CiteULike is a free online bibliography manager. Register and you can start organising your references online.

The Effect of Blockade of Tumor Necrosis Factor alpha on VLA-1+T-Cells in Rheumatoid Arthritis Patients. Export

J Clin Immunol (22 September 2007)

Citation Format

[Posts]

View FullText article


shimi002's tags for this article

arthritis vla-1

X Reviews [Write a review of this article]

X Find related articles from these CiteULike users

X Find related articles with these CiteULike tags

X Posting History

X Abstract

The alpha1beta1 integrin, very late antigen (VLA)-1, characterizes collagen adherent interferon (IFN) gamma producing memory T cells in inflamed synovium. We now report that the mean percentage of VLA-1+ T cells is significantly lower among peripheral blood mononuclear cells of rheumatoid patients responsive to antitumor necrosis factor (TNF) alpha therapy than of those with active disease not receiving therapy. Neutralization of TNFalpha during in vitro polyclonal activation of VLA-1- T cells reduced differentiation to expression of VLA-1 and inhibited secretion of IFNgamma, but did not affect integrin expression on in vivo differentiated VLA-1+ T cells. Moreover, synovial fluids of patients relapsing during and after therapy were enriched in VLA-1+ T cells and lines derived from VLA-1+ T cells in peripheral blood of treated patients retained collagen binding and secreted IFN gamma. Thus, whereas therapy decreases VLA-1+ T cells in rheumatoid arthritis patients, a subset is resistant and contributes to residual and recurring inflammation.


X BibTeX record

X RIS record


Privacy Statement | Terms & Conditions
CiteULike organises scholarly (or academic) papers or literature and provides bibliographic (which means it makes bibliographies) for universities and higher education establishments. It helps undergraduates and postgraduates. People studying for PhDs or in postdoctoral (postdoc) positions. The service is similar in scope to EndNote or RefWorks or any other reference manager like BibTeX, but it is a social bookmarking service for scientists and humanities researchers.