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Two distinct mechanisms underlie progesterone-induced proliferation in the mammary gland
The mouse mammary gland develops postnatally under the control of female reproductive hormones. Estrogens and progesterone trigger morphogenesis by poorly understood mechanisms acting on a subset ofExpand
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CD11b+ Monocytes Abrogate Th17 CD4+ T Cell-Mediated Experimental Autoimmune Myocarditis1
Experimental autoimmune myocarditis (EAM) represents a Th17 T cell-mediated mouse model of postinflammatory heart disease. In BALB/c wild-type mice, EAM is a self-limiting disease, peaking 21 daysExpand
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Interferon-gamma regulates idiopathic pneumonia syndrome, a Th17+CD4+ T-cell-mediated graft-versus-host disease.
RATIONALE Pulmonary complications of hematopoietic stem cell transplantation include infections and graft-versus-host diseases, such as idiopathic pneumonia syndrome (IPS). Conflicting data existExpand
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Heart-Infiltrating Prominin-1+/CD133+ Progenitor Cells Represent the Cellular Source of Transforming Growth Factor &bgr;–Mediated Cardiac Fibrosis in Experimental Autoimmune Myocarditis
Rationale: Myocardial fibrosis is a hallmark of inflammation-triggered end-stage heart disease, a common cause of heart failure in young patients. Objective: We used CD4+ T-cell–mediated experimentalExpand
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Prominin-1/CD133+ lung epithelial progenitors protect from bleomycin-induced pulmonary fibrosis.
RATIONALE The mouse model of bleomycin-induced lung injury offers an approach to study idiopathic pulmonary fibrosis, a progressive interstitial lung disease with poor prognosis. ProgenitorExpand
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Vaccination with Flt3L-induced CD8α+ dendritic cells prevents CD4+ T helper cell-mediated experimental autoimmune myocarditis.
Experimental autoimmune myocarditis (EAM) represents a CD4(+) T helper (Th) cell-mediated mouse model of inflammatory heart disease. Interferon (IFN)-γ, typically produced by Th1 cells, reduces EAMExpand
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Determination of liver specific toxicities in rat hepatocytes by high content imaging during 2-week multiple treatment.
DILI is a major safety issue during drug development and one of the leading causes for market withdrawal. Despite many efforts made in the past, the prediction of DILI using in vitro models remainsExpand
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Profibrotic potential of Prominin-1+ epithelial progenitor cells in pulmonary fibrosis
BackgroundIn idiopathic pulmonary fibrosis loss of alveolar epithelium induces inflammation of the pulmonary tissue followed by accumulation of pathogenic myofibroblasts leading eventually toExpand
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