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Bob1 enhances RORγt-mediated IL-17A expression in Th17 cells through interaction with RORγt.

Ippei Ikegami1, Hiromi Takaki1, Shiori Kamiya2

  • 1Department of Human Immunology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, S1W17, Chuo-ku, Sapporo, 060-8556, Japan.

Biochemical and Biophysical Research Communications
|May 20, 2019
PubMed
Summary

POU domain class 2-associating factor 1 (Bob1) enhances IL-17A expression in T helper 17 (Th17) cells by interacting with RORγt. This interaction is crucial for Th17 cell differentiation and plays a role in autoimmune diseases.

Keywords:
Bob1EAE/MSIL-17RORγtTh17

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Area of Science:

  • Immunology
  • Molecular Biology
  • Autoimmune Diseases

Background:

  • POU domain class 2-associating factor 1 (Bob1) is primarily expressed in B cells and regulates B cell homeostasis and humoral immunity.
  • Bob1's function in T cell subsets like follicular helper T cells, Th1, and Th2 cells is established, but its role in other T cell subsets remained unclear.
  • Experimental autoimmune encephalomyelitis (EAE) is a T cell-mediated autoimmune disease model.

Purpose of the Study:

  • To investigate the role of Bob1 in T helper 17 (Th17) cell differentiation and function.
  • To elucidate the molecular mechanism by which Bob1 influences Th17 cell activity.
  • To determine Bob1's involvement in autoimmune diseases mediated by Th17 cells.

Main Methods:

  • Utilized Bob1 knockout (KO) mice to study EAE susceptibility.
  • Analyzed Th17 cell differentiation in Bob1 KO T cells.
  • Investigated the interaction between Bob1 and RORγt using biochemical assays.
  • Assessed IL-17A transcription activity and the formation of a DNA-Oct1-Bob1 ternary complex.

Main Results:

  • Bob1 KO mice exhibited resistance to MOG35-55-induced EAE.
  • Bob1 KO T cells showed defects in Th17 differentiation.
  • Bob1 directly interacts with the ligand-binding domain of RORγt, enhancing IL-17A transcription.
  • Bob1-mediated IL-17A induction requires the formation of a DNA-Oct1-Bob1 ternary complex.

Conclusions:

  • Bob1 enhances IL-17A expression in Th17 cells both in vivo and in vitro through interaction with RORγt.
  • Bob1 plays a critical role in Th17 cell differentiation and function.
  • Bob1 is implicated as a pivotal factor in Th17-mediated autoimmune diseases like EAE.