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Kamran Ghoreschi

Researcher at Charité

Publications -  193
Citations -  11082

Kamran Ghoreschi is an academic researcher from Charité. The author has contributed to research in topics: Medicine & Psoriasis. The author has an hindex of 41, co-authored 144 publications receiving 8966 citations. Previous affiliations of Kamran Ghoreschi include Ludwig Maximilian University of Munich & University Hospital Heidelberg.

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Journal ArticleDOI

Generation of pathogenic T H 17 cells in the absence of TGF-β signalling

Kamran Ghoreschi, +20 more
- 21 Oct 2010 - 
TL;DR: In this article, the authors show that T(H)17 differentiation can occur in the absence of TGF-β signalling, without the need of transforming growth factor (TGF)-β1.
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Janus kinases in immune cell signaling.

Kamran Ghoreschi, +2 more
- 01 Mar 2009 - 
TL;DR: existing knowledge on Jak signaling pathways and fundamental work on their biochemical structure and intracellular interactions allow us to develop new strategies for controlling autoimmune diseases or malignancies by developing selective Jak inhibitors, which are now coming into clinical use.
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Guidelines for the use of flow cytometry and cell sorting in immunological studies (second edition)

Andrea Cossarizza, +462 more
- 01 Oct 2019 - 
TL;DR: These guidelines are a consensus work of a considerable number of members of the immunology and flow cytometry community providing the theory and key practical aspects offlow cytometry enabling immunologists to avoid the common errors that often undermine immunological data.
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Opposing regulation of the locus encoding IL-17 through direct, reciprocal actions of STAT3 and STAT5.

Xiang-Ping Yang, +12 more
- 01 Mar 2011 - 
TL;DR: Deletion of the gene encoding the transcription factor STAT3 in T cells abrogated IL-17 production and attenuated autoimmunity associated with IL-2 deficiency and 'Titration' of the relative activation of STAT3 and STAT5 modulated the specification of cells to the IL- 17-producing helper T cell (TH17 cell) subset.
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Modulation of Innate and Adaptive Immune Responses by Tofacitinib (CP-690,550)

Kamran Ghoreschi, +19 more
- 01 Apr 2011 - 
TL;DR: In a model of established arthritis, CP-690,550 rapidly improved disease by inhibiting the production of inflammatory mediators and suppressing STAT1-dependent genes in joint tissue through a mechanism likely involving the inhibition of STAT1 signaling.