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

Copyright © 2024 Elsevier Inc. All rights reserved.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 269(2024) vom: 15. Dez., Seite 110402
Auteur principal: Shyanti, Ritis Kumar (Auteur)
Autres auteurs: Haque, Mazharul, Singh, Rajesh, Mishra, Manoj
Format: Article en ligne
Langue:English
Publié: 2024
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Review CD1d Cytokines Invariant natural killer T cells Lipid antigens Tumor immunity Antigens, CD1d CD1D protein, human
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520 |a 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 
650 4 |a Journal Article 
650 4 |a Review 
650 4 |a CD1d 
650 4 |a Cytokines 
650 4 |a Invariant natural killer T cells 
650 4 |a Lipid antigens 
650 4 |a Tumor immunity 
650 7 |a Antigens, CD1d  |2 NLM 
650 7 |a CD1D protein, human  |2 NLM 
700 1 |a Haque, Mazharul  |e verfasserin  |4 aut 
700 1 |a Singh, Rajesh  |e verfasserin  |4 aut 
700 1 |a Mishra, Manoj  |e verfasserin  |4 aut 
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