| http://purl.uniprot.org/citations/7492435 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/7492435 | http://www.w3.org/2000/01/rdf-schema#comment | "Stimulation of human immunodeficiency virus type 1 (HIV-1)-infected donor peripheral blood mononuclear cells (PBMCs) via the TCR-CD3 complex induces HIV-1 production in vitro (Zarling JM, et al.: Nature [London] 1990;347:92; Haffar OK, et al.: J Virol 1992;66:4279; Moran PM, et al.: AIDS Res Hum Retroviruses 1993;9:455). However, in addition to the primary stimulatory signal delivered through the TCR-CD3 complex, optimal T cell activation requires secondary or costimulatory signals delivered via various T cell accessory proteins (Alton A, et al.: Adv Immunol 1990;48:227). In this article we explore the role of costimulation of T cells via CD28 in HIV-1 replication. Ligation of CD28 with either a CD28-specific MAb or by coculture of PBMCs with Chinese hamster ovary (CHO) cell lines stably expressing either of the CD28 counterreceptors, B7-1 (CD80) or B7-2 (CD86), concomitant with stimulation via CD3, results in increased virus replication compared to stimulation via CD3 alone. CD28 ligation also augments de novo infection of CD3-stimulated seronegative donor PBMCs with cell-free virus. Increased virus replication following CD28 ligation is not solely attributed to increased levels of endogenous IL-2, because addition of an anti-IL-2-neutralizing antibody only partially inhibits the response. In contrast, interfering with the interaction between CD28 and its counterreceptors on antigen-presenting cells (APCs) using CTLA4Ig effectively inhibits virus replication. At high concentrations CTLA4Ig also reduces cell proliferation. These in vitro results suggest that CD28 plays a central role in HIV-1 replication and that interfering with the CD28 costimulatory pathway may modify the course of HIV-1 infection."xsd:string |
| http://purl.uniprot.org/citations/7492435 | http://purl.org/dc/terms/identifier | "doi:10.1089/aid.1995.11.885"xsd:string |
| http://purl.uniprot.org/citations/7492435 | http://purl.uniprot.org/core/author | "Linsley P.S."xsd:string |
| http://purl.uniprot.org/citations/7492435 | http://purl.uniprot.org/core/author | "Smithgall M.D."xsd:string |
| http://purl.uniprot.org/citations/7492435 | http://purl.uniprot.org/core/author | "Haffar O.K."xsd:string |
| http://purl.uniprot.org/citations/7492435 | http://purl.uniprot.org/core/author | "Wong J.G."xsd:string |
| http://purl.uniprot.org/citations/7492435 | http://purl.uniprot.org/core/date | "1995"xsd:gYear |
| http://purl.uniprot.org/citations/7492435 | http://purl.uniprot.org/core/name | "AIDS Res Hum Retroviruses"xsd:string |
| http://purl.uniprot.org/citations/7492435 | http://purl.uniprot.org/core/pages | "885-892"xsd:string |
| http://purl.uniprot.org/citations/7492435 | http://purl.uniprot.org/core/title | "Costimulation of CD4+ T cells via CD28 modulates human immunodeficiency virus type 1 infection and replication in vitro."xsd:string |
| http://purl.uniprot.org/citations/7492435 | http://purl.uniprot.org/core/volume | "11"xsd:string |
| http://purl.uniprot.org/citations/7492435 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/7492435 |
| http://purl.uniprot.org/citations/7492435 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/7492435 |
| http://purl.uniprot.org/uniprot/P10747#attribution-3E46EBCF0BDB749E00ED63C3935677B2 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/7492435 |