한빛사
>
한빛사논문
한빛사논문
- 조회3,043
Immunol. Rev., Volume 266, Issue 1, pages 134–144, July 2015 | DOI: 10.1111/imr.12303
Molecular mechanism and cellular function of MHCII ubiquitination
Abstract
Jaehak Oh and Jeoung-Sook Shin*
Department of Microbiology and Immunology, Sandler Asthma Basic Research Center, University of California San Francisco, San Francisco, CA, USA
* Correspondence to : Jeoung-Sook Shin, 513 Parnassus Avenue, HSE-201 San Francisco, CA 94143, USA
Summary
The major histocompatibility complex class II (MHCII) is ubiquitinated via the evolutionarily conserved lysine in the cytoplasmic tail of the β chain in dendritic cells (DCs) and B cells. The ubiquitination is mediated by the membrane-associated RING-CH1 (MARCH1) ubiquitin ligase although it can be also mediated by the homologous ligase MARCH8 in model cell lines. The ubiquitination promotes MHCII endocytosis and lysosomal sorting that results in a reduction in the level of MHCII at cell surface. Functionally, MHCII ubiquitination serves as a means by which DCs suppress MHCII expression and reduce antigen presentation in response to the immune regulatory cytokine interleukin-10 (IL-10) and regulatory T cells. Recently, additional roles of MHCII ubiquitination have emerged. MHCII ubiquitination promoted DC production of inflammatory cytokines in response to the Toll-like receptor ligands. It also potentiated DC ability to activate antigen-specific naive CD4+ T cells while limiting the amount of antigens presented at cell surface. Similarly, MHCII ubiquitination promoted DC activation of CD4+ thymocytes supporting regulatory T-cell development independent of its effect of limiting antigen presentation. Thus, ubiquitination appears to confer MHCII a function independent of presenting antigens by a mechanism yet to be identified.
Keywords : MHCII ; ubiquitination; MARCH ; dendritic cell ; TLR ; regulatory T cell
논문정보
- Review Paper
- 2015년 07월 (BRIC 등록일 2015-06-29)
- 국외 연구진
- 생명과학 > 면역학
댓글 작성 로그인
팝업 닫기관련 링크
연구자 키워드
관련분야 연구자보기
소속기관 논문보기
관련분야 논문보기
