J
Jun-ichi Inobe
Researcher at Brigham and Women's Hospital
Publications - 13
Citations - 4038
Jun-ichi Inobe is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Antigen & Interleukin 4. The author has an hindex of 13, co-authored 13 publications receiving 3999 citations.
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Journal ArticleDOI
Regulatory T cell clones induced by oral tolerance: suppression of autoimmune encephalomyelitis
TL;DR: Mucosally derived TH2-like clones induced by oral antigen can actively regulate immune responses in vivo and may represent a different subset of T cells.
Journal ArticleDOI
Peripheral deletion of antigen-reactive T cells in oral tolerance.
Youhai H. Chen,Jun-ichi Inobe,Reinhard Marks,Patricia A. Gonnella,Vijay K. Kuchroo,Howard L. Weiner +5 more
TL;DR: It is reported that oral antigen can delete antigen-reactive T cells in Peyer's patches, in mice transgenic for the ovalbumin-specific T-cell receptor genes, and was dependent on dosage and frequency of feeding.
Journal ArticleDOI
Oral tolerance in myelin basic protein T-cell receptor transgenic mice: suppression of autoimmune encephalomyelitis and dose-dependent induction of regulatory cells.
TL;DR: It is demonstrated that MBP-specific T cells can differentiate in vivo into encephalitogenic or regulatory T cells depending upon the context by which they are exposed to antigen.
Journal ArticleDOI
IL‐4 is a differentiation factor for transforming growth factor‐β secreting Th3 cells and oral administration of IL‐4 enhances oral tolerance in experimental allergic encephalomyelitis
Jun-ichi Inobe,Anthony J. Slavin,Yoshinori Komagata,Youhai H. Chen,Liming Liu,Howard L. Weiner +5 more
TL;DR: IL‐4 is a differentiation factor for TGF‐β‐secreting Th3 cells and oral IL‐4 has a synergistic effect on low‐dose oral tolerance that is associated with increased TGF-β secretion.
Journal Article
Induction of oral tolerance to myelin basic protein in CD8-depleted mice: both CD4+ and CD8+ cells mediate active suppression.
TL;DR: It is demonstrated that CD4+ cells in the absence of CD8+ cells can mediate the active suppression component of oral tolerance in mice and that there is a reciprocal relationship between Th1- and Th2-type cytokine production associated with oral tolerization.