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Cheryl M. Sweeney

Researcher at University College Dublin

Publications -  25
Citations -  3323

Cheryl M. Sweeney is an academic researcher from University College Dublin. The author has contributed to research in topics: Psoriasis & Hidradenitis suppurativa. The author has an hindex of 16, co-authored 24 publications receiving 2859 citations. Previous affiliations of Cheryl M. Sweeney include Trinity College, Dublin.

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Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity.

TL;DR: It is shown that gammadelta T cells express IL-23R and the transcription factor RORgammat and produce IL-17, IL-21, and IL-22 in response to IL-1beta andIL-23, without T cell receptor engagement.
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T cells in multiple sclerosis and experimental autoimmune encephalomyelitis

TL;DR: The contribution of Th1, Th17, γδ, CD8+ and regulatory T cells as well as the possible development of new therapeutic approaches for MS based on manipulating these T cell subtypes are reviewed.
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Dysregulated cytokine expression in lesional and nonlesional skin in hidradenitis suppurativa.

TL;DR: There is a dearth of information on the precise pathogenesis of hidradenitis suppurativa, but immune dysregulation is implicated and its role in infectious disease is implicated.
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Attenuating Regulatory T Cell Induction by TLR Agonists through Inhibition of p38 MAPK Signaling in Dendritic Cells Enhances Their Efficacy as Vaccine Adjuvants and Cancer Immunotherapeutics

TL;DR: It is demonstrated that the adjuvant activity of TLR agonists is compromised by coinduction of Treg cells, but this can be overcome by inhibiting p38 signaling in DC, and p38 is an important therapeutic target.
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IL-27 mediates the response to IFN-β therapy in multiple sclerosis patients by inhibiting Th17 cells.

TL;DR: The findings suggest that IFN-β mediates its therapeutic effects in MS at at least in part via the induction of IL-27, and that IL- 27 may represent an alternative therapy for MS patients that do not respond to IFn-β.