Prednisolone treatment induces tolerogenic dendritic cells and a regulatory milieu in myasthenia gravis patients

Luther, Claudia; Adamopoulou, Eleni; Stoeckle, Christina; Brucklacher-Waldert, Verena; Rosenkranz, Daniela; Stoltze, Lars; Lauer, Sigrid; Poeschel, Simone; Melms, Arthur; Tolosa, Eva (2009). Prednisolone treatment induces tolerogenic dendritic cells and a regulatory milieu in myasthenia gravis patients. Journal of immunology, 183(2), pp. 841-8. Bethesda, Md.: American Association of Immunologists 10.4049/jimmunol.0802046

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FOXP3-expressing naturally occurring CD4(+)CD25(high) T regulatory cells (Treg) are relevant in the control of autoimmunity, and a defect in this cell population has been observed in several human autoimmune diseases. We hypothesized that altered functions of peripheral Treg cells might play a role in the immunopathogenesis of myasthenia gravis, a T cell-dependent autoimmune disease characterized by the presence of pathogenic autoantibodies specific for the nicotinic acetylcholine receptor. We report in this study a significant decrease in the in vitro suppressive function of peripheral Treg cells isolated from myasthenia patients in comparison to those from healthy donors. Interestingly, Treg cells from prednisolone-treated myasthenia gravis patients showed an improved suppressive function compared with untreated patients, suggesting that prednisolone may play a role in the control of the peripheral regulatory network. Indeed, prednisolone treatment prevents LPS-induced maturation of monocyte-derived dendritic cells by hampering the up-regulation of costimulatory molecules and by limiting secretion of IL-12 and IL-23, and enhancing IL-10. In addition, CD4(+) T cells cultured in the presence of such tolerogenic dendritic cells are hyporesponsive and can suppress autologous CD4(+) T cell proliferation. The results shown in this study indicate that prednisolone treatment promotes an environment that favors immune regulation rather than inflammation.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Pharmacology

UniBE Contributor:

Merz, Christina

ISSN:

0022-1767

Publisher:

American Association of Immunologists

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 15:10

Last Modified:

04 May 2014 23:22

Publisher DOI:

10.4049/jimmunol.0802046

PubMed ID:

19542375

Web of Science ID:

000267812600008

URI:

https://boris.unibe.ch/id/eprint/30703 (FactScience: 194979)

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