E
Eva V. Acosta-Rodríguez
Researcher at National University of Cordoba
Publications - 17
Citations - 4356
Eva V. Acosta-Rodríguez is an academic researcher from National University of Cordoba. The author has contributed to research in topics: B cell & Polyclonal B cell response. The author has an hindex of 14, co-authored 17 publications receiving 4119 citations.
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Journal ArticleDOI
Surface phenotype and antigenic specificity of human interleukin 17–producing T helper memory cells
Eva V. Acosta-Rodríguez,Laura Rivino,Jens Geginat,David Jarrossay,Marco Gattorno,Antonio Lanzavecchia,Federica Sallusto,Giorgio Napolitani +7 more
TL;DR: It is demonstrated that human TH-17 cells have distinct migratory capacity and antigenic specificities and a link between microbial products, T helper cell differentiation and homing in response to fungal antigens is established.
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Interleukins 1beta and 6 but not transforming growth factor-beta are essential for the differentiation of interleukin 17-producing human T helper cells.
TL;DR: These results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH- 17 cells in humans and mice.
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Trypanosoma cruzi trans-sialidase initiates a program independent of the transcription factors RORγt and Ahr that leads to IL-17 production by activated B cells.
Daniela A. Bermejo,Shaun W. Jackson,Shaun W. Jackson,Melisa Gorosito-Serrán,Eva V. Acosta-Rodríguez,Maria C. Amezcua-Vesely,Blythe D. Sather,Blythe D. Sather,Akhilesh Kumar Singh,Akhilesh Kumar Singh,Socheath Khim,Socheath Khim,Juan Mucci,Denny Liggitt,Oscar Campetella,Mohamed Oukka,Mohamed Oukka,Adriana Gruppi,David J. Rawlings,David J. Rawlings +19 more
TL;DR: It is found that exposure to parasite-derived trans-sialidase in vitro was sufficient to trigger modification of the cell-surface mucin CD45, which led to signaling dependent on the kinase Btk and production of IL-17F via a transcriptional program independent of the transcription factors RORγt and Ahr.
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Prostaglandin E2 enhances Th17 responses via modulation of IL-17 and IFN-gamma production by memory CD4+ T cells.
TL;DR: It is reported here that prostaglandin E2 (PGE2) can directly modulate cytokine production by human memory CD4+ T cells and suggest a novel mechanism by which inhibitors of prostaglandsin synthesis, such as COX‐2 inhibitors, exert their anti‐inflammatory effect.
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Galectin-3 mediates IL-4-induced survival and differentiation of B cells: functional cross-talk and implications during Trypanosoma cruzi infection.
Eva V. Acosta-Rodríguez,Carolina L. Montes,Claudia Cristina Motran,Elina I. Zuniga,Fu-Tong Liu,Gabriel A. Rabinovich,Adriana Gruppi +6 more
TL;DR: Evidence is provided of a novel role for Gal-3 as an intracellular mediator of B cell survival and a checkpoint in IL-4-induced B cell commitment toward a memory phenotype.