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Dermatology Research and Practice
Volume 2010 (2010), Article ID 657406, 11 pages
Review Article

Metastatic Melanomas Express Inhibitory Low Affinity Fc Gamma Receptor and Escape Humoral Immunity

1INSERM, U872, Microenvironnement Immunitaire et Tumeurs, Equipe 13, Centre de Recherche des Cordeliers, 75006 Paris, France
2UMRS 872, Universite Pierre et Marie Curie, 75005 Paris, France
3UMRS 872, Universite Paris Descartes, 75006 Paris, France
4The Feinstein Institute for Medical Research, North-Shore Long Island Jewish Health System, Manhassett, NY 11030, USA
5Unite d'Allergologie Moleculaire et Cellulaire, Institut Pasteur, 75724 Paris, France
6Department of Immunology, National Jewish Health, University of Colorado, Denver, CO 80045, USA

Received 16 December 2009; Accepted 1 April 2010

Academic Editor: Keith Hoek

Copyright © 2010 Joel F. G. Cohen-Solal 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.


Our research, inspired by the pioneering works of Isaac Witz in the 1980s, established that 40% of human metastatic melanomas express ectopically inhibitory Fc gamma receptors (Fc 𝛾 RIIB), while they are detected on less than 5% of primary cutaneous melanoma and not on melanocytes. We demonstrated that these tumoral Fc 𝛾 RIIB act as decoy receptors that bind the Fc portion of antimelanoma IgG, which may prevent Fc recognition by the effector cells of the immune system and allow the metastatic melanoma to escape the humoral/natural immune response. The Fc 𝛾 RIIB is able to inhibit the ADCC (antibody dependent cell cytotoxicity) in vitro. Interestingly, the percentage of melanoma expressing the Fc 𝛾 RIIB is high (70%) in organs like the liver, which is rich in patrolling NK (natural killer) cells that exercise their antitumoral activity by ADCC. We found that this tumoral Fc 𝛾 RIIB is fully functional and that its inhibitory potential can be triggered depending on the specificity of the anti-tumor antibody with which it interacts. Together these observations elucidate how metastatic melanomas interact with and potentially evade humoral immunity and provide direction for the improvement of anti-melanoma monoclonal antibody therapy.