Galectin-1 expression in CD8+ T lymphocytes controls inflammation in contact hypersensitivity
| Autor: | Raquel Castillo-González, Hortensia de la Fuente, Francisco Sánchez-Madrid, María Laura Saiz, Manuel Fresno, Nieves Fernández-Gallego, Marta Ramírez-Huesca, María N. Navarro, Danay Cibrian |
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| Přispěvatelé: | UAM. Departamento de Biología Molecular, UAM. Departamento de Medicina, Ministerio de Economía y Competitividad (España), Comunidad de Madrid, Fundación Ramón Areces, Fundación Ciencias de la Salud, Fundación BBVA, Fundació La Marató de TV3, La Caixa |
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Adoptive cell transfer Regulatory T cell Gamma-Delta T-Cells Inflammation Dermatology Biochemistry 03 medical and health sciences 0302 clinical medicine Immune system medicine Cytotoxic T cell Molecular Biology Allergic contact dermatitis Skin Chemistry Molecule Cell Biology medicine.disease Biología y Biomedicina / Biología 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Immunology Effector medicine.symptom Contact dermatitis CD8 LFA-1 |
| Zdroj: | Digital.CSIC. Repositorio Institucional del CSIC instname Biblos-e Archivo. Repositorio Institucional de la UAM |
| Popis: | Allergic contact dermatitis, also known as contact hypersensitivity, is a frequent T-cell‒mediated inflammatory skin disease characterized by red, itchy, swollen, and cracked skin. It is caused by the direct contact with an allergen and/or irritant hapten. Galectin-1 (Gal-1) is a β-galactoside‒binding lectin, which is highly expressed in several types of immune cells. The role of endogenous Gal-1 in contact hypersensitivity is not known. We found that Gal-1‒deficient mice display more sustained and prolonged skin inflammation than wild-type mice after oxazolone treatment. Gal-1‒deficient mice have increased CD8 T cells and neutrophilic infiltration in the skin. After the sensitization phase, Gal-1‒depleted mice showed an increased frequency of central memory CD8 T cells and IFN-γ secretion by CD8 T cells. The absence of Gal-1 does not affect the migration of transferred CD4 and CD8 T cells from the blood to the lymph nodes or to the skin. The depletion of CD4 T lymphocytes as well as adoptive transfer experiments demonstrated that endogenous expression of Gal-1 on CD8 T lymphocytes exerts a major role in the control of contact hypersensitivity model. These data underscore the protective role of endogenous Gal-1 in CD8 but not CD4 T cells in the development of allergic contact dermatitis. Spanish Ministry of Economy and Competitiveness, grant S2017/BMD-3671-INFLAMUNE-CM from the Comunidad de Madrid, a grant from the Ramón Areces Foundation Ciencias de la Vida y la Salud (XIX Concurso-2018), and a grant from Ayudas Fundación BBVA a Equipos de Investigación Científica (BIOMEDICINA-2018), the Fundacio´ Marato´ TV3 (grant 122/C/2015), and La Caixa Banking Foundation (HR17-00016) |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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