resident MΦs were observed in the target tissue of the SS model. Comprehensive gene expression analysis of chemokines revealed effective production of CCL22 by the CD11b MΦs. CCL22 upregulated the migratory activity of CD4 T cells by increasing CCR4, a receptor of CCL22, on T cells in the SS model. In addition, CCL22 enhanced IFN-γ production of T cells of the SS model, thereby suggesting that CCL22 may impair the local immune tolerance in the target organ of the SS model. Moreover, administration of anti-CCL22 antibody suppressed autoimmune lesions in the SS model. Finally, histopathological analysis revealed numerous CCL22-producing MΦs in the minor salivary gland tissue specimens of the SS patients. CCL22-producing tissue-resident MΦs may control autoimmune lesions by enhancing T cell response in the SS model. These results suggest that specific chemokines and their receptors may serve as novel therapeutic or diagnostic targets for SS. Macrophages (MΦs) are critical regulators of immune response and serve as a link between innate and acquired immunity. The precise mechanism of involvement of tissue-resident MΦs in the pathogenesis of autoimmune diseases is not clear. Here, using a murine model for Sjögren's syndrome (SS), we investigated the role of tissue-resident MΦs in the onset and development of autoimmunity. Two unique populations of CD11bhigh and CD11blow resident MΦs were observed in the target tissue of the SS model. Comprehensive gene expression analysis of chemokines revealed effective production of CCL22 by the CD11bhigh MΦs. CCL22 upregulated the migratory activity of CD4+ T cells by increasing CCR4, a receptor of CCL22, on T cells in the SS model. In addition, CCL22 enhanced IFN-γ production of T cells of the SS model, thereby suggesting that CCL22 may impair the local immune tolerance in the target organ of the SS model. Moreover, administration of anti-CCL22 antibody suppressed autoimmune lesions in the SS model. Finally, histopathological analysis revealed numerous CCL22-producing MΦs in the minor salivary gland tissue specimens of the SS patients. CCL22-producing tissue-resident MΦs may control autoimmune lesions by enhancing T cell response in the SS model. These results suggest that specific chemokines and their receptors may serve as novel therapeutic or diagnostic targets for SS. Macrophages (MΦs) are critical regulators of immune response and serve as a link between innate and acquired immunity. The precise mechanism of involvement of tissue-resident MΦs in the pathogenesis of autoimmune diseases is not clear. Here, using a murine model for Sjögren's syndrome (SS), we investigated the role of tissue-resident MΦs in the onset and development of autoimmunity. Two unique populations of CD11b high and CD11b low resident MΦs were observed in the target tissue of the SS model. Comprehensive gene expression analysis of chemokines revealed effective production of CCL22 by the CD11b high MΦs. CCL22 upregulated the migratory activity of CD4 + T cells by increasing CCR4, a receptor of CCL22, on T cells in the SS model. In addition, CCL22 enhanced IFN-γ production of T cells of the SS model, thereby suggesting that CCL22 may impair the local immune tolerance in the target organ of the SS model. Moreover, administration of anti-CCL22 antibody suppressed autoimmune lesions in the SS model. Finally, histopathological analysis revealed numerous CCL22-producing MΦs in the minor salivary gland tissue specimens of the SS patients. CCL22-producing tissue-resident MΦs may control autoimmune lesions by enhancing T cell response in the SS model. These results suggest that specific chemokines and their receptors may serve as novel therapeutic or diagnostic targets for SS. |
| Author | Ishimaru, Naozumi Arakaki, Rieko Kudo, Yasusei Otsuka, Kunihiro Azuma, Masayuki Yamada, Akiko Ushio, Aya Tsunematsu, Takaaki Aota, Keiko |
| AuthorAffiliation | 1 Department of Oral Molecular Pathology, Tokushima University Graduate School of Biomedical Sciences , Tokushima , Japan 2 Department of Pathology and Laboratory Medicine, Tokushima University Graduate School of Biomedical Sciences , Tokushima , Japan 3 Department of Oral Medicine, Tokushima University Graduate School of Biomedical Sciences , Tokushima , Japan |
| AuthorAffiliation_xml | – name: 3 Department of Oral Medicine, Tokushima University Graduate School of Biomedical Sciences , Tokushima , Japan – name: 1 Department of Oral Molecular Pathology, Tokushima University Graduate School of Biomedical Sciences , Tokushima , Japan – name: 2 Department of Pathology and Laboratory Medicine, Tokushima University Graduate School of Biomedical Sciences , Tokushima , Japan |
| Author_xml | – sequence: 1 givenname: Aya surname: Ushio fullname: Ushio, Aya – sequence: 2 givenname: Rieko surname: Arakaki fullname: Arakaki, Rieko – sequence: 3 givenname: Kunihiro surname: Otsuka fullname: Otsuka, Kunihiro – sequence: 4 givenname: Akiko surname: Yamada fullname: Yamada, Akiko – sequence: 5 givenname: Takaaki surname: Tsunematsu fullname: Tsunematsu, Takaaki – sequence: 6 givenname: Yasusei surname: Kudo fullname: Kudo, Yasusei – sequence: 7 givenname: Keiko surname: Aota fullname: Aota, Keiko – sequence: 8 givenname: Masayuki surname: Azuma fullname: Azuma, Masayuki – sequence: 9 givenname: Naozumi surname: Ishimaru fullname: Ishimaru, Naozumi |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30467506$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright © 2018 Ushio, Arakaki, Otsuka, Yamada, Tsunematsu, Kudo, Aota, Azuma and Ishimaru. 2018 Ushio, Arakaki, Otsuka, Yamada, Tsunematsu, Kudo, Aota, Azuma and Ishimaru |
| Copyright_xml | – notice: Copyright © 2018 Ushio, Arakaki, Otsuka, Yamada, Tsunematsu, Kudo, Aota, Azuma and Ishimaru. 2018 Ushio, Arakaki, Otsuka, Yamada, Tsunematsu, Kudo, Aota, Azuma and Ishimaru |
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| Keywords | salivary gland chemokine tissue-resident macrophage autoimmunity Sjögren's syndrome T cell response |
| Language | English |
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| Title | CCL22-Producing Resident Macrophages Enhance T Cell Response in Sjögren's Syndrome |
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