Aidan T. Miller

ORCID: 0000-0002-4931-9747
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Immune Response and Inflammation
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • CAR-T cell therapy research
  • Neurological Disorders and Treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • IL-33, ST2, and ILC Pathways
  • Clostridium difficile and Clostridium perfringens research
  • Alzheimer's disease research and treatments
  • Amoebic Infections and Treatments
  • Parkinson's Disease Mechanisms and Treatments
  • Parasitic Infections and Diagnostics

University of Alabama at Birmingham
2023-2024

Washington University in St. Louis
2019-2022

Both higher- and lower-affinity self-reactive CD4+ T cells are expanded in autoimmunity; however, their individual contribution to disease remains unclear. We addressed this question using peptide-MHCII chimeric antigen receptor (pMHCII-CAR) specifically deplete peptide-reactive mice. Integration of improvements CAR engineering with TCR repertoire analysis was critical for interrogating vivo the role affinity autoimmunity. Our original MOG35-55 pMHCII-CAR, which targeted only higher-affinity...

10.1126/sciimmunol.abo0777 article EN Science Immunology 2022-10-07

The success of B cell depletion therapies and identification leptomeningeal ectopic lymphoid tissue (ELT) in patients with multiple sclerosis (MS) has renewed interest the antibody-independent pathogenic functions cells during neuroinflammation. timing location antigen presentation MS its animal model experimental autoimmune encephalomyelitis (EAE) remain undefined. Using a new EAE system that incorporates temporal regulation MHCII expression by myelin-specific cells, we observed rapid...

10.1073/pnas.1909098116 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2019-11-07

Abstract Lewy pathology due to alpha-synuclein (α-syn) inclusions is one of the major hallmarks Parkinson’s Disease (PD). β-Amyloid (Aβ) and phosphorylated-tau, pathologies usually found in Alzheimer’s (AD), have also been implicated PD, with over 50% patients exhibited co-expression these proteins (co-pathologies). In both AD PD postmortem tissue, neuroinflammation – activation microglia resident macrophages infiltration immune cells from periphery, including T monocytes–are drivers...

10.1101/2024.10.13.618101 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-10-13

Abstract Maintenance of immune homeostasis to the intestinal mictrobiota is dependent on a population effector regulatory T (eTreg) cells that develop from microbiota-reactive induced (i)Treg cells. A cardinal feature eTreg their production IL-10, which plays non-redundant role in tolerance commensal microbes. Here, we identify an unexpected for IL-2-induced Stat3 signaling program iTreg cell differentiation and Il10 transcriptional competency. IL-2 proved be both necessary sufficient...

10.1101/2023.09.26.559434 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-09-28
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