MR1 deficiency enhances IL-17-mediated allergic contact dermatitis
Major histocompatibility complex (MHC) class Ib molecules present antigens to subsets of T cells primarily involved in host defense against pathogenic microbes and influence the development of immune-mediated diseases. The MHC class Ib molecule MHC-related protein 1 (MR1) functions as a platform to...
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2023-06-01
|
| Series: | Frontiers in Immunology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2023.1215478/full |
| _version_ | 1797799488977371136 |
|---|---|
| author | Naoya Imahashi Naoya Imahashi Masashi Satoh Masashi Satoh Emanuela Clemente Emanuela Clemente Kazuhisa Yoshino Mario Di Gioacchino Mario Di Gioacchino Kazuya Iwabuchi Kazuya Iwabuchi |
| author_facet | Naoya Imahashi Naoya Imahashi Masashi Satoh Masashi Satoh Emanuela Clemente Emanuela Clemente Kazuhisa Yoshino Mario Di Gioacchino Mario Di Gioacchino Kazuya Iwabuchi Kazuya Iwabuchi |
| author_sort | Naoya Imahashi |
| collection | DOAJ |
| description | Major histocompatibility complex (MHC) class Ib molecules present antigens to subsets of T cells primarily involved in host defense against pathogenic microbes and influence the development of immune-mediated diseases. The MHC class Ib molecule MHC-related protein 1 (MR1) functions as a platform to select MR1-restricted T cells, including mucosal-associated invariant T (MAIT) cells in the thymus, and presents ligands to them in the periphery. MAIT cells constitute an innate-like T-cell subset that recognizes microbial vitamin B2 metabolites and plays a defensive role against microbes. In this study, we investigated the function of MR1 in allergic contact dermatitis (ACD) by examining wild-type (WT) and MR1-deficient (MR1-/-) mice in which ACD was induced with 2,4-dinitrofluorobenzene (DNFB). MR1-/- mice exhibited exaggerated ACD lesions compared with WT mice. More neutrophils were recruited in the lesions in MR1-/- mice than in WT mice. WT mice contained fewer MAIT cells in their skin lesions following elicitation with DNFB, and MR1-/- mice lacking MAIT cells exhibited a significant increase in IL-17-producing αβ and γδ T cells in the skin. Collectively, MR1-/- mice displayed exacerbated ACD from an early phase with an enhanced type 3 immune response, although the precise mechanism of this enhancement remains elusive. |
| first_indexed | 2024-03-13T04:20:41Z |
| format | Article |
| id | doaj.art-5a184c8dec8544e3993d7af9ff153563 |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-03-13T04:20:41Z |
| publishDate | 2023-06-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-5a184c8dec8544e3993d7af9ff1535632023-06-20T10:23:28ZengFrontiers Media S.A.Frontiers in Immunology1664-32242023-06-011410.3389/fimmu.2023.12154781215478MR1 deficiency enhances IL-17-mediated allergic contact dermatitisNaoya Imahashi0Naoya Imahashi1Masashi Satoh2Masashi Satoh3Emanuela Clemente4Emanuela Clemente5Kazuhisa Yoshino6Mario Di Gioacchino7Mario Di Gioacchino8Kazuya Iwabuchi9Kazuya Iwabuchi10Program in Cellular Immunology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, JapanDepartment of Immunology, School of Medicine, Kitasato University, Sagamihara, JapanProgram in Cellular Immunology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, JapanDepartment of Immunology, School of Medicine, Kitasato University, Sagamihara, JapanProgram in Cellular Immunology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, JapanCenter for Advanced Studies and Technology (CAST), G. d’Annunzio University of Chieti-Pescara, Chiete, ItalyDepartment of Anesthesiology, School of Medicine, Kitasato University, Sagamihara, JapanCenter for Advanced Studies and Technology (CAST), G. d’Annunzio University of Chieti-Pescara, Chiete, ItalyInstitute of Clinical Immunotherapy and Advanced Biological Treatments, Pescara, ItalyProgram in Cellular Immunology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, JapanDepartment of Immunology, School of Medicine, Kitasato University, Sagamihara, JapanMajor histocompatibility complex (MHC) class Ib molecules present antigens to subsets of T cells primarily involved in host defense against pathogenic microbes and influence the development of immune-mediated diseases. The MHC class Ib molecule MHC-related protein 1 (MR1) functions as a platform to select MR1-restricted T cells, including mucosal-associated invariant T (MAIT) cells in the thymus, and presents ligands to them in the periphery. MAIT cells constitute an innate-like T-cell subset that recognizes microbial vitamin B2 metabolites and plays a defensive role against microbes. In this study, we investigated the function of MR1 in allergic contact dermatitis (ACD) by examining wild-type (WT) and MR1-deficient (MR1-/-) mice in which ACD was induced with 2,4-dinitrofluorobenzene (DNFB). MR1-/- mice exhibited exaggerated ACD lesions compared with WT mice. More neutrophils were recruited in the lesions in MR1-/- mice than in WT mice. WT mice contained fewer MAIT cells in their skin lesions following elicitation with DNFB, and MR1-/- mice lacking MAIT cells exhibited a significant increase in IL-17-producing αβ and γδ T cells in the skin. Collectively, MR1-/- mice displayed exacerbated ACD from an early phase with an enhanced type 3 immune response, although the precise mechanism of this enhancement remains elusive.https://www.frontiersin.org/articles/10.3389/fimmu.2023.1215478/fullinnate T cellsdelayed-type hypersensitivityneutrophilsgamma/delta T cellsallergy |
| spellingShingle | Naoya Imahashi Naoya Imahashi Masashi Satoh Masashi Satoh Emanuela Clemente Emanuela Clemente Kazuhisa Yoshino Mario Di Gioacchino Mario Di Gioacchino Kazuya Iwabuchi Kazuya Iwabuchi MR1 deficiency enhances IL-17-mediated allergic contact dermatitis Frontiers in Immunology innate T cells delayed-type hypersensitivity neutrophils gamma/delta T cells allergy |
| title | MR1 deficiency enhances IL-17-mediated allergic contact dermatitis |
| title_full | MR1 deficiency enhances IL-17-mediated allergic contact dermatitis |
| title_fullStr | MR1 deficiency enhances IL-17-mediated allergic contact dermatitis |
| title_full_unstemmed | MR1 deficiency enhances IL-17-mediated allergic contact dermatitis |
| title_short | MR1 deficiency enhances IL-17-mediated allergic contact dermatitis |
| title_sort | mr1 deficiency enhances il 17 mediated allergic contact dermatitis |
| topic | innate T cells delayed-type hypersensitivity neutrophils gamma/delta T cells allergy |
| url | https://www.frontiersin.org/articles/10.3389/fimmu.2023.1215478/full |
| work_keys_str_mv | AT naoyaimahashi mr1deficiencyenhancesil17mediatedallergiccontactdermatitis AT naoyaimahashi mr1deficiencyenhancesil17mediatedallergiccontactdermatitis AT masashisatoh mr1deficiencyenhancesil17mediatedallergiccontactdermatitis AT masashisatoh mr1deficiencyenhancesil17mediatedallergiccontactdermatitis AT emanuelaclemente mr1deficiencyenhancesil17mediatedallergiccontactdermatitis AT emanuelaclemente mr1deficiencyenhancesil17mediatedallergiccontactdermatitis AT kazuhisayoshino mr1deficiencyenhancesil17mediatedallergiccontactdermatitis AT mariodigioacchino mr1deficiencyenhancesil17mediatedallergiccontactdermatitis AT mariodigioacchino mr1deficiencyenhancesil17mediatedallergiccontactdermatitis AT kazuyaiwabuchi mr1deficiencyenhancesil17mediatedallergiccontactdermatitis AT kazuyaiwabuchi mr1deficiencyenhancesil17mediatedallergiccontactdermatitis |