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Volume 2010 (2010), Article ID 130646, 9 pages
Review Article

Rationale for Targeting CD6 as a Treatment for Autoimmune Diseases

1EA2216 Immunology and Pathology and IFR 148 ScInBioS, European University of Brittany, BP 824, 29609 Brest, France
2Experimental Immunotherapy Department, Center for Molecular Immunology, P.O. Box 16040, 11600 La Havana, Cuba
3Laboratory of Immunology, CHU Brest, Brest University Medical School Hospital, BP 824, 29609 Brest, France

Received 16 August 2010; Accepted 22 December 2010

Academic Editor: Deh-Ming Chang

Copyright © 2010 Ruby Alonso-Ramirez 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.


CD6 is a 105–130 kDa surface glycoprotein expressed on the majority of T cells and a subset of B cells. The human cd6 gene maps to chromosome 11, and the expression of its protein product is tightly regulated. CD6 mediates cellular adhesion migration across the endothelial and epithelial cells. In addition, it participates in the antigen presentation by B cells and the subsequent proliferation of T cells. CD6 may bind in trans to surface glycoproteins (such as ALCAM and 3A11), or to microbial lipopolysaccharides, and may bind in cis to endogenous ligands (such as CD3 and CD5), and thereby deliver a costimulatory signal. Transinteractions are reinforced during autoimmune diseases (e.g., rheumatoid arthritis (RA), Sjögren's syndrome, and multiple sclerosis) and some cancers. Based on experimental data and on clinical results in RA and psoriasis, we believe that the recent humanized anti-CD6-specific mAb T1h may act as a regulator of the immunological response in addition to its function as an anti-T- and -B cell agent.