Donald M. Rodriguez

ORCID: 0000-0002-2534-1480
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About
Contact & Profiles
Research Areas
  • 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,...

10.1172/jci81151 article EN Journal of Clinical Investigation 2015-10-19

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...

10.1126/science.adk3248 article EN Science 2025-02-27

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...

10.1101/379453 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2018-08-02

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...

10.4049/jimmunol.208.supp.169.15 article EN The Journal of Immunology 2022-05-01
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