Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |
lüll Identification of a potential HIV-induced source of bystander-mediated apoptosis in T cells: upregulation of trail in primary human macrophages by HIV-1 tat Zhang M; Li X; Pang X; Ding L; Wood O; Clouse K; Hewlett I; Dayton AIJ Biomed Sci 2001[May]; 8 (3): 290-6The induction of apoptosis in T cells by bystander cells has been repeatedly implicated as a mechanism contributing to the T cell depletion seen in HIV infection. It has been shown that apoptosis could be induced in T cells from asymptomatic HIV-infected individuals in a Fas-independent, TNF-related apoptosis-inducing ligand (TRAIL)-dependent manner if the cells were pretreated with anti-CD3. It has also been shown that T cells from HIV-infected patients were even more sensitive to TRAIL induction of apoptosis than they were to Fas induction. Recently, it has been reported that in an HIV-1 SCID-Hu model, the vast majority of the T cell apoptosis is not associated with p24 and is therefore produced by bystander effects. Furthermore, few apoptotic cells were associated with neighboring cells which were positive for either Fas ligand or TNF. However, most of the apoptotic cells were associated with TRAIL-positive cells. The nature of these TRAIL-positive cells was undetermined. Here, we report that HIV infection of primary human macrophages switches on abundant TRAIL production both at the RNA and protein levels. Furthermore, more macrophages produce TRAIL than are infected by HIV, indicating that a bystander mechanism may, at least in part, upregulate TRAIL. Exogenously supplied HIV-1 Tat protein upregulates TRAIL production by primary human macrophages to an extent indistinguishable from infection. The results suggest a model in which HIV-1-infected cells produce extracellular Tat protein, which in turn upregulates TRAIL in macrophages which then can induce apoptosis in bystander T cells.|*Apoptosis/drug effects[MESH]|*Up-Regulation/drug effects[MESH]|Apoptosis Regulatory Proteins[MESH]|Cells, Cultured[MESH]|Flow Cytometry[MESH]|Gene Products, tat/*metabolism/pharmacology[MESH]|HIV-1/*physiology[MESH]|Humans[MESH]|Macrophages/drug effects/*metabolism/virology[MESH]|Membrane Glycoproteins/biosynthesis/genetics/*metabolism[MESH]|RNA, Messenger/genetics/metabolism[MESH]|T-Lymphocytes/*cytology/drug effects[MESH]|TNF-Related Apoptosis-Inducing Ligand[MESH]|Tumor Necrosis Factor-alpha/biosynthesis/genetics/*metabolism[MESH]|tat Gene Products, Human Immunodeficiency Virus[MESH] |