Journal of Clinical and Cellular Immunology
Open Access
ISSN: 2155-9899
ISSN: 2155-9899
Josef Bodor1,2, Petr Kobylka1, Radek Klubal3, Karola Schaefer4 and Jan van Lunzen4
1Institute of Hematology and Blood Transfusion, Czech Republic 2Johannes Gutenberg University, Germany 3Czech Genetic Bank, Czech Republic 4University Medical Center Hamburg - Eppendorf, Germany
Posters-Accepted Abstracts: J Clin Cell Immunol
The goal of our work is to develop insight and understanding of the effect of deleting the chemokine receptor CCR5 in T cells, and its interplay with immune regulation of human immunodeficiency virus type � 1 (HIV-1), to enable a novel technology platform to cure HIV disease. A critical point is the use hematopoietic stem cell (HSC) transplantation of the cells resistant to HIV such as CCR5��32 cells, which harbor deletion in the CCR5 promoter. Such mutation confer resistance to CCR5-tropic HIV-1 in homozygous individuals and could cure HIV-1 disease based on the outcome of bone marrow engraftment in HIV+ leukemic patients using a CCR5��32 homozygous donor (�Berlin Patient�). However, a shift of HIV tropism to CXCR-4 tropic strains of HIV-1 might be limiting after HSC transplantation with CCR5��32/��32 mutation since it could lead to recurrence of viremia (�Essen patient�). In addition, patients receiving allogeneic bone marrow transplantation often suffer from graft versushost disease (GvHD), and for that reason HIV infection is not considered an indication, unless a hematologic malignancy warrants transplantation. To advance this field, it is, however, vital to search for novel determinants to HIV susceptibility using genome-wide analyses and exploit mechanisms, which play a crucial role in repression of CD4+ T conventional cells (Tcons) by naturally occurring CD4+CD25+ T regulatory cells (nTregs). In order to ameliorate GvHD further understanding of the mechanisms of immunological self tolerance will also provide insights into how strong immune responses such as graft rejection could be restrained and engraftment of HIV resistant cells in HIV+ leukemic patients could be augmented.
Email: bodor@unimainz.de