Optimizing iNKT-driven immune responses against cancer by modulating CD1d in tumor and antigen presenting cells.

Autor: Shyanti RK; Cancer Research Center, Department of Biological Sciences, Alabama State University, AL 36104, USA., Haque M; Cancer Research Center, Department of Biological Sciences, Alabama State University, AL 36104, USA., Singh R; Microbiology, Biochemistry, and Immunology, Cancer Health Equity Institute, Morehouse School of Medicine, Atlanta, GA, USA., Mishra M; Cancer Research Center, Department of Biological Sciences, Alabama State University, AL 36104, USA. Electronic address: mmishra@alasu.edu.
Jazyk: angličtina
Zdroj: Clinical immunology (Orlando, Fla.) [Clin Immunol] 2024 Dec; Vol. 269, pp. 110402. Date of Electronic Publication: 2024 Nov 17.
DOI: 10.1016/j.clim.2024.110402
Abstrakt: Two major antigen processing pathways represent protein Ags through major histocompatibility complexes (MHC class I and II) or lipid Ags through CD1 molecules influence the tumor immune response. Invariant Natural Killer T cells (iNKT) manage a significant role in cancer immunotherapy. CD1d, found on antigen-presenting cells (APCs), presents lipid Ags to iNKT cells. In many cancers, the number and function of iNKT cell are compromised, leading to immune evasion. Additionally impaired motility of iNKT cells may contribute to poor tumor prognosis. Emerging evidences suggest that CD1d, itself also influences cancer progression. Patient databases further highlight the importance of CD1d expression in different cancers and its correlation with patient survival outcomes. The ability of iNKT cells to activate and enhance the immune response renders them an attractive target for cancer immunotherapy. This review discusses all the possible ways of cancer immune evasion and restoration of immune responses mediated by CD1d-iNKT interactions.
Competing Interests: Declaration of competing interest The authors declare no conflict of interest.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
Externí odkaz: