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Hogan RJ, VanBeek J, Broussard DR, et al. Identification of MHC class II-associated peptides that promote the presentation of toxic shock syndrome toxin-1 to T cells. J Immunol. 2001;166(11):6514-22doi: 10.4049/jimmunol.166.11.6514.
Hogan, R. J., VanBeek, J., Broussard, D. R., Surman, S. L., & Woodland, D. L. (2001). Identification of MHC class II-associated peptides that promote the presentation of toxic shock syndrome toxin-1 to T cells. Journal of immunology (Baltimore, Md. : 1950), 166(11), 6514-22. https://doi.org/10.4049/jimmunol.166.11.6514
Hogan, R J, et al. "Identification of MHC class II-associated peptides that promote the presentation of toxic shock syndrome toxin-1 to T cells." Journal of immunology (Baltimore, Md. : 1950) vol. 166,11 (2001): 6514-22. doi: https://doi.org/10.4049/jimmunol.166.11.6514
Hogan RJ, VanBeek J, Broussard DR, Surman SL, Woodland DL. Identification of MHC class II-associated peptides that promote the presentation of toxic shock syndrome toxin-1 to T cells. J Immunol. 2001 Jun 01;166(11):6514-22. doi: 10.4049/jimmunol.166.11.6514. PMID: 11359802.
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J Immunol. 2001 Jun 01;166(11):6514-22. doi: 10.4049/jimmunol.166.11.6514.

Identification of MHC class II-associated peptides that promote the presentation of toxic shock syndrome toxin-1 to T cells.

Journal of immunology (Baltimore, Md. : 1950)

R J Hogan, J VanBeek, D R Broussard, S L Surman, D L Woodland

Affiliations

  1. Trudeau Institute, Saranac Lake, 100 Algonquin Avenue, NY 12983, USA.

PMID: 11359802 DOI: 10.4049/jimmunol.166.11.6514

Abstract

Previous studies have shown that the DM-deficient cell line, T2-I-A(b), is very inefficient at presenting toxic shock syndrome toxin 1 (TSST-1) to T cells, suggesting that I-A(b)-associated peptides play an essential role in the presentation of this superantigen. Consistent with this, the loading of an I-A(b)-binding peptide, staphylococcal enterotoxin B 121-136, onto T2-I-A(b) cells enhanced TSST-1 presentation >1000-fold. However, despite extensive screening, no other peptides have been identified that significantly promote TSST-1 presentation. In addition, the peptide effect on TSST-1 presentation has been demonstrated only in the context of the tumor cell line T2-I-A(b). Here we show that peptides that do not promote TSST-1 presentation can be converted into "promoting" peptides by the progressive truncation of C-terminal residues. These studies result in the identification of two peptides derived from IgGV heavy chain and I-Ealpha proteins that are extremely strong promoters of TSST-1 presentation (47,500- and 12,000-fold, respectively). We have also developed a system to examine the role of MHC class II-associated peptides in superantigen presentation using splenic APC taken directly ex vivo. The data confirmed that the length of the MHC class II-bound peptide plays a critical role in the presentation of TSST-1 by splenic APC and showed that different subpopulations of APC are equally peptide dependent in TSST-1 presentation. Finally, we demonstrated that the presentation of staphylococcal enterotoxin A, like TSST-1, is peptide dependent, whereas staphylococcal enterotoxin B presentation is peptide independent.

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