UCL logo

UCL Discovery

UCL home » Library Services » Electronic resources » UCL Discovery

Integrin signalling defects in T-lymphocytes in systemic lupus erythematosus

Ng, TTC; Collins, IE; Kanner, SB; Humphries, MJ; Amft, N; Wickremasinghe, RG; D'Cruz, D; ... Morrow, WJW; + view all (1999) Integrin signalling defects in T-lymphocytes in systemic lupus erythematosus. LUPUS , 8 (1) 39 - 51.

Full text not available from this repository.

Abstract

Objective: To establish the relationship between T cell responses to integrin coreceptor stimulation and B cell hyperreactivity as measured by pathologic autoantibody production.Methods: Peripheral blood mononuclear cells from 42 patients with SLE according to the American Rheumatism Association criteria were examined for their ability to adhere to plate-immobilised fibronectin. Go-stimulation assays were performed on the same cells using anti-CD3 antibody alone or co-immobilised with an anti-beta(1)-integrin antibody. Proliferative responses were measured by (3)[H]thymidine pulsing on day 3 and activation was determined using a commercial protein kinase C assay, the protocol being established by our group in association with Promega. beta(1)-Integrin expression was established by FAGS analysis.Results: An impaired PKC response to integrin-mediated activation was found in T-lymphocytes from 6/21 (29%) SLE patients, which correlated significantly with an absence of anti-dsDNA antibody in patient sera, irrespective of prednisolone treatment. Integrin co-stimulation of TcR/CD3-induced proliferation and T cell adhesion to fibronectin were also impaired among 5/21 (24%) and 6/15 (40%) patients studied, respectively.Conclusion: We hypothesise that the integrity of beta(1)-integrin signalling pathways may influence pathological antibody production in SLE by affecting T-lymphocyte activation and interactions between T- and B-lymphocytes.

Type: Article
Title: Integrin signalling defects in T-lymphocytes in systemic lupus erythematosus
Keywords: fibronectin, integrin, protein kinase C, signalling, SLE, T cell co-stimulation, PROTEIN-KINASE-C, CELL-ADHESION MOLECULE-1, NEUTROPHIL CHEMOTACTIC FACTOR, MURINE LUPUS, GENE-EXPRESSION, TYROSINE PHOSPHORYLATION, EXTRACELLULAR-MATRIX, ENDOTHELIAL-CELLS, PERMISSIVE ACTIVATION, LPR/LPR MICE
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute > Research Department of Haematology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute > Research Department of Oncology
URI: http://discovery.ucl.ac.uk/id/eprint/121874
Downloads since deposit
0Downloads
Download activity - last month
Download activity - last 12 months
Downloads by country - last 12 months

Archive Staff Only

View Item View Item