A5071465797- Immune Cell Function and Interaction
- Diabetes and associated disorders
- T-cell and B-cell Immunology
- Allergic Rhinitis and Sensitization
- Asthma and respiratory diseases
- Virus-based gene therapy research
- Immune Response and Inflammation
- Dermatology and Skin Diseases
- TGF-β signaling in diseases
- Immunotherapy and Immune Responses
- Neonatal Respiratory Health Research
- Immune cells in cancer
- Diabetes Management and Research
- Animal Virus Infections Studies
- Viral gastroenteritis research and epidemiology
- Cell Adhesion Molecules Research
- Pancreatic function and diabetes
University of Miami
2024
La Jolla Institute for Immunology
2006-2012
Imperial College London
2002-2005
University of Connecticut
2005
Lung Institute
2003
A defining characteristic of persistent viral infections is the loss and functional inactivation antiviral effector T cells, which prevents clearance. Interleukin-10 (IL-10) suppresses cellular immune responses by modulating function cells antigen-presenting cells. In this paper, we report that IL-10 production drastically increased in mice persistently infected with lymphocytic choriomeningitis virus. vivo blockade receptor (IL-10R) a neutralizing antibody resulted rapid resolution...
Transforming growth factor-beta (TGF-beta) can exhibit strong immune suppression but has also been shown to promote T-cell growth. We investigated the differential effect of this cytokine on CD8(+) T-cells in autoimmunity and antiviral immunity.We used mouse models for virally induced type 1 diabetes conjunction with transgenic systems enabling manipulation TGF-beta expression or signaling vivo.Surprisingly, when expressed selectively pancreas, reduced apoptosis differentiated autoreactive...
During an autoimmune process, the autoaggressive response spreads from initiating autoantigen to other antigens expressed in target organ. Based on evidence experimental models for multiple sclerosis, such “antigenic spreading” can play important role exacerbation of clinical disease. We evaluated whether pathogenesis spontaneous diabetes NOD mice could be accelerated a similar way when novel was pancreatic β-cells. Unexpectedly, we found that expression lymphocytic choriomeningitis virus...
Human Fms‐like Tyrosine Kinase3‐L (huFlt3‐L) treatment of prediabetic NOD mice has been shown to increase the intrinsically low numbers myeloid dendritic cells in these mice, while decreasing insulitis and delaying progression diabetes. In this study, we investigated influence huFlt3‐L on diabetes onset LCMV‐induced RIP‐GP (fast onset) or RIP‐NP (slow C57Bl/6 mouse models T1D. We showed that have no intrinsic abnormality DC subset development during LCMV infection. As expected, dramatically...