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STRL33, A novel chemokine receptor-like protein, functions as a fusion cofactor for both macrophage-tropic and T cell line-tropic HIV-1.

Liao F, Alkhatib G, Peden KW, Sharma G, Berger EA, Farber JM - J. Exp. Med. (1997)

Bottom Line: Of greatest interest, STRL33, in contrast with CXCR4 or CCR5, was able to function as a cofactor for fusion mediated by Envs from both T cell line-tropic and macrophage-tropic HIV-1 strains.Despite the sequence similarities between STRL33 and chemokine receptors, STRL33-transfected cell lines did not respond to any in a panel of chemokines.Based on the pattern of tissue expression of the STRL33 mRNA, and given the ability of STRL33 to function with Envs of differing tropisms, STRL33 may play a role in the establishment and/or progression of HIV-1 infection.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.

ABSTRACT
The chemokine receptors CXCR4, CCR2B, CCR3, and CCR5 have recently been shown to serve along with CD4 as coreceptors for HIV-1. The tropisms of HIV-1 strains for subgroups of CD4(+) cells can be explained, at least partly, by the selective use of G protein-coupled receptors (GPCRs). We have identified a novel human gene, STRL33, located on chromosome 3 that encodes a GPCR with sequence similarity to chemokine receptors and to chemokine receptor-like orphan receptors. STRL33 is expressed in lymphoid tissues and activated T cells, and is induced in activated peripheral blood lymphocytes. When transfected into nonhuman NIH 3T3 cells expressing human CD4, the STRL33 cDNA rendered these cells competent to fuse with cells expressing HIV-1 envelope glycoproteins (Envs). Of greatest interest, STRL33, in contrast with CXCR4 or CCR5, was able to function as a cofactor for fusion mediated by Envs from both T cell line-tropic and macrophage-tropic HIV-1 strains. STRL33-transfected Jurkat cell lines also supported enhanced productive infection with HIV-1 compared with control Jurkat cells. Despite the sequence similarities between STRL33 and chemokine receptors, STRL33-transfected cell lines did not respond to any in a panel of chemokines. Based on the pattern of tissue expression of the STRL33 mRNA, and given the ability of STRL33 to function with Envs of differing tropisms, STRL33 may play a role in the establishment and/or progression of HIV-1 infection.

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The expression of STRL33 in human tissues. Blots were prepared by the supplier (Clontech, Palo Alto, CA) from 1.2% agarose–formaldehyde gels containing ∼2 μg poly(A)+ RNA per lane. Hybridizations  were done using a 32P-labeled STRL33 ORF probe and blots were  washed according to the instructions of the manufacturer. The blot prepared from lymphoid tissue (left) was exposed for 2 d, and the blot from  other selected tissues (right) was exposed for 8 d.
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Figure 3: The expression of STRL33 in human tissues. Blots were prepared by the supplier (Clontech, Palo Alto, CA) from 1.2% agarose–formaldehyde gels containing ∼2 μg poly(A)+ RNA per lane. Hybridizations were done using a 32P-labeled STRL33 ORF probe and blots were washed according to the instructions of the manufacturer. The blot prepared from lymphoid tissue (left) was exposed for 2 d, and the blot from other selected tissues (right) was exposed for 8 d.

Mentions: Fig. 3 shows the expression of the STRL33 gene in selected human tissues. There is an mRNA species of ∼2.1 kb prominently expressed in lymphoid tissue; a species of ∼2.5 kb in placenta; low abundance species of 2.1-2.4 kb expressed in pancreas, liver, lung, and heart; and low abundance larger species in a variety of tissues. The conspicuous expression of the STRL33 gene in T cells, activated PBL, and lymphoid tissues is consistent with the presumption that STRL33 is a chemokine receptor.


STRL33, A novel chemokine receptor-like protein, functions as a fusion cofactor for both macrophage-tropic and T cell line-tropic HIV-1.

Liao F, Alkhatib G, Peden KW, Sharma G, Berger EA, Farber JM - J. Exp. Med. (1997)

The expression of STRL33 in human tissues. Blots were prepared by the supplier (Clontech, Palo Alto, CA) from 1.2% agarose–formaldehyde gels containing ∼2 μg poly(A)+ RNA per lane. Hybridizations  were done using a 32P-labeled STRL33 ORF probe and blots were  washed according to the instructions of the manufacturer. The blot prepared from lymphoid tissue (left) was exposed for 2 d, and the blot from  other selected tissues (right) was exposed for 8 d.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196334&req=5

Figure 3: The expression of STRL33 in human tissues. Blots were prepared by the supplier (Clontech, Palo Alto, CA) from 1.2% agarose–formaldehyde gels containing ∼2 μg poly(A)+ RNA per lane. Hybridizations were done using a 32P-labeled STRL33 ORF probe and blots were washed according to the instructions of the manufacturer. The blot prepared from lymphoid tissue (left) was exposed for 2 d, and the blot from other selected tissues (right) was exposed for 8 d.
Mentions: Fig. 3 shows the expression of the STRL33 gene in selected human tissues. There is an mRNA species of ∼2.1 kb prominently expressed in lymphoid tissue; a species of ∼2.5 kb in placenta; low abundance species of 2.1-2.4 kb expressed in pancreas, liver, lung, and heart; and low abundance larger species in a variety of tissues. The conspicuous expression of the STRL33 gene in T cells, activated PBL, and lymphoid tissues is consistent with the presumption that STRL33 is a chemokine receptor.

Bottom Line: Of greatest interest, STRL33, in contrast with CXCR4 or CCR5, was able to function as a cofactor for fusion mediated by Envs from both T cell line-tropic and macrophage-tropic HIV-1 strains.Despite the sequence similarities between STRL33 and chemokine receptors, STRL33-transfected cell lines did not respond to any in a panel of chemokines.Based on the pattern of tissue expression of the STRL33 mRNA, and given the ability of STRL33 to function with Envs of differing tropisms, STRL33 may play a role in the establishment and/or progression of HIV-1 infection.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.

ABSTRACT
The chemokine receptors CXCR4, CCR2B, CCR3, and CCR5 have recently been shown to serve along with CD4 as coreceptors for HIV-1. The tropisms of HIV-1 strains for subgroups of CD4(+) cells can be explained, at least partly, by the selective use of G protein-coupled receptors (GPCRs). We have identified a novel human gene, STRL33, located on chromosome 3 that encodes a GPCR with sequence similarity to chemokine receptors and to chemokine receptor-like orphan receptors. STRL33 is expressed in lymphoid tissues and activated T cells, and is induced in activated peripheral blood lymphocytes. When transfected into nonhuman NIH 3T3 cells expressing human CD4, the STRL33 cDNA rendered these cells competent to fuse with cells expressing HIV-1 envelope glycoproteins (Envs). Of greatest interest, STRL33, in contrast with CXCR4 or CCR5, was able to function as a cofactor for fusion mediated by Envs from both T cell line-tropic and macrophage-tropic HIV-1 strains. STRL33-transfected Jurkat cell lines also supported enhanced productive infection with HIV-1 compared with control Jurkat cells. Despite the sequence similarities between STRL33 and chemokine receptors, STRL33-transfected cell lines did not respond to any in a panel of chemokines. Based on the pattern of tissue expression of the STRL33 mRNA, and given the ability of STRL33 to function with Envs of differing tropisms, STRL33 may play a role in the establishment and/or progression of HIV-1 infection.

Show MeSH
Related in: MedlinePlus