- T-cell and B-cell Immunology
- Immune Cell Function and Interaction
- Immunotherapy and Immune Responses
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Racial and Ethnic Identity Research
- Otitis Media and Relapsing Polychondritis
- Cell Adhesion Molecules Research
- CAR-T cell therapy research
- Innovations in Medical Education
- Galectins and Cancer Biology
- Latin American and Latino Studies
- Primary Care and Health Outcomes
- Peptidase Inhibition and Analysis
- IL-33, ST2, and ILC Pathways
- Vascular Anomalies and Treatments
- Diversity and Career in Medicine
University of Chicago
2022-2025
Yale University
2015-2019
Virginia Mason Medical Center
2013
FOXP3+ Tregs are central for the maintenance of self-tolerance and can be defective in autoimmunity. In multiple sclerosis type-1 diabetes, dysfunctional is partially mediated by a population IFNγ-secreting Tregs. It was previously reported that increased NaCl concentrations promote induction proinflammatory Th17 cells high-salt diets exacerbate experimental models Here, we have shown increasing NaCl, either vitro or murine via diet, markedly impairs Treg function. IFNγ secretion Tregs,...
During infections, CD4 + Foxp3 regulatory T (Treg) cells must control autoreactive conventional (Tconv) cell responses against self-peptide antigens while permitting those pathogen-derived “nonself” peptides. We defined the basis of this selectivity using mice in which Treg reactive to a single prostate-specific were selectively depleted. found that self-peptide-specific dispensable for Tconv matched specificity at homeostasis. However, they required such and prevent autoimmunity toward...
Abstract Foxp3 + regulatory T cells (Tregs) are the central component of peripheral immune tolerance. While dysregulation Treg cytokine signature has been observed in autoimmune diseases such as multiple sclerosis (MS) and type 1 diabetes, mechanisms balancing pro- anti-inflammatory production not known. Here, we identify imbalance between IFNγ IL-10 a shared signature, present patients with MS under high salt conditions. By performing RNA-seq analysis on human subpopulations, β-catenin key...
Abstract In both humans and mice, self-reactive CD4+ T cells are implicated in a range of autoinflammatory processes. To promote disease, such must evade clonal deletion the thymus, as well intrinsic extrinsic regulation mechanisms periphery, including anergy regulatory cell-mediated suppression. However, impact cell receptor (TCR) - peptide/MHC class II (pMHCII) binding properties on autoimmune potential self-specific their susceptibility to immune remains incompletely defined. Much...