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Marcel B. M. Teunissen

Researcher at University of Amsterdam

Publications -  90
Citations -  5590

Marcel B. M. Teunissen is an academic researcher from University of Amsterdam. The author has contributed to research in topics: Psoriasis & T cell. The author has an hindex of 36, co-authored 88 publications receiving 5129 citations. Previous affiliations of Marcel B. M. Teunissen include Royal Tropical Institute.

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Interleukin-17 and interferon-gamma synergize in the enhancement of proinflammatory cytokine production by human keratinocytes.

TL;DR: It is indicated that IL-17 is a proinflammatory cytokine, which could amplify the development of cutaneous inflammation and may support the maintenance of chronic dermatoses, through stimulation of keratinocytes to augment their secretion of pro inflammatory cytokines.
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In Vitro and In Situ Expression of IL-23 by Keratinocytes in Healthy Skin and Psoriasis Lesions: Enhanced Expression in Psoriatic Skin

TL;DR: In this paper, the authors investigated whether human keratinocytes can express IL-23, a newly defined IFN-gamma-inducing cytokine composed of a unique p19 subunit and a p40 subunit shared with IL-12.
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Overrepresentation of IL-17A and IL-22 Producing CD8 T Cells in Lesional Skin Suggests Their Involvement in the Pathogenesis of Psoriasis

TL;DR: The increased presence of Tc17 and Tc22 cells in lesional psoriatic skin suggests that these types of CD8 T cells play a significant role in the pathogenesis of psoriasis and demonstrates plasticity in their cytokine production profile.
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Composition of innate lymphoid cell subsets in the human skin: enrichment of NCR(+) ILC3 in lesional skin and blood of psoriasis patients.

TL;DR: Significant increased proportions of NCR(+) ILC3 were present in lesional skin and peripheral blood of psoriasis patients as compared with skin and blood of healthy individuals, respectively, whereas the proportions of ILC2 and CD161(+ ILC1 remained unchanged.
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Psoriasis: dysregulation of innate immunity.

TL;DR: The current understanding of the function of natural killer T cells in innate immunity and their potential to control acquired specific immunity, as well as the remarkable efficacy of antitumour necrosis factor‐α biological treatments in psoriasis, forces the current T‐cell hypothesis of Psoriasis pathogenesis to refine.