NEUROIMMUNOLOGYB7-homolog 1 expression by human glioma: a new mechanism of immune evasionWilmotte, Rick1 2; Burkhardt, Karim3; Kindler, Vincent4; Belkouch, Marie-Claude1; Dussex, Géraldine1; Tribolet, Nicolas de2; Walker, Paul R.1; Dietrich, Pierre-Yves1 CAAuthor Information 1Laboratory of Tumor Immunology, Division of Oncology 2Department of Neurosurgery 3Divisions of Neuropathology 4Hematology, University Hospital Geneva, Geneva, Switzerland CACorresponding Author: firstname.lastname@example.org Received 10 May 2005; accepted 12 May 2005 NeuroReport: July 13th, 2005 - Volume 16 - Issue 10 - p 1081-1085 Buy SDC Abstract Immunosuppressive soluble factors such as transforming growth factor β and cell surface molecules such as FasL may contribute to the immune evasion of malignant glioma. B7 homolog 1 is a member of the B7 family of costimulatory molecules implicated in the negative regulation of T cell immune responses. Here, we show that human glioma cell lines express B7 homolog 1 protein that reduces interferon-γ production by activated T cells. The expression of B7 homolog 1 in vivo was demonstrated in a large series of human glioma samples, with a significant correlation between the level of B7 homolog 1 expression and the tumor grade. Overall, our data suggest that B7 homolog 1 may be involved in the immune evasion of glioma and encourage the blockade of this pathway in future immunotherapies. © 2005 Lippincott Williams & Wilkins, Inc.