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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 354068, 19 pages
http://dx.doi.org/10.1155/2010/354068
Review Article

Bridging Innate and Adaptive Antitumor Immunity Targeting Glycans

1Department of Pathology, Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, 4301 West Markham St., Slot no.824, Little Rock, AR 72205, USA
2Bioinformatics Centre, Institute of Microbial Technology, Sector 39A, Chandigarh 160036, India

Received 26 January 2010; Accepted 22 April 2010

Academic Editor: Hanchun Yang

Copyright © 2010 Anastas Pashov et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Effective immunotherapy for cancer depends on cellular responses to tumor antigens. The role of major histocompatibility complex (MHC) in T-cell recognition and T-cell receptor repertoire selection has become a central tenet in immunology. Structurally, this does not contradict earlier findings that T-cells can differentiate between small hapten structures like simple glycans. Understanding T-cell recognition of antigens as defined genetically by MHC and combinatorially by T cell receptors led to the “altered self” hypothesis. This notion reflects a more fundamental principle underlying immune surveillance and integrating evolutionarily and mechanistically diverse elements of the immune system. Danger associated molecular patterns, including those generated by glycan remodeling, represent an instance of altered self. A prominent example is the modification of the tumor-associated antigen MUC1. Similar examples emphasize glycan reactivity patterns of antigen receptors as a phenomenon bridging innate and adaptive but also humoral and cellular immunity and providing templates for immunotherapies.