CD49a Expression Defines Tissue-Resident CD8+ T Cells Poised for Cytotoxic Function in Human Skin
Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker that differentiates CD8+ Trm cells on a compartmental and functional basis. In human skin epithelia, CD8+CD49a+ Trm cells produced interferon...
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| Published in | Immunity (Cambridge, Mass.) Vol. 46; no. 2; pp. 287 - 300 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
21.02.2017
Elsevier Limited Cell Press |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker that differentiates CD8+ Trm cells on a compartmental and functional basis. In human skin epithelia, CD8+CD49a+ Trm cells produced interferon-γ, whereas CD8+CD49a− Trm cells produced interleukin-17 (IL-17). In addition, CD8+CD49a+ Trm cells from healthy skin rapidly induced the expression of the effector molecules perforin and granzyme B when stimulated with IL-15, thereby promoting a strong cytotoxic response. In skin from patients with vitiligo, where melanocytes are eradicated locally, CD8+CD49a+ Trm cells that constitutively expressed perforin and granzyme B accumulated both in the epidermis and dermis. Conversely, CD8+CD49a– Trm cells from psoriasis lesions predominantly generated IL-17 responses that promote local inflammation in this skin disease. Overall, CD49a expression delineates CD8+ Trm cell specialization in human epithelial barriers and correlates with the effector cell balance found in distinct inflammatory skin diseases.
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•CD49a expression marks CD8+ Trm cells poised for IFN-γ production in human skin•IL-15 drives potent cytotoxic capacity in CD49a+ Trm cells•IL-17 is preferentially produced by CD49a− CD8+ Trm cells in the skin•CD49a+ versus CD49- Trm cell functional dichotomy is preserved in vitiligo and psoriasis
Tissue-resident memory T (Trm) cells provide localized adaptive immunity in peripheral tissues. Cheuk et al. identify cytotoxic CD49a+CD8+ Trm cells and IL-17-producing CD49a−CD8+ Trm cells in healthy human skin. The functional dichotomy of pathogenic Trm cells based on CD49a expression is preserved in focal skin diseases vitiligo and psoriasis. |
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| AbstractList | Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker that differentiates CD8+ Trm cells on a compartmental and functional basis. In human skin epithelia, CD8+CD49a+ Trm cells produced interferon-γ, whereas CD8+CD49a− Trm cells produced interleukin-17 (IL-17). In addition, CD8+CD49a+ Trm cells from healthy skin rapidly induced the expression of the effector molecules perforin and granzyme B when stimulated with IL-15, thereby promoting a strong cytotoxic response. In skin from patients with vitiligo, where melanocytes are eradicated locally, CD8+CD49a+ Trm cells that constitutively expressed perforin and granzyme B accumulated both in the epidermis and dermis. Conversely, CD8+CD49a– Trm cells from psoriasis lesions predominantly generated IL-17 responses that promote local inflammation in this skin disease. Overall, CD49a expression delineates CD8+ Trm cell specialization in human epithelial barriers and correlates with the effector cell balance found in distinct inflammatory skin diseases.
