ArticleCell reports2025
Defective removal of invariant chain peptides from MHC class II suppresses tumor antigen presentation and promotes tumor growth.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Review
- Astragalus polysaccharide antagonized anti PD-1 efficacy in melanoma through inhibiting JAK-STAT1/CIITA and TLR/NF-κB signaling.Frontiers in immunology · 2026Article
- Longitudinal Imaging of the Premalignant Tumor Microenvironment Reveals Transient Myeloid States Predictive of Tumor Fate.bioRxiv : the preprint server for biology · 2025Article
- Cathepsin S: molecular mechanisms in inflammatory and immunological processes.Frontiers in immunology · 2025Review
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Authors and funding
4 authors.
Funding
Abstract
Tumor-draining lymph node dendritic cells (DCs) are poor stimulators of tumor antigen-specific CD4 T cells; however, the mechanism behind this defect is unclear. We now show that, in tumor-draining lymph node DCs, a large proportion of major histocompatibility complex class II (MHC-II) molecules retains the class II-associated invariant chain peptide (CLIP) fragment of the invariant chain bound to the MHC-II peptide binding groove due to reduced expression of the peptide editor H2-M and enhanced activity of the CLIP-generating proteinase cathepsin S. The net effect of this is that MHC-II molecules are unable to efficiently bind antigenic peptides. DCs in mice expressing a mutation in the invariant chain sequence that results in enhanced MHC-II-CLIP accumulation are poor stimulators of CD4 T cells and have diminished anti-tumor responses. Our data reveal a previously unknown mechanism of immune evasion in which enhanced expression of MHC-II-CLIP complexes on tumor-draining lymph node DCs limits MHC-II availability for tumor peptides.
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