| http://purl.uniprot.org/citations/9108410 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/9108410 | http://www.w3.org/2000/01/rdf-schema#comment | "CD44 is a widely distributed cell surface glycoprotein whose principal ligand has been identified as hyaluronic acid (HA), a major component of the extracellular matrix (ECM). Recent studies have demonstrated that activation through CD44 leads to induction of effector function in T cells and macrophages. In the current study, we investigated whether HA or monoclonal antibodies (MoAbs) against CD44 would induce a proliferative response in mouse lymphocytes. Spleen cells from normal and nude, but not severe combined immunodeficient mice, exhibited strong proliferative responsiveness to stimulation with soluble HA or anti-CD44 MoAbs. Furthermore, purified B cells, but not T cells, were found to respond to HA. HA was unable to stimulate T cells even in the presence of antigen presenting cells (APC) and was unable to act as a costimulus in the presence of mitogenic or submitogenic concentrations of anti-CD3 MoAbs. In contrast, stimulation of B cells with HA in vitro, led to B-cell differentiation as measured by production of IgM antibodies in addition to increased expression of CD44 and decreased levels of CD45R. The fact that the B cells were responding directly to HA through its binding to CD44 and not to any contaminants or endotoxins was demonstrated by the fact that F(ab)2 fragments of anti-CD44 MoAbs or soluble CD44 fusion proteins could significantly inhibit the HA-induced proliferation of B cells. Also, HA-induced proliferation of B cells was not affected by the addition of polymixin B, and B cells from lipopolysaccharide (LPS)-unresponsive C3H/HeJ strain responded strongly to stimulation with HA. Furthermore, HA, but not chondroitin-sulfate, another major component of the ECM, induced B-cell activation. It was also noted that injection of HA intraperitoneally, triggered splenic B cell proliferation in vivo. Together, the current study demonstrates that interaction between HA and CD44 can regulate murine B-cell effector functions and that such interactions may play a critical role during normal or autoimmune responsiveness of B cells."xsd:string |
| http://purl.uniprot.org/citations/9108410 | http://purl.uniprot.org/core/author | "Nagarkatti M."xsd:string |
| http://purl.uniprot.org/citations/9108410 | http://purl.uniprot.org/core/author | "Nagarkatti P.S."xsd:string |
| http://purl.uniprot.org/citations/9108410 | http://purl.uniprot.org/core/author | "Rafi A."xsd:string |
| http://purl.uniprot.org/citations/9108410 | http://purl.uniprot.org/core/date | "1997"xsd:gYear |
| http://purl.uniprot.org/citations/9108410 | http://purl.uniprot.org/core/name | "Blood"xsd:string |
| http://purl.uniprot.org/citations/9108410 | http://purl.uniprot.org/core/pages | "2901-2908"xsd:string |
| http://purl.uniprot.org/citations/9108410 | http://purl.uniprot.org/core/title | "Hyaluronate-CD44 interactions can induce murine B-cell activation."xsd:string |
| http://purl.uniprot.org/citations/9108410 | http://purl.uniprot.org/core/volume | "89"xsd:string |
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