F. Tacchini-Cottier

Discipline

Sociology (2) History, Philosophy and Sociology of Sciences (1)

Type

Articles (28) Reviews (4)

Co-author

Date

Source

Keyword

Leishmania (24) infection (23) Infection (23) Cells (22) parasite (18) Mice (17) Expression (16) disease (12) Development (12) Immune response (12) disease (12) show (11) Neutrophils (11) Control (10) Parasites (10) Leishmaniasis (10) Parasites (10) skin (8) Skin (8) Leishmaniasis, Cutaneous (8) Impact (8) Blood (8) Animals (8) Addition (8) Susceptibility (8) T cells (7) Secretion (6) Pathogenic microorganisms (6) Secretion (6) Pathogens (6)

Documents written by F. Tacchini-Cottier (28) | is about F. Tacchini-Cottier (0)

The c-MET receptor tyrosine kinase contributes to neutrophil-driven pathology in cutaneous leishmaniasis.
K. Passelli et al.
The Impact of Neutrophil Recruitment to the Skin on the Pathology Induced by Leishmania Infection.
K. Passelli et al. (2021)
Neutrophil Activation: Influence of Antimony Tolerant and Susceptible Clinical Strains of L. (V.) panamensis and Meglumine Antimoniate.
O.L. Fernández et al. (2021)
Evaluation of a New Topical Treatment for the Control of Cutaneous Leishmaniasis.
B. Martínez-Salazar et al. (Nov 17, 2020)
Deletion of Interleukin-4 Receptor Alpha-Responsive Keratinocytes in BALB/c Mice Does Not Alter Susceptibility to Cutaneous Leishmaniasis.
M. Govender et al.
Resistance of Leishmania (Viannia) Panamensis to Meglumine Antimoniate or Miltefosine Modulates Neutrophil Effector Functions.
I.B. Regli et al. (2018)
Neutrophils enhance early Trypanosoma brucei infection onset.
G. Caljon et al. (2018)
Survival Mechanisms Used by Some Leishmania Species to Escape Neutrophil Killing
I.B. Regli et al. (Nov 16, 2017)
IL-4Rα Signaling in Keratinocytes and Early IL-4 Production Are Dispensable for Generating a Curative T Helper 1 Response in Leishmania major-Infected C57BL/6 Mice.
M. Descatoire et al. (2017)
Notch regulates Th17 differentiation and controls trafficking of IL-17 and metabolic regulators within Th17 cells in a context-dependent manner.
M. Coutaz et al. (Dec 15, 2016)
Rapid Sequestration of Leishmania mexicana by Neutrophils Contributes to the Development of Chronic Lesion.
B.P. Hurrell et al. (2015)
Exposure to Leishmania braziliensis triggers neutrophil activation and apoptosis.
S.A. Falcão et al. (2015)
Blocking Junctional Adhesion Molecule C Enhances Dendritic Cell Migration and Boosts the Immune Responses against Leishmania major.
R. Ballet et al. (2014)
Specific fibroblastic niches in secondary lymphoid organs orchestrate distinct Notch-regulated immune responses.
N. Fasnacht et al. (2014)
Repeated exposure to Lutzomyia intermedia sand fly saliva induces local expression of interferon-inducible genes both at the site of injection in mice and in human blood.
T. Weinkopff et al. (2014)
A scoring method to standardize lesion monitoring following intra-dermal infection of Leishmania parasites in the murine ear
S. Schuster et al. (2014)
TREM-1 deficiency can attenuate disease severity without affecting pathogen clearance.
B. Weber et al. (2014)
Arginase activity in the blood of patients with visceral leishmaniasis and HIV infection.
Y. Takele et al. (2013)
Arginase activity - a marker of disease status in patients with visceral leishmaniasis in ethiopia.
T. Abebe et al. (2013)
Redundant Notch1 and Notch2 signaling is necessary for IFNγ secretion by T helper 1 cells during infection with Leishmania major.
F. Auderset et al. (2012)
Local increase of arginase activity in lesions of patients with cutaneous leishmaniasis in ethiopia.
T. Abebe et al. (2012)
Does T Helper Differentiation Correlate with Resistance or Susceptibility to Infection with L. major? Some Insights From the Murine Model.
F. Tacchini-Cottier et al. (2012)
Regulatory B cells shape the development of Th2 immune responses in BALB/c mice infected with Leishmania major through IL-10 production.
C. Ronet et al. (2010)
The prominent role of neutrophils during the initial phase of infection by Leishmania parasites.
M. Charmoy et al. (2010)
In leishmaniasis due to Leishmania guyanensis infection, distinct intralesional interleukin-10 and Foxp3 mRNA expression are associated with unresponsiveness to treatment.
E. Bourreau et al. (2009)

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