## Abstract Protease inhibitor (PI) therapy for the treatment of patients infected with human immunodeficiency virus is frequently associated with insulin resistance and diabetic complications. These adverse effects of PI treatment result to a large extent from their inhibition of insulinβstimulate
LPS-induced expression of a novel chemokine receptor (L-CCR) in mouse glial cells in vitro and in vivo
β Scribed by Mike W. Zuurman; Joost Heeroma; Nieske Brouwer; Hendrikus W.G.M. Boddeke; Knut Biber
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 332 KB
- Volume
- 41
- Category
- Article
- ISSN
- 0894-1491
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β¦ Synopsis
Abstract
There is increasing evidence that chemokines, specialized regulators of the peripheral immune system, are also involved in the physiology and pathology of the CNS. It is known that glial cells (astrocytes and microglia) express various chemokine receptors like CCR1, β3, β5, and CXCR4. We have investigated the possible expression of the known CC chemokine receptors (CCR1β8 and D6) in murine glial cells. In addition, we examined possible glial expression of the orphan CC chemokine receptor LβCCR that has been identified previously in murine macrophages. We report here expression of LβCCR mRNA in murine astrocytes and microglia. Furthermore, LβCCR mRNA expression was strongly induced after application of bacterial lipopolysaccharide (LPS), both in vitro and in vivo. Functional studies and binding experiments using biotinylated monocyte chemoattractant protein (MCP)β1 (CCL2) indicate that CCL2 could be a candidate chemokine ligand for glial LβCCR. Based on the data presented, it is suggested that LβCCR is a functional glial chemokine receptor that is important in neuroimmunology. GLIA 41:327β336, 2003. Β© 2003 WileyβLiss, Inc.
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