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Sublingual macrophage-associated ILDR2 contributes to immune tolerance via Treg induction.
Biochem Biophys Res Commun
January 2025
Department of Oral Biology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, 113-8549, Japan; Department of Molecular Immunology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. Electronic address:
The sublingual mucosa (SLM) has been used for sublingual immunotherapy (SLIT) which has the potential to induce antigen-specific immune tolerance. We previously demonstrated the CD206 macrophages that were increased in the SLM after repeated antigen exposure. These macrophages showed high expression of the gene encoding ILDR2 (Ig-like domain-containing receptor 2), an immune checkpoint molecule.
View Article and Find Full Text PDFSiglec15/TGF-β bispecific antibody mediates synergistic anti-tumor response against 4T1 triple negative breast cancer in mice.
Bioeng Transl Med
September 2024
Division of Pharmacoengineering and Molecular Pharmaceutics Eshelman School of Pharmacy, University of North Carolina Chapel Hill North Carolina USA.
An ideal tumor-specific immunomodulatory therapy should both preferentially target the tumor, while simultaneously reduce the immunosuppressive environment within the tumor. This guiding principle led us to explore engineering Siglec-15 (S15) targeted bispecific antibody (bsAb) to enhance therapy against triple negative breast cancer (TNBC). S15 appears to be exclusively expressed on macrophages and diverse tumor cells, including human and mouse 4T1 TNBC.
View Article and Find Full Text PDFBlockade of CCR5 T Cell Accumulation in the Tumor Microenvironment Optimizes Anti-TGF-β/PD-L1 Bispecific Antibody.
Adv Sci (Weinh)
November 2024
Cancer Center, Shanxi Bethune Hospital, Shanxi Academy of Medical Science, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, 030032, P. R. China.
Article Synopsis
- The study investigates the bispecific antibody YM101, which shows better results than anti-PD-L1 alone in fighting tumors, but still fails to completely eliminate tumors in mice, indicating other immunosuppressive factors in the tumor microenvironment (TME).
- Researchers used single-cell RNA sequencing (scRNA-seq) to analyze changes in the TME caused by YM101, discovering increased immune cell populations boosting antitumor activity, yet also finding immunosuppressive CCR5 T cells.
- To improve YM101's effectiveness, the researchers combined it with Maraviroc, a CCR5 antagonist, which reduced the harmful CCR5 T cells and enhanced the overall antitumor immune response, suggesting that targeting CCR5 could
EGFR mutations induce the suppression of CD8 T cell and anti-PD-1 resistance via ERK1/2-p90RSK-TGF-β axis in non-small cell lung cancer.
J Transl Med
July 2024
Department of Medical Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, West Huaihai Road 241, Shanghai, 200030, China.
Background: Non-small cell lung cancer (NSCLC) patients with EGFR mutations exhibit an unfavorable response to immune checkpoint inhibitor (ICI) monotherapy, and their tumor microenvironment (TME) is usually immunosuppressed. TGF-β plays an important role in immunosuppression; however, the effects of TGF-β on the TME and the efficacy of anti-PD-1 immunotherapy against EGFR-mutated tumors remain unclear.
Methods: Corresponding in vitro studies used the TCGA database, clinical specimens, and self-constructed mouse cell lines with EGFR mutations.
Short-term cultured tumor fragments to study immunotherapy combinations based on CD137 (4-1BB) agonism.
Oncoimmunology
July 2024
Immunology, Navarra Institute for Health Research (IdiSNA), Pamplona, Spain.
Biomarkers for cancer immunotherapy are an unmet medical need. The group of Daniela Thommen at the NKI recently reported on novel methodologies based on short-term cultures of patient-derived tumor fragments whose cytokine concentrations in the supernatants and activation markers on infiltrating T cells were associated with clinical response to PD-1 blockade. We set up a similar culture technology with tumor-derived fragments using mouse tumors transplanted into syngeneic immunocompetent mice to test an agonist anti-CD137 mAb and its combinations with anti-PD-1 and/or anti-TGF-β.
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