Karlhans F. Che
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Karlhans F. Che has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
Davorka Messmer
University of California at San Diego, Moores Cancer Center La Jolla, CA, USA
1 shared publication- Esaki Muthu Shankar
Infection and Inflammation, Department of Biotechnology, Central University of Tamil Nadu, Thiruvarur, India
1 shared publication Jeffrey D. Lifson
AIDS and Cancer Virus Program, SAIC Frederick Inc., National Cancer Institute at Frederick Maryland, MD, USA
1 shared publication- Marie Larsson
Molecular Medicine and Virology, Department of Biomedical and Clinical Sciences, Linköping University
1 shared publication Nina Bhardwaj
New York University School of Medicine New York, NY, USA
1 shared publicationRachel L. Sabado
New York University School of Medicine New York, NY, USA
1 shared publication
Latest Publications
- Open Access
- 29 July 2010
- Published by Wiley in European Journal of Immunology
- Vol. 40 (8) , 2248-2258
HIV‐1 impairs in vitro priming of naïve T cells and gives rise to contact‐dependent suppressor T cells
Priming of T cells in lymphoid tissues of HIV‐infected individuals occurs in the presence of HIV‐1. DC in this milieu activate T cells and disseminate HIV‐1 to newly activated T cells, the outcome of which may have serious implications in the development of optimal antiviral responses. We investigated the effects of HIV‐1 on DC–naïve T‐cell interactions using an allogeneic in vitro system. Our data demonstrate a dramatic decrease in the primary expansion of naïve T cells when cultured with HIV‐1‐exposed DC. CD4+ and CD8+ T cells showed enhanced expression of PD‐1 and TRAIL, whereas CTLA‐4 expression was observed on CD4+ T cells. It is worth noting that T cells primed in the presence of HIV‐1 suppressed priming of other naïve T cells in a contact‐dependent manner. We identified PD‐1, CTLA‐4, and TRAIL pathways as responsible for this suppresion, as blocking these negative molecules restored T‐cell proliferation to a higher degree. In conclusion, the presence of HIV‐1 during DC priming produced cells with inhibitory effects on T‐cell activation and proliferation, i.e. suppressor T cells, a mechanism that could contribute to the enhancement of HIV‐1 pathogenesis.
- 29 July 2010
- Published by Wiley in European Journal of Immunology
- Vol. 40 (8) , 2248-2258
Open AccessHIV‐1 impairs in vitro priming of naïve T cells and gives rise to contact‐dependent suppressor T cells
Priming of T cells in lymphoid tissues of HIV‐infected individuals occurs in the presence of HIV‐1. DC in this milieu activate T cells and disseminate HIV‐1 to newly activated T cells, the outcome of which may have serious implications in the development of optimal antiviral responses. We investigated the effects of HIV‐1 on DC–naïve T‐cell interactions using an allogeneic in vitro system. Our data demonstrate a dramatic decrease in the primary expansion of naïve T cells when cultured with HIV‐1‐exposed DC. CD4+ and CD8+ T cells showed enhanced expression of PD‐1 and TRAIL, whereas CTLA‐4 expression was observed on CD4+ T cells. It is worth noting that T cells primed in the presence of HIV‐1 suppressed priming of other naïve T cells in a contact‐dependent manner. We identified PD‐1, CTLA‐4, and TRAIL pathways as responsible for this suppresion, as blocking these negative molecules restored T‐cell proliferation to a higher degree. In conclusion, the presence of HIV‐1 during DC priming produced cells with inhibitory effects on T‐cell activation and proliferation, i.e. suppressor T cells, a mechanism that could contribute to the enhancement of HIV‐1 pathogenesis.