[Display omitted]
•CD49a expression marks CD8+ Trm cells poised for IFN-γ production in human skin•IL-15 drives potent cytotoxic capacity in CD49a+ Trm cells•IL-17 is preferentially produced by CD49a− CD8+ Trm cells in the skin•CD49a+ versus CD49- Trm cell functional dichotomy is preserved in vitiligo and psoriasis
Tissue-resident memory T (Trm) cells provide localized adaptive immunity in peripheral tissues. Cheuk et al. identify cytotoxic CD49a+CD8+ Trm cells and IL-17-producing CD49a−CD8+ Trm cells in healthy human skin. The functional dichotomy of pathogenic Trm cells based on CD49a expression is preserved in focal skin diseases vitiligo and psoriasis. Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker that differentiates CD8 + Trm cells on a compartmental and functional basis. In human skin epithelia, CD8 + CD49a + Trm cells produced interferon-γ, whereas CD8 + CD49a − Trm cells produced interleukin-17 (IL-17). In addition, CD8 + CD49a + Trm cells from healthy skin rapidly induced the expression of the effector molecules perforin and granzyme B when stimulated with IL-15, thereby promoting a strong cytotoxic response. In skin from patients with vitiligo, where melanocytes are eradicated locally, CD8 + CD49a + Trm cells that constitutively expressed perforin and granzyme B accumulated both in the epidermis and dermis. Conversely, CD8 + CD49a – Trm cells from psoriasis lesions predominantly generated IL-17 responses that promote local inflammation in this skin disease. Overall, CD49a expression delineates CD8 + Trm cell specialization in human epithelial barriers and correlates with the effector cell balance found in distinct inflammatory skin diseases. • CD49a expression marks CD8 + Trm cells poised for IFN-γ production in human skin • IL-15 drives potent cytotoxic capacity in CD49a + Trm cells • IL-17 is preferentially produced by CD49a − CD8 + Trm cells in the skin • CD49a + versus CD49 - Trm cell functional dichotomy is preserved in vitiligo and psoriasis Tissue-resident memory T (Trm) cells provide localized adaptive immunity in peripheral tissues. Cheuk et al. identify cytotoxic CD49a + CD8 + Trm cells and IL-17-producing CD49a − CD8 + Trm cells in healthy human skin. The functional dichotomy of pathogenic Trm cells based on CD49a expression is preserved in focal skin diseases vitiligo and psoriasis. Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker that differentiates CD8+Trm cells on a compartmental and functional basis. In human skin epithelia, CD8+CD49a+Trm cells produced interferon-γ, whereas CD8+CD49a-Trm cells produced interleukin-17 (IL-17). In addition, CD8+CD49a+Trm cells from healthy skin rapidly induced the expression of the effector molecules perforin and granzyme B when stimulated with IL-15, thereby promoting a strong cytotoxic response. In skin from patients with vitiligo, where melanocytes are eradicated locally, CD8+CD49a+Trm cells that constitutively expressed perforin and granzyme B accumulated both in the epidermis and dermis. Conversely, CD8+CD49a-Trm cells from psoriasis lesions predominantly generated IL-17 responses that promote local inflammation in this skin disease. Overall, CD49a expression delineates CD8+Trm cell specialization in human epithelial barriers and correlates with the effector cell balance found in distinct inflammatory skin diseases. Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker that differentiates CD8+ Trm cells on a compartmental and functional basis. In human skin epithelia, CD8+CD49a+ Trm cells produced interferon- gamma , whereas CD8+CD49a- Trm cells produced interleukin-17 (IL-17). In addition, CD8+CD49a+ Trm cells from healthy skin rapidly induced the expression of the effector molecules perforin and granzyme B when stimulated with IL-15, thereby promoting a strong cytotoxic response. In skin from patients with vitiligo, where melanocytes are eradicated locally, CD8+CD49a+ Trm cells that constitutively expressed perforin and granzyme B accumulated both in the epidermis and dermis. Conversely, CD8+CD49a- Trm cells from psoriasis lesions predominantly generated IL-17 responses that promote local inflammation in this skin disease. Overall, CD49a expression delineates CD8+ Trm cell specialization in human epithelial barriers and correlates with the effector cell balance found in distinct inflammatory skin diseases. Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker that differentiates CD8 Trm cells on a compartmental and functional basis. In human skin epithelia, CD8 CD49a Trm cells produced interferon-γ, whereas CD8 CD49a Trm cells produced interleukin-17 (IL-17). In addition, CD8 CD49a Trm cells from healthy skin rapidly induced the expression of the effector molecules perforin and granzyme B when stimulated with IL-15, thereby promoting a strong cytotoxic response. In skin from patients with vitiligo, where melanocytes are eradicated locally, CD8 CD49a Trm cells that constitutively expressed perforin and granzyme B accumulated both in the epidermis and dermis. Conversely, CD8 CD49a Trm cells from psoriasis lesions predominantly generated IL-17 responses that promote local inflammation in this skin disease. Overall, CD49a expression delineates CD8 Trm cell specialization in human epithelial barriers and correlates with the effector cell balance found in distinct inflammatory skin diseases. Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker that differentiates CD8+ Trm cells on a compartmental and functional basis. In human skin epithelia, CD8+CD49a+ Trm cells produced interferon-γ, whereas CD8+CD49a- Trm cells produced interleukin-17 (IL-17). In addition, CD8+CD49a+ Trm cells from healthy skin rapidly induced the expression of the effector molecules perforin and granzyme B when stimulated with IL-15, thereby promoting a strong cytotoxic response. In skin from patients with vitiligo, where melanocytes are eradicated locally, CD8+CD49a+ Trm cells that constitutively expressed perforin and granzyme B accumulated both in the epidermis and dermis. Conversely, CD8+CD49a- Trm cells from psoriasis lesions predominantly generated IL-17 responses that promote local inflammation in this skin disease. Overall, CD49a expression delineates CD8+ Trm cell specialization in human epithelial barriers and correlates with the effector cell balance found in distinct inflammatory skin diseases.Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker that differentiates CD8+ Trm cells on a compartmental and functional basis. In human skin epithelia, CD8+CD49a+ Trm cells produced interferon-γ, whereas CD8+CD49a- Trm cells produced interleukin-17 (IL-17). In addition, CD8+CD49a+ Trm cells from healthy skin rapidly induced the expression of the effector molecules perforin and granzyme B when stimulated with IL-15, thereby promoting a strong cytotoxic response. In skin from patients with vitiligo, where melanocytes are eradicated locally, CD8+CD49a+ Trm cells that constitutively expressed perforin and granzyme B accumulated both in the epidermis and dermis. Conversely, CD8+CD49a- Trm cells from psoriasis lesions predominantly generated IL-17 responses that promote local inflammation in this skin disease. Overall, CD49a expression delineates CD8+ Trm cell specialization in human epithelial barriers and correlates with the effector cell balance found in distinct inflammatory skin diseases. |
| Author | Schlums, Heinrich Gallais Sérézal, Irène Michaëlsson, Jakob Blomqvist, Lennart Eidsmo, Liv Folkersen, Lasse Martini, Elisa Marquardt, Nicole Mjösberg, Jenny Introini, Andrea Ståhle, Mona Forkel, Marianne Gibbs, Anna Cheuk, Stanley Chiang, Samuel C. Bryceson, Yenan T. Tjernlund, Annelie Höög, Charlotte Ehrström, Marcus Detlofsson, Ebba |
| AuthorAffiliation | 8 Broegelmann Research Laboratory, Department of Clinical Science, University of Bergen, Bergen 5021, Norway 1 Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden 3 Dermatology Department, Karolinska University Hospital, Stockholm 141 86, Sweden 5 Center for Biological Sequence Analysis, Department of Systems Biology, Technical University of Denmark, Building 208, DK-2800 Kongens Lyngby 2800, Denmark 6 Unit for Endocrinology and Diabetes, Department of Medicine, Huddinge, Karolinska Institutet, Stockholm 171 77, Sweden 2 Center for Hematology and Regenerative Medicine, Department of Medicine Huddinge, Karolinska Institutet, Stockholm 171 77, Sweden 4 Unit for Inflammation, Gastroenterology and Rheumatology, Department of Medicine, Huddinge, Karolinska Institutet, Stockholm 171 77, Sweden 7 Department of Reconstructive Plastic Surgery, Karolinska University Hospital Solna, Stockholm 171 76, Sweden |
| AuthorAffiliation_xml | – name: 1 Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden – name: 6 Unit for Endocrinology and Diabetes, Department of Medicine, Huddinge, Karolinska Institutet, Stockholm 171 77, Sweden – name: 3 Dermatology Department, Karolinska University Hospital, Stockholm 141 86, Sweden – name: 7 Department of Reconstructive Plastic Surgery, Karolinska University Hospital Solna, Stockholm 171 76, Sweden – name: 2 Center for Hematology and Regenerative Medicine, Department of Medicine Huddinge, Karolinska Institutet, Stockholm 171 77, Sweden – name: 5 Center for Biological Sequence Analysis, Department of Systems Biology, Technical University of Denmark, Building 208, DK-2800 Kongens Lyngby 2800, Denmark – name: 8 Broegelmann Research Laboratory, Department of Clinical Science, University of Bergen, Bergen 5021, Norway – name: 4 Unit for Inflammation, Gastroenterology and Rheumatology, Department of Medicine, Huddinge, Karolinska Institutet, Stockholm 171 77, Sweden |
