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The Immune Checkpoint HLA-G 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (20 May 2023) | Viewed by 2549

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Guest Editor
1. Commissariat à l'Energie Atomique et aux Energies Alternatives, Direction de la Recherche Fondamentale, Institut de Biologie François Jacob, Service de Recherches en Hémato-Immunologie, 75475 Paris, France
2. Institut de Recherche Saint-Louis, Université de Paris, UMR 976, 75475 Paris, France
3. Hôpital Saint-Louis, 1 Avenue Claude Vellefaux, CEDEX 10, 75475 Paris, France
Interests: immune checkpoints; gene regulation; immunogenetics
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Special Issue Information

Dear Colleagues, 

The immune checkpoint HLA-G is a non-classical HLA-class I molecule primarily expressed in extravillous trophoblast cells; it was first described to play a critical role in protecting the fetus from destruction by the maternal immune system. While HLA-G expression in healthy tissues is restricted to immune-privileged sites, it is upregulated in several pathological situations and may be beneficial (allogenic transplantation, autoimmune diseases) or harmful (cancer, viral and parasitic infections) for patients. Unlike other checkpoints, the interaction of HLA-G with ILT-2 and ILT-4 receptors inhibits all actors and blocks all stages of an immune response, from APC activation and effector priming to the function of fully activated CTLs, NK cells or B cells.

The aim of this Special Issue is to present recent advances in HLA-G regulation and HLA-G function in the context of pregnancy, transplantation, cancer, infectious diseases, chronic inflammatory pathologies and autoimmunity. HLA-G can be considered on its own or in conjunction with other known immune checkpoints. In addition, research papers and review articles on the development of therapeutic and monitoring tools involving HLA-G and its receptors are also of interest.

Dr. Philippe Moreau
Guest Editor

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16 pages, 2532 KiB  
Article
The Severity of COVID-19 Affects the Plasma Soluble Levels of the Immune Checkpoint HLA-G Molecule
by Jéssica F. C. Cordeiro, Talita M. Fernandes, Diana M. Toro, Pedro V. da Silva-Neto, Vinícius E. Pimentel, Malena M. Pérez, Jonatan C. S. de Carvalho, Thais F. C. Fraga-Silva, Camilla N. S. Oliveira, Jamille G. M. Argolo, Augusto M. Degiovani, Fátima M. Ostini, Enrico F. Puginna, João S. da Silva, Isabel K. F. M. Santos, Vânia L. D. Bonato, Cristina R. B. Cardoso, Marcelo Dias-Baruffi, Lúcia H. Faccioli, Eduardo A. Donadi, Carlos A. Sorgi, Ana P. M. Fernandes and on behalf of the IMMUNOCOVID Study Groupadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2022, 23(17), 9736; https://doi.org/10.3390/ijms23179736 - 27 Aug 2022
Cited by 5 | Viewed by 2233
Abstract
The non-classical histocompatibility antigen G (HLA-G) is an immune checkpoint molecule that has been implicated in viral disorders. We evaluated the plasma soluble HLA-G (sHLA-G) in 239 individuals, arranged in COVID-19 patients (n = 189) followed up at home or in a [...] Read more.
The non-classical histocompatibility antigen G (HLA-G) is an immune checkpoint molecule that has been implicated in viral disorders. We evaluated the plasma soluble HLA-G (sHLA-G) in 239 individuals, arranged in COVID-19 patients (n = 189) followed up at home or in a hospital, and in healthy controls (n = 50). Increased levels of sHLA-G were observed in COVID-19 patients irrespective of the facility care, gender, age, and the presence of comorbidities. Compared with controls, the sHLA-G levels increased as far as disease severity progressed; however, the levels decreased in critically ill patients, suggesting an immune exhaustion phenomenon. Notably, sHLA-G exhibited a positive correlation with other mediators currently observed in the acute phase of the disease, including IL-6, IL-8 and IL-10. Although sHLA-G levels may be associated with an acute biomarker of COVID-19, the increased levels alone were not associated with disease severity or mortality due to COVID-19. Whether the SARS-CoV-2 per se or the innate/adaptive immune response against the virus is responsible for the increased levels of sHLA-G are questions that need to be further addressed. Full article
(This article belongs to the Special Issue The Immune Checkpoint HLA-G 2.0)
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