BRIEF RESEARCH REPORT article
Front. Cell. Infect. Microbiol.
Sec. Microbes and Innate Immunity
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1618339
This article is part of the Research TopicEmerging Mechanisms of Host-Pathogen Interactions and immune responsesView all 6 articles
Specific inflammatory stimuli that engage innate immune sensors induce novel CD103 expression profiles in macrophages
Provisionally accepted
- Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Canada
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The integrin CD103 is an adhesion molecule that facilitates immune cell retention in epithelial tissues through its interaction with E-cadherin. It is a marker for certain CD8+ T-cell subpopulations and conventional type 1 dendritic cells (cDC1), but its presence on macrophages remains poorly characterized. Macrophage differentiation is influenced by M-CSF and GM-CSF, and we investigated whether macrophages can also express CD103 under inflammatory conditions. We examined baseline CD103 expression in bone marrow-derived macrophages (BMDMs) differentiated in M-CSF or GM-CSF and then stimulated them with pathogen-associated molecular patterns (PAMPs) or examined them following viral infection. We found that CD103 is minimally expressed at baseline but is selectively upregulated in M-CSF-differentiated macrophages after stimulation with endosomal TLR agonists. Mechanistically, p38 MAPK inhibition prevented CD103 upregulation, suggesting that this process is mediated by p38 MAPK signaling. Furthermore, in vivo LCMV infection induced CD103 expression on peritoneal macrophages. These findings demonstrate that macrophages can express CD103 under specific inflammatory conditions, challenging the assumption that CD103 is restricted to T cells and dendritic cells. This study expands our understanding of CD103 beyond its recognized roles in T cells and DCs, providing new insight into its regulation by macrophages.
Keywords: CD103/ITGAE, macrophage, Inflammation, TLR, virus, innate immunity
Received: 25 Apr 2025; Accepted: 04 Jun 2025.
Copyright: © 2025 Bouzeineddine, Talbot, Basta and Gee. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Sam Basta, Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Canada
Katrina Gee, Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Canada
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