Abstract
The current study was aimed at investigating the effect of HIV-1 protein Tat on the retinal neurosensory cell line R28. Exposure of Tat resulted in induction of pro-inflammatory mediators such as CXCL10 and TNF-α in addition to the activation marker GFAP in these cells. Conditioned media from Tat-treated R28 cells was able to induce monocyte migration, an effect that was blocked by CXCR3 antagonist. Complementary studies in the HIV-1 Tat-transgenic mice, showed a complete absence of the nuclear layer and the outer photoreceptor segments of the retina with a concomitant increase in glial activation. These findings lend support to the observation in post-HAART era of increased incidence of immune response-mediated retinal degeneration. These findings have direct relevance to diseases such as immune response uveitis and patients recovering from CMV retinitis.
| Original language | English |
|---|---|
| Pages (from-to) | 399-408 |
| Number of pages | 10 |
| Journal | Journal of Neuroimmune Pharmacology |
| Volume | 6 |
| Issue number | 3 |
| DOIs | |
| State | Published - Sep 2011 |
Keywords
- Chemokine
- HIV
- Retina
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