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Dendritic Cell Activation Prevents MHC Class II Ubiquitination and Promotes MHC Class II Survival Regardless of the Activation Stimulus

  1. Author:
    Walseng, E.
    Furuta, K.
    Goldszmid, R. S.
    Weih, K. A.
    Sher, A.
    Roche, P. A.

  2. Author Address

    [Walseng, Even; Furuta, Kazuyuki; Weih, Karis A.; Roche, Paul A.] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. [Goldszmid, Romina S.; Sher, Alan] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. [Goldszmid, Romina S.] NCI, Expt Immunol Lab, Canc & Inflammat Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.;Roche, PA, NCI, Expt Immunol Branch, NIH, Bldg 10,Rm 4B36, Bethesda, MD 20892 USA.;paul.roche@nih.gov
    1. Year: 2010
    2. Date: Dec
  2. Journal: Journal of Biological Chemistry
    1. 285
    2. 53
    3. Pages: 41749-41754
  4. Type of Article: Article
  5. ISSN: 0021-9258
  1. Abstract:

    The expression of MHC class II (MHC-II) on the surface of antigen-presenting cells, such as dendritic cells (DCs), is tightly regulated during cellular activation. Many cells, including DCs, are activated following stimulation of innate Toll-like receptors (TLRs) by products of microorganisms. In the resting (immature) state, MHC-II is ubiquitinated in immature DCs and is rapidly degraded; however, after activation of these cells with MyD88-dependent TLR ligands, MHC-II ubiquitination is blocked, and MHC-II survival is prolonged. We now show that DC activation using MyD88-dependent TLR ligands, MyD88-independent TLR ligands, and even infection with the intracellular parasite Toxoplasma gondii leads to identical changes in MHC-II expression, ubiquitination, and surface stability, revealing a conserved role for enhanced MHC-II stability after DC activation by different stimuli.

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External Sources

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  2. DOI: 10.1074/jbc.M110.157586
  3. View record in Web of Science®
  4. WOS: 000285622600062

Library Notes

  1. Fiscal Year: FY2010-2011
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