M
Martin Pelletier
Researcher at Laval University
Publications - 68
Citations - 4409
Martin Pelletier is an academic researcher from Laval University. The author has contributed to research in topics: Cytokine & Proinflammatory cytokine. The author has an hindex of 28, co-authored 64 publications receiving 3469 citations. Previous affiliations of Martin Pelletier include University of Verona & Institut national de la recherche scientifique.
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Journal ArticleDOI
In Vivo and In Vitro Roles of IL-21 in Inflammation
TL;DR: IL-21 is found to be a proinflammatory cytokine, but not a neutrophil agonist, and it is proposed that IL-21 attracts neutrophils indirectly in vivo via a mechanism independent of IL-6,CCL3, CCL5, and CXCL2 production.
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Human neutrophils interact with both 6-sulfo LacNAc+ DC and NK cells to amplify NK-derived IFNγ: role of CD18, ICAM-1, and ICAM-3
Claudio Costantini,Federica Calzetti,Omar Perbellini,Alessandra Micheletti,Claudia Scarponi,Silvia Lonardi,Martin Pelletier,Knut Schäkel,Giovanni Pizzolo,Fabio Facchetti,William Vermi,Cristina Albanesi,Marco A. Cassatella +12 more
TL;DR: Colocalization of neutrophils, NK cells, and slanDCs, as well as of IL-12p70 and IFNγ, in inflamed tissues of Crohn disease and psoriasis provides strong evidence for a novel cellular and cytokine cooperation within the innate immune system in which neutrophil act as amplifiers of NK cell/slanDC-mediated responses.
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Mechanisms involved in interleukin-15-induced suppression of human neutrophil apoptosis: role of the anti-apoptotic Mcl-1 protein and several kinases including Janus kinase-2, p38 mitogen-activated protein kinase and extracellular signal-regulated kinases-1/2
TL;DR: It is concluded that IL‐15 delays neutrophil apoptosis via several pathways, and that Mcl‐1 and several kinases contribute to this.
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The TNF-Family Ligand TL1A and Its Receptor DR3 Promote T Cell–Mediated Allergic Immunopathology by Enhancing Differentiation and Pathogenicity of IL-9–Producing T Cells
Arianne C. Richard,Cuiyan Tan,Eric T. Hawley,Julio Gomez-Rodriguez,Ritobrata Goswami,Xiang-Ping Yang,Anthony C. Cruz,Pallavi Penumetcha,Erika T. Hayes,Martin Pelletier,Odile Gabay,Matthew C. Walsh,John R. Ferdinand,Andrea Keane-Myers,Yongwon Choi,John J. O'Shea,Aymen Al-Shamkhani,Mark H. Kaplan,Igal Gery,Richard M. Siegel,Françoise Meylan +20 more
TL;DR: It is found that TL1A potently promotes generation of murine T cells producing IL-9 (Th9) by signaling through DR3 in a cell-intrinsic manner, and this data identifyTL1A–DR3 interactions as a novel pathway that promotes Th9 differentiation and pathogenicity.
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Mechanisms Involved in Spontaneous and Viscum album Agglutinin-I-Induced Human Neutrophil Apoptosis: Viscum album Agglutinin-I Accelerates the Loss of Antiapoptotic Mcl-1 Expression and the Degradation of Cytoskeletal Paxillin and Vimentin Proteins Via Caspases
TL;DR: It is concluded that VAA-I needs to be internalized to mediate apoptosis and that its activity is not dependent on a cell surface receptor-mediated pathway.