The primate lentiviral receptor Bonzo/STRL33 is coordinately regulated with CCR5 and its expression pattern is conserved between human and mouse

Citation
D. Unutmaz et al., The primate lentiviral receptor Bonzo/STRL33 is coordinately regulated with CCR5 and its expression pattern is conserved between human and mouse, J IMMUNOL, 165(6), 2000, pp. 3284-3292
Citations number
57
Categorie Soggetti
Immunology
Journal title
JOURNAL OF IMMUNOLOGY
ISSN journal
00221767 → ACNP
Volume
165
Issue
6
Year of publication
2000
Pages
3284 - 3292
Database
ISI
SICI code
0022-1767(20000915)165:6<3284:TPLRBI>2.0.ZU;2-S
Abstract
Chemokines play necessary and important roles in regulating the trafficking of lymphocytes to intra- or interlymphoid tissues as well as to sites of i nflammation. The complex migratory patterns of lymphoid lineage cells is go verned by subset-specific expression of chemokine receptors and their acces s to specific ligands, Several chemokine receptors and chemokine receptor-l ike orphan receptors also serve, in conjunction with CD4, as coreceptors fo r infection by human and simian immunodeficiency viruses (HIV and SIV), Her e we show that the expression pattern of Bonzo/STRL33, an orphan SIV/HIV co receptor, is highly restricted to the memory subset of T tells and is up-re gulated upon stimulation of these cells with IL-2 or IL-15, Both the patter n and the regulation of Bonzo expression closely paralleled that of CC fami ly chemokine receptors CCR5 or CCR6 and inversely correlated with CXCR4 exp ression. However, in striking contrast to CCR5, Bonzo expression was not do wn-modulated by PMA or mitogen stimulation of T cells, Targeted replacement of the Bonzo gene with a gene encoding green fluorescent protein in mice r evealed that the expression and cytokine regulation of mouse Bonzo are comp arable to those of its human counterpart. The similar expression and regula tion patterns of Bonzo and the HIV coreceptor CCR5 may have implications fo r understanding the role of HIV/SIV receptors in viral evolution and pathog enesis.