Ogunjimi B.,University of Antwerp |
Smits E.,Laboratory of Experimental Hematology |
Hens N.,University of Antwerp |
Hens N.,Hasselt University |
And 7 more authors.
Viral Immunology | Year: 2011
Varicella-zoster virus (VZV) causes both primary varicella, and through reactivation of the virus, herpes zoster. It is hypothesized that VZV-immune adults may reduce the probability of developing herpes zoster through exposure to varicella. In this study we examine the existence of immunological boosting in VZV-immune adults after close contact with primary varicella. We followed-up 18 parents with household exposure to primary varicella for 1 y. Fifteen age-matched healthy and 20 older volunteers served as control groups. Cellular (IFN-γ ELISPOT) and humoral responses were measured. Data analyses were performed by t-tests and linear mixed models. The young control group only showed higher cellular responses than the older control group and the exposed group 1 mo after exposure. The exposed group had a strong tendency toward higher cellular responses compared to the older control group, reaching significance 1 y post-exposure. The best fitting linear mixed model predicts a decline in cellular response of 50% between 1 wk and 1 mo post-exposure, followed by an increase to attain an 80% higher level at 1 y compared to the first week post-exposure. No significant results emerged based on the humoral response of the individual parents in the exposed group, despite a general tendency toward higher antibody concentrations in the exposed versus the control groups. No significant difference in humoral immunity was found between the control groups. One year after initial re-exposure to VZV, VZV-immune adults showed a rise in cellular response as assessed by IFN-γ ELISPOT, and steady-state levels for the humoral response. Copyright 2011, Mary Ann Liebert, Inc.
Van Acker H.H.,Laboratory of Experimental Hematology |
Anguille S.,Laboratory of Experimental Hematology |
Van Tendeloo V.F.,Laboratory of Experimental Hematology |
Lion E.,Laboratory of Experimental Hematology
OncoImmunology | Year: 2015
Gamma delta (γδ) T cells are the all-rounders of our immune-system with their major histocompatibility complex-unrestricted cytotoxicity, capacity to secrete immunosti-mulatory cytokines and ability to promote the generation of tumor antigen-specific CD8+ and CD4+ T cell responses. Dendritic cell (DC)-based vaccine therapy has the prospective to harness these unique features of the γδ T cells in the fight against cancer. In this review, we will discuss our current knowledge on DC-mediated γδ T cell activation and related opportunities for tumor immunologists. © 2015 The Author(s). Published with license by Taylor & Francis Group, LLC.