HIV-1 NL4-3, but Not IIIB, Inhibits JAK3/STAT5 Activation in CD4+ T Cells
Copyright policy )HIV-1 NL4-3, but Not IIIB, Inhibits JAK3/STAT5 Activation in CD4+ T Cells
HIV-1 infection leads to T cell dysfunction and apoptosis in vivo and in vitro. The shared common gamma chain of IL-2R and its associated Janus kinase, JAK3, are indispensable for normal T cell function and survival. We have reported that CD4 ligation with HIV gp120 inhibits T cell receptor-induced activation and expression of JAK3. We have also shown that while some strains of HIV-1, such as NL4-3, induce apoptosis of infected CD4(+) T cells, other strains, such as HIV-1 IIIB, do not. Interestingly, we show here that infection of CD4(+) T cells with HIV-1 NL4-3, but not IIIB, inhibited activation and expression of JAK3. NL4-3-infected T cells were unable to upregulate JAK3 expression following stimulation through TCR/CD3. In addition, NL4-3, but not IIIB, inhibited tyrosine phosphorylation and expression of STAT5, a downstream target of JAK3. These data suggest a correlation between apoptosis of HIV-1-infected T cells and inhibition of the JAK3/STAT5 activation pathway.
- University of Pennsylvania United States
- Children's Hospital of Philadelphia United States
- UNIVERSITY OF PENNSYLVANIA
CD4-Positive T-Lymphocytes, CD3 Complex, Receptors, Antigen, T-Cell, Apoptosis, Lymphocyte Activation, AIDS/HIV, Virology, T lymphocyte, STAT5 Transcription Factor, Humans, Phosphorylation, STAT5, Janus Kinase 3, Protein-Tyrosine Kinases, Milk Proteins, NL4-3, DNA-Binding Proteins, Receptor-CD3 Complex, Antigen, T-Cell, IIIB, HIV-1, Trans-Activators, JAK3, signal transduction, Signal Transduction
CD4-Positive T-Lymphocytes, CD3 Complex, Receptors, Antigen, T-Cell, Apoptosis, Lymphocyte Activation, AIDS/HIV, Virology, T lymphocyte, STAT5 Transcription Factor, Humans, Phosphorylation, STAT5, Janus Kinase 3, Protein-Tyrosine Kinases, Milk Proteins, NL4-3, DNA-Binding Proteins, Receptor-CD3 Complex, Antigen, T-Cell, IIIB, HIV-1, Trans-Activators, JAK3, signal transduction, Signal Transduction
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