Jonathan Jung
University of Massachusetts Medical School
4 Papers
Jonathan Jung is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Synapse & T-cell receptor. The author has an hindex of 4, co-authored 4 publications.
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Papers
Targeted Complement Inhibition at Synapses Prevents Microglial Synaptic Engulfment and Synapse Loss in Demyelinating Disease.
Sebastian Werneburg,Jonathan Jung,Rejani B. Kunjamma,Seung Kwon Ha,Nicholas J. Luciano,Cory M. Willis,Guangping Gao,Natalia P. Biscola,Leif A. Havton,Stephen J. Crocker,Brian Popko,Daniel S. Reich,Dorothy P. Schafer +12 more
TL;DR: Results indicate that microglia eliminate synapses through the alternative complement cascade in demyelinating disease and identify a strategy to prevent synapse loss that may be broadly applicable to other neurodegenerative diseases.
335
Hydrophobic CDR3 residues promote the development of self-reactive T cells
Brian D. Stadinski,Karthik Shekhar,Iria Gomez-Tourino,Jonathan Jung,Katsuhiro Sasaki,Andrew K. Sewell,Mark Peakman,Arup K. Chakraborty,Eric S. Huseby +8 more
TL;DR: The interfacial hydrophobicity of amino acids at positions 6 and 7 of the complementarity-determining region CDR3β robustly promoted the development of self-reactive TCRs, providing a means for distinguishing normal T cell repertoires versus autoimmunity-prone T cell repertoireires.
156
Targeted complement inhibition at synapses prevents microglial synaptic engulfment and synapse loss in demyelinating disease
Sebastian Werneburg,Jonathan Jung,Rejani B. Kunjamma,Seung Kwon Ha,Nicholas J. Luciano,Cory M. Willis,Guangping Gao,Stephen J. Crocker,Brian Popko,Daniel S. Reich,Dorothy P. Schafer +10 more
TL;DR: In postmortem human MS tissue and in nonhuman primate and mouse MS models profound synapses loss and microglial synaptic engulfment are identified and a novel gene therapy approach is provided to prevent synapse loss by microglia, which may be broadly applicable to other neurodegenerative diseases.
13
Hydrophobic CDR3 residues promote the development of self-reactive T cells
Brian D. Stadinski,Karthik Shekhar,Iria Gomez-Tourino,Jonathan Jung,Katsuhiro Sasaki,Andrew K. Sewell,Mark Peakman,Arup K. Chakraborty,Eric S. Huseby +8 more
- 01 Jun 2016
TL;DR: In this paper, the authors found that the interfacial hydrophobicity of amino acids at positions 6 and 7 of the complementarity-determining region CDR3β robustly promoted the development of self-reactive TCRs.