T lymphocytes in patients with primary vasculitis: expansion of CD8 + T cells with the propensity to activate polymorphonuclear neutrophils. Rheumatology (Oxford, England) [Rheumatology (Oxford)] Journal article | | Title | T lymphocytes in patients with primary vasculitis: expansion of CD8 + T cells with the propensity to activate polymorphonuclear neutrophils. | | Author(s) | Iking-Konert C, Vogl T, Prior B, Wagner C, Sander O, Bleck E, Ostendorf B, Schneider M, Andrassy K, Hänsch GM | | Institution | Rheumatology, Department of Endocrinology, Diabetology and Rheumatology, Heinrich-Heine-University of Duesseldorf, Institute for Immunology, Ruprecht-Karls University of Heidelberg, Klinik für Unfallchirurgie und Orthopädie, Berufsgenossenschaftliche Unfallklinik Ludwigshafen and Medizinische Klinik, Ruprecht-Karls University of Heidelberg, Germany. | | Source | Rheumatology (Oxford) 2008 Mar 17. | | Abstract | Objectives. To gain insight into the immune pathogenesis of primary ANCA-associated vasculitides, the prevalence of circulating T lymphocytes expressing CD11b as a marker for activation was analysed in patients with WG or microscopic polyangiitis. Methods. Receptor expression and IFNgamma synthesis were measured in T cells of patients with active disease by cytofluorometry and compared with expression in patients in remission and in healthy donors.
Results. During active disease, a small but conspicuous population of CD8+CD28+CD11b+ was found which produced IFNgamma. In healthy donors and in patients in remission or undergoing immunosuppressive therapy, CD11b was exclusively associated with CD8+CD28- cells, the latter being more frequent in patients with long-lasting or severe disease. In vitro experiments confirmed that CD11b is up-regulated when T cells are activated. After multiple rounds of restimulation, the CD11b expression persists whereas CD28 expression is lost, compatible with the notion that CD8+CD28+CD11b+ represents a transient phenotype in the course of T-cell activation. The IFNgamma-producing T cells activated polymorphonuclear neutrophils (PMN) to express MHC class II, thus generating the same PMN phenotype as in patients with active ANCA-associated vasculitis. A similar PMN phenotype could be generated by cultivation with supernatants of activated T cells or by IFNgamma alone, but not by antibodies to proteinase 3.
Conclusions. In active primary vasculitis, a small population of CD8+ T cells, identified by the expression of CD11b, expands, producing IFNgamma. These T cells could activate PMN, thus generating a long-living and potentially destructive PMN phenotype. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 18346977 |
|
|
| |
Advertise on this site.
| | |
|
