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Peer-reviewedCC BY 4.0Frontiers in Immunology

MHC-II+ G-MDSC expressing CD80, CD86, or ICOSL are associated with pro-inflammatory CD4+ T cells phenotypes in the lungs of lupus-prone mice

  • Felipe R. Uribe1,2
  • Sebastián A. Echeverría-Araya1,2
  • Grabiel J. García-Velázquez1,2
  • Karissa Chávez-Villacreses1,2
  • Benjamín Díaz-López1,2
  • Valeria Salazar-Montoya1,2
  • Alison Sepúlveda-Pontigo1,2
  • Jocelyn Tobar2,3
  • Felipe Simon2,3
  • Rodolfo Paredes4,5
  • Felipe Melo-González2,6
  • Katina Schinnerling2,6
4 more authors
  • Juan P. Mackern-Oberti7,8
  • Abel E. Vasquez9,10
  • Karen Bohmwald11
  • Jorge A. Soto1,2
11 affiliations
  1. 1Laboratory of Virology and Integrative Translational Immunology, Faculty of Life Sciences, Universidad Andres Bello
  2. 2Center for Research on Pandemic Resilience, Faculty of Life Sciences and Institute of Public Health, Universidad Andres Bello
  3. 3Millenium Institute of Immunology and Immunotherapy
  4. 4Veterinary School, Faculty of Life Science, Universidad Andres Bello
  5. 5One Health Institute, Faculty of Life Sciences, Universidad Andres Bello
  6. 6Translational Immunology Laboratory, Faculty of Life Sciences, Universidad Andres Bello
  7. 7Universidad Nacional de Cuyo, Faculty of Medical Sciences
  8. 8Instituto de Medicina y Biología Experimental de Cuyo (IMBECU), Centro Científico Tecnológico (CCT), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET)
  9. 9School of Veterinary Medicine, Faculty of Medicine and Health Sciences, Universidad Mayor
  10. 10Center for Biomedicine, Universidad Mayor
  11. 11Instituto de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Autónoma de Chile
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Abstract

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that affects various tissues of the body. One of these tissues is the lung, in which pleuropulmonary manifestations commonly occur. In these patients, homeostasis is disrupted, characterized by a decrease in T reg and an increase in T h1 and T h2 cells. Myeloid-derived suppressor cells (MDSCs) are a cell population characterized by their ability to suppress the T cell response; however, in recent years, the presence of major histocompatibility complex class II (MHC-II) molecules on MDSCs has been reported. Nevertheless, the presence of costimulatory molecules, such as CD80, CD86, and ICOSL, has not been studied yet in MDSCs expressing MHC-II in the context of SLE. In this study, we evaluated the pulmonary microenvironment in SLE mice from an immunological and histological perspective. We observed increased pro-inflammatory cytokines and cellular infiltration in lungs of SLE mice. We also observed MDSC MHC-II cells expressing CD80, CD86, and ICOSL in this tissue, along with alterations of CD4 ⁺ T cells subsets, characterized by a decrease in IL-10 frequency in SLE mice. Moreover, we observed that G-MDSCs MHC-II expressing CD80, CD86, or ICOSL correlate positively with phenotypes of CD4 ⁺ T cells that produce IL-17 and IFN-γ. For this reason, we suggest that MHC-II ⁺ G-MDSC cells may contribute to an inflammatory environment that triggers tissue damage in the lungs of SLE mice.

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Cite

BibTeXRIS
BibTeX
@article{uribe2026mhcii,
  title = {{MHC-II+ G-MDSC expressing CD80, CD86, or ICOSL are associated with pro-inflammatory CD4+ T cells phenotypes in the lungs of lupus-prone mice}},
  author = {Felipe R. Uribe and Sebastián A. Echeverría-Araya and Grabiel J. García-Velázquez and Karissa Chávez-Villacreses and Benjamín Díaz-López and Valeria Salazar-Montoya and Alison Sepúlveda-Pontigo and Jocelyn Tobar and Felipe Simon and Rodolfo Paredes and Felipe Melo-González and Katina Schinnerling and Juan P. Mackern-Oberti and Abel E. Vasquez and Karen Bohmwald and Jorge A. Soto},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1891967},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1891967/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - MHC-II+ G-MDSC expressing CD80, CD86, or ICOSL are associated with pro-inflammatory CD4+ T cells phenotypes in the lungs of lupus-prone mice
AU  - Felipe R. Uribe
AU  - Sebastián A. Echeverría-Araya
AU  - Grabiel J. García-Velázquez
AU  - Karissa Chávez-Villacreses
AU  - Benjamín Díaz-López
AU  - Valeria Salazar-Montoya
AU  - Alison Sepúlveda-Pontigo
AU  - Jocelyn Tobar
AU  - Felipe Simon
AU  - Rodolfo Paredes
AU  - Felipe Melo-González
AU  - Katina Schinnerling
AU  - Juan P. Mackern-Oberti
AU  - Abel E. Vasquez
AU  - Karen Bohmwald
AU  - Jorge A. Soto
PY  - 2026
DA  - 2026/10/26
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1891967
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1891967/full
AB  - Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that affects various tissues of the body. One of these tissues is the lung, in which pleuropulmonary manifestations commonly occur. In these patients, homeostasis is disrupted, characterized by a decrease in T reg and an increase in T h1 and T h2 cells. Myeloid-derived suppressor cells (MDSCs) are a cell population characterized by their ability to suppress the T cell response; however, in recent years, the presence of major histocompatibility complex class II (MHC-II) molecules on MDSCs has been reported. Nevertheless, the presence of costimulatory molecules, such as CD80, CD86, and ICOSL, has not been studied yet in MDSCs expressing MHC-II in the context of SLE. In this study, we evaluated the pulmonary microenvironment in SLE mice from an immunological and histological perspective. We observed increased pro-inflammatory cytokines and cellular infiltration in lungs of SLE mice. We also observed MDSC MHC-II cells expressing CD80, CD86, and ICOSL in this tissue, along with alterations of CD4 ⁺ T cells subsets, characterized by a decrease in IL-10 frequency in SLE mice. Moreover, we observed that G-MDSCs MHC-II expressing CD80, CD86, or ICOSL correlate positively with phenotypes of CD4 ⁺ T cells that produce IL-17 and IFN-γ. For this reason, we suggest that MHC-II ⁺ G-MDSC cells may contribute to an inflammatory environment that triggers tissue damage in the lungs of SLE mice.
SN  - 1664-3224
ER  -