Jonathan B. Johnnidis

ORCID: 0000-0003-4308-2504
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Immunotherapy and Immune Responses
  • Hippo pathway signaling and YAP/TAZ
  • Hematopoietic Stem Cell Transplantation
  • Adrenal Hormones and Disorders
  • Epigenetics and DNA Methylation
  • MicroRNA in disease regulation
  • Cancer Cells and Metastasis
  • Cancer-related molecular mechanisms research
  • CAR-T cell therapy research
  • Cancer-related Molecular Pathways
  • Circular RNAs in diseases

Translational Therapeutics (United States)
2021

University of Pennsylvania
2011-2021

Whitehead Institute for Biomedical Research
2007-2008

Massachusetts Institute of Technology
2008

Harvard University
2005

UNC Lineberger Comprehensive Cancer Center
2005

Brigham and Women's Hospital
2005

Joslin Diabetes Center
2005

Chronic infections strain the regenerative capacity of antiviral T lymphocyte populations, leading to failure in long-term immunity. The cellular and molecular events controlling this capacity, however, are unknown. We found that two distinct states virus-specific CD8(+) cells exist chronically infected mice humans. Differential expression T-box transcription factors T-bet Eomesodermin (Eomes) facilitated cooperative maintenance pool during chronic viral infection. T-bet(hi) displayed low...

10.1126/science.1229620 article EN Science 2012-11-29

Autoimmune regulator (aire) is a transcription factor that controls the self-reactivity of T cell repertoire. Although previous results indicate it exerts this function in part by promoting ectopic expression battery peripheral-tissue antigens epithelial cells thymic medulla, recent data argue for additional roles negative selection thymocytes medullary cells. As one approach to exploring such roles, we performed computational analyses microarray on RNA transcripts from aire-deficient versus...

10.1073/pnas.0502670102 article EN Proceedings of the National Academy of Sciences 2005-05-09

Memory CD8(+) T cells are characterized by more rapid and robust effector function upon infection compared with naive cells, but factors governing gene responsiveness incompletely understood. We sought to understand transcriptional control of the genes IFN-γ (Ifng), granzyme B (Gzmb), perforin 1 (Prf1) in murine memory characterizing their profiles chromatin states during lymphocytic choriomeningitis virus infection. Each has a distinct profile resting following restimulation. Primary leads...

10.4049/jimmunol.1003741 article EN The Journal of Immunology 2011-01-29
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