Impaired assembly yet normal trafficking of MHC class I molecules in Tapasin mutant mice

Andres G. Grandea, Tatiana N. Golovina, Sara E. Hamilton, Venkataraman Sriram, Thomas Spies, Randy R. Brutkiewicz, John T. Harty, Laurence C. Eisenlohr, Luc Van Kaer

Research output: Contribution to journalArticle

166 Scopus citations

Abstract

Loading of peptides onto major histocompatibility complex class I molecules involves a multifactorial complex that includes tapasin (TPN), a membrane protein that tethers empty class I glycoproteins to the transporter associated with antigen processing. To evaluate the in vivo role of TPN, we have generated Tpn mutant mice. In these animals, most class I molecules exit the endoplasmic reticulum (ER) in the absence of stably bound peptides. Consequently, mutant animals have defects in class I cell surface expression, antigen presentation, CD8+ T cell development, and immune responses. These findings reveal a critical role of TPN for ER retention of empty class I molecules. Tpn mutant animals should prove useful for studies on alternative antigen-processing pathways that involve post-ER peptide loading.

Original languageEnglish (US)
Pages (from-to)213-222
Number of pages10
JournalImmunity
Volume13
Issue number2
DOIs
StatePublished - Jan 1 2000

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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    Grandea, A. G., Golovina, T. N., Hamilton, S. E., Sriram, V., Spies, T., Brutkiewicz, R. R., Harty, J. T., Eisenlohr, L. C., & Van Kaer, L. (2000). Impaired assembly yet normal trafficking of MHC class I molecules in Tapasin mutant mice. Immunity, 13(2), 213-222. https://doi.org/10.1016/S1074-7613(00)00021-2