CD1c is a group 1 CD1 molecule expressed predominantly by human conventional dendritic cells (cDC2) and functions as a lipid antigen-presenting molecule that activates antigen-specific T-cell responses through presentation of structurally diverse endogenous and microbial lipids
[1][2]. Mechanistically, CD1c participates in adaptive immune regulation by presenting mycobacterial lipids, phosphatidylinositol, phosphatidylcholine, sulfatides, and lipopeptide antigens, thereby supporting T-cell activation and interferon-γ production during antimicrobial immune responses
[1]. CD1c
+ dendritic cells also produce IL-12p70, IL-1β, IL-6, and IL-23 following innate immune stimulation and promote both Th1 and Th17 effector differentiation, linking antigen presentation to inflammatory cytokine networks
[3]. In autoimmune and inflammatory settings, activated CD1c
+ dendritic cells have been implicated in pathogenic Th1/Th17 immune responses, highlighting their relevance in disease-associated immune activation
[3]. Compared with related CD1 isoforms, including CD1a and CD1b, CD1c exhibits distinct structural features that enable presentation of a broader repertoire of lipid-based antigens, supporting functional specialization within the group 1 CD1 family
[1][2]. Within the CD1c
+ dendritic-cell compartment, CD14
+ and CD14
− subsets display divergent transcriptional and functional characteristics, with CD14
+ populations expressing monocyte-associated markers and showing reduced T-cell stimulatory capacity
[4]. Furthermore, CD1c
+CD163
+ dendritic-cell subsets can prime CD8
+CD103
+ T cells through TGF-β signaling and are associated with tissue-resident memory T-cell responses in tumor microenvironments, supporting their utility in tumor immunology research models
[5].