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Wiki Education Foundation-supported course assignment

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This article was the subject of a Wiki Education Foundation-supported course assignment, between 4 January 2021 and 15 March 2021. Further details are available on the course page. Student editor(s): Immcarle143.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 22:04, 17 January 2022 (UTC)[reply]

Wiki Education Foundation-supported course assignment

[edit]

This article is or was the subject of a Wiki Education Foundation-supported course assignment. Further details are available on the course page. Student editor(s): Immcarle57.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 22:56, 16 January 2022 (UTC)[reply]

Immunodominant epitope selection

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What is 'immunodominant epitope selection,' and how does it differs from other types (if any) of epitope selection? I look forward to learning more about this and HLA-DO as I update the HLA-DO Wiki page. Immcarle57 (talk) 02:00, 9 January 2018 (UTC)[reply]

Possible Sources

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  1. Chen, Xinjian, and Peter E. Jensen. "Biological Function of HLA-DO (H2-O)." Critical Reviews in Immunology 34.3 (2014).
  2. Guce, Abigail I., et al. "HLA-DO acts as a substrate mimic to inhibit HLA-DM by a competitive mechanism." Nature Structural and Molecular Biology 20.1 (2013): 90.
  3. Jiang, Wei, et al. "pH-susceptibility of HLA-DO tunes DO/DM ratios to regulate HLA-DM catalytic activity." Scientific reports 5 (2015): 17333.
  4. Mellins, Elizabeth D., and Lawrence J. Stern. "HLA-DM and HLA-DO, key regulators of MHC-II processing and presentation." Current opinion in immunology 26 (2014): 115-122.
  5. Poluektov, Yuri O., AeRyon Kim, and Scheherazade Sadegh-Nasseri. "HLA-DO and its role in MHC class II antigen presentation." Frontiers in immunology 4 (2013): 260.
  6. Poluektov, Yuri O., et al. "HLA-DO as the optimizer of epitope selection for MHC class II antigen presentation." PLoS One 8.8 (2013): e71228.
  7. Pezeshki, Abdul Mohammad, et al. "HLA-DO increases bacterial superantigen binding to human MHC molecules by inhibiting dissociation of class II-associated invariant chain peptides." Human immunology 74.10 (2013): 1280-1287.

Guce, A.I., Mortimer, S.E., Yoon, T., Painter, C.A., Jiang, W., Mellins, E.D., and Stern, L.J. (2013). HLA-DO acts as a substrate mimic to inhibit HLA-DM by a competitive mechanism. Nat Struct Mol Biol 20, 90–98.

van Ham, S.M., Tjin, E.P.M., Lillemeier, B.F., Grüneberg, U., van Meijgaarden, K.E., Pastoors, L., Verwoerd, D., Tulp, A., Canas, B., Rahman, D., et al. (1997). HLA-DO is a negative modulator of HLA-DM-mediated MHC class II peptide loading. Current Biology 7, 950–957.

Liljedahl, M., Kuwana, T., Fung-Leung, W.P., Jackson, M.R., Peterson, P.A., and Karlsson, L. (1996). HLA-DO is a lysosomal resident which requires association with HLA-DM for efficient intracellular transport. The EMBO Journal 15, 4817–4824.

Mellins, E.D., and Stern, L.J. (2014). HLA-DM and HLA-DO, key regulators of MHC-II processing and presentation. Current Opinion in Immunology 26, 115–122.

Poluektov, Y.O., Kim, A., and Sadegh-Nasseri, S. (2013). HLA-DO and Its Role in MHC Class II Antigen Presentation. Front. Immunol. 4.

Shiina, T., Hosomichi, K., Inoko, H., and Kulski, J.K. (2009). The HLA genomic loci map: expression, interaction, diversity and disease. Journal of Human Genetics 54, 15–39.

Welsh, R.A., and Sadegh-Nasseri, S. (2020). The love and hate relationship of HLA-DM/DO in the selection of immunodominant epitopes. Current Opinion in Immunology 64, 117–123. HLA-DM - an overview | ScienceDirect Topics. — Preceding unsigned comment added by Immcarle143 (talkcontribs) 01:15, 30 January 2021 (UTC)[reply]

Welsh RA, Song N, Foss CA, Boronina T, Cole RN, Sadegh-Nasseri S. Lack of the MHC class II chaperone H2-O causes susceptibility to autoimmune diseases.PLoS Biol. 2020 Feb 18;18(2):e3000590. doi: 10.1371/journal.pbio.3000590. eCollection 2020 Feb. — Preceding unsigned comment added by Narenge.blossom (talkcontribs) 04:39, 10 March 2021 (UTC)[reply]