| Author_xml | – sequence: 1 givenname: Stanley surname: Cheuk fullname: Cheuk, Stanley organization: Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 2 givenname: Heinrich surname: Schlums fullname: Schlums, Heinrich organization: Center for Hematology and Regenerative Medicine, Department of Medicine Huddinge, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 3 givenname: Irène surname: Gallais Sérézal fullname: Gallais Sérézal, Irène organization: Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 4 givenname: Elisa surname: Martini fullname: Martini, Elisa organization: Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 5 givenname: Samuel C. surname: Chiang fullname: Chiang, Samuel C. organization: Center for Hematology and Regenerative Medicine, Department of Medicine Huddinge, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 6 givenname: Nicole surname: Marquardt fullname: Marquardt, Nicole organization: Dermatology Department, Karolinska University Hospital, Stockholm 141 86, Sweden – sequence: 7 givenname: Anna surname: Gibbs fullname: Gibbs, Anna organization: Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 8 givenname: Ebba surname: Detlofsson fullname: Detlofsson, Ebba organization: Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 9 givenname: Andrea surname: Introini fullname: Introini, Andrea organization: Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 10 givenname: Marianne surname: Forkel fullname: Forkel, Marianne organization: Dermatology Department, Karolinska University Hospital, Stockholm 141 86, Sweden – sequence: 11 givenname: Charlotte surname: Höög fullname: Höög, Charlotte organization: Unit for Inflammation, Gastroenterology and Rheumatology, Department of Medicine, Huddinge, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 12 givenname: Annelie surname: Tjernlund fullname: Tjernlund, Annelie organization: Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 13 givenname: Jakob surname: Michaëlsson fullname: Michaëlsson, Jakob organization: Dermatology Department, Karolinska University Hospital, Stockholm 141 86, Sweden – sequence: 14 givenname: Lasse surname: Folkersen fullname: Folkersen, Lasse organization: Center for Biological Sequence Analysis, Department of Systems Biology, Technical University of Denmark, Building 208, DK-2800 Kongens Lyngby 2800, Denmark – sequence: 15 givenname: Jenny surname: Mjösberg fullname: Mjösberg, Jenny organization: Dermatology Department, Karolinska University Hospital, Stockholm 141 86, Sweden – sequence: 16 givenname: Lennart surname: Blomqvist fullname: Blomqvist, Lennart organization: Unit for Endocrinology and Diabetes, Department of Medicine, Huddinge, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 17 givenname: Marcus surname: Ehrström fullname: Ehrström, Marcus organization: Department of Reconstructive Plastic Surgery, Karolinska University Hospital Solna, Stockholm 171 76, Sweden – sequence: 18 givenname: Mona surname: Ståhle fullname: Ståhle, Mona organization: Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 19 givenname: Yenan T. surname: Bryceson fullname: Bryceson, Yenan T. email: yenan.bryceson@ki.se organization: Center for Hematology and Regenerative Medicine, Department of Medicine Huddinge, Karolinska Institutet, Stockholm 171 77, Sweden – sequence: 20 givenname: Liv surname: Eidsmo fullname: Eidsmo, Liv email: liv.eidsmo@ki.se organization: Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28214226$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:135255884$$DView record from Swedish Publication Index |
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| Keywords | granzyme B perforin immunopathology CD49a tissue resident T cells psoriasis vitiligo IL-15 Skin cytotoxicity |
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| License | This is an open access article under the CC BY-NC-ND license. Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
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| Snippet | Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker... Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker... |
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| SubjectTerms | Biopsy CD49a CD8-Positive T-Lymphocytes - immunology Cell Separation Councils Cytotoxicity Cytotoxicity, Immunologic - immunology Deoxyribonucleic acid DNA Experiments Flow Cytometry granzyme B Humans IL-15 Immunologic Memory - immunology immunopathology Integrin alpha1 - biosynthesis Integrin alpha1 - immunology Localization Lymphocyte Activation - immunology Lymphocytes Microscopy, Confocal perforin Psoriasis Psoriasis - immunology Skin Skin - immunology T cell receptors T-Lymphocyte Subsets - immunology tissue resident T cells Vitiligo Vitiligo - immunology |
| Title | CD49a Expression Defines Tissue-Resident CD8+ T Cells Poised for Cytotoxic Function in Human Skin |
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