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Galectin-1 Expression in CD8+ T Lymphocytes Controls Inflammation in Contact Hypersensitivity.

Authors
  • Castillo-González, Raquel1
  • Cibrian, Danay2
  • Fernández-Gallego, Nieves3
  • Ramírez-Huesca, Marta4
  • Saiz, María Laura5
  • Navarro, María N6
  • Fresno, Manuel6
  • de la Fuente, Hortensia2
  • Sánchez-Madrid, Francisco7
  • 1 Immunology Service, Hospital de la Princesa, Universidad Autónoma de Madrid, Instituto de Investigación Sanitaria del Hospital Universitario de La Princesa, Madrid, Spain; Department of Medicine, Universidad Autónoma de Madrid, Madrid, Spain; Department of Intercellular Communication in the Inflammatory Response, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain. , (Spain)
  • 2 Immunology Service, Hospital de la Princesa, Universidad Autónoma de Madrid, Instituto de Investigación Sanitaria del Hospital Universitario de La Princesa, Madrid, Spain; Department of Medicine, Universidad Autónoma de Madrid, Madrid, Spain; Department of Intercellular Communication in the Inflammatory Response, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; CIBER de Enfermedades Cardiovasculares, Carlos III Health Institute, Madrid, Spain. , (Spain)
  • 3 Department of Medicine, Universidad Autónoma de Madrid, Madrid, Spain; Department of Intercellular Communication in the Inflammatory Response, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain. , (Spain)
  • 4 Department of Intercellular Communication in the Inflammatory Response, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain. , (Spain)
  • 5 Immunology Service, Hospital de la Princesa, Universidad Autónoma de Madrid, Instituto de Investigación Sanitaria del Hospital Universitario de La Princesa, Madrid, Spain; Department of Medicine, Universidad Autónoma de Madrid, Madrid, Spain. , (Spain)
  • 6 Department of Immune System Development and Function, Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain. , (Spain)
  • 7 Immunology Service, Hospital de la Princesa, Universidad Autónoma de Madrid, Instituto de Investigación Sanitaria del Hospital Universitario de La Princesa, Madrid, Spain; Department of Medicine, Universidad Autónoma de Madrid, Madrid, Spain; Department of Intercellular Communication in the Inflammatory Response, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; CIBER de Enfermedades Cardiovasculares, Carlos III Health Institute, Madrid, Spain. Electronic address: [email protected] , (Spain)
Type
Published Article
Journal
Journal of Investigative Dermatology
Publisher
Elsevier
Publication Date
Jun 01, 2021
Volume
141
Issue
6
Identifiers
DOI: 10.1016/j.jid.2020.10.020
PMID: 33181141
Source
Medline
Language
English
License
Unknown

Abstract

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. Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

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