Ham-2 corrects the class I antigen-processing defect in RMA-S cells

Michelle Attaya, Stephen Jameson, Coleen K. Martinez, Evan Hermel, Carla Aldrich, James Forman, Kirsten Fischer Lindahl, Michael J. Bevan, John J. Monaco

Research output: Contribution to journalArticlepeer-review

293 Scopus citations


THE murine major histocompatibility complex (MHC) contains two genes (Ham-1 and Ham-2) that encode members of a super-family of ATP-dependent transport proteins1,2. These genes are believed to mediate the transport of peptide antigen from the cytoplasm into the lumen of the endoplasmic reticulum for binding by MHC class I molecules. Evidence for such a function has come from the rescue of class I surface expression by a cloned copy of the human homologue of Ham-1, PSF-1, in a human cell line that is defective in antigen processing3. A mutant murine cell line, RMA-S, has an identical antigen-processing-defective phenotype4,5. Here we show that expression of a cloned copy of the Ham-2 gene in RMA-S cells results in recovery of the ability to process and present class I-restricted antigens to cytotoxic T lymphocytes, and in partial recovery of class I surface expression. Processing defects for classical (H-2 K and D) and non-classical (Qal and HMT) class I molecules are corrected by Ham-2. These data indicate that both MHC-linked transporter genes are probably required for class I antigen processing, and that the functional transporter in this pathway may consist of a Ham-l/Ham-2 heterodimer.

Original languageEnglish (US)
Pages (from-to)647-649
Number of pages3
Issue number6361
StatePublished - 1992


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