The major histocompatibility complex class II-linked cim locus controls the kinetics of intracellular transport of a classical class I molecule

• Published in: The Journal of experimental medicine Vol. 173; no. 4; pp. 913 - 921
• Main Authors: Powis, S J, Howard, J C, Butcher, G W
• Format: Journal Article
• Language: English
• Published: New York, NY Rockefeller University Press 01.04.1991; The Rockefeller University Press
• Subjects: Animals; Antigens; Biological and medical sciences; Biological Transport; Cell Compartmentation; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Histocompatibility antigens (hla, h-2 and other systems); Histocompatibility Antigens Class I - metabolism; Lymphocytes - metabolism; Major Histocompatibility Complex; Mice; Molecular immunology; Protein Processing, Post-Translational; Rats; Transfection; Flow cytometry; Intracellular transport; Rat; Gene product; Major histocompatibility system; Rodentia; Class II histocompatibility antigen; Vertebrata; Immunoprecipitation reaction; Regulation(control); Mammalia; Locus; Mechanism of action; Class I histocompatibility antigen
• ISSN: 0022-1007; 1540-9538
• DOI: 10.1084/jem.173.4.913

The dominant trans-acting major histocompatibility complex (MHC)-linked class I modifier (cim) locus, previously recognized through its ability to determine altered alloantigenicity of a rat class I molecule, RT1.A3, is shown here to influence class I intracellular transport. The MHC recombinant laboratory rat strains PVG.R1 and PVG.R8 display unusually long retention of RT1.Aa within the endoplasmic reticulum or cis-Golgi. In appropriate F1 hybrid cells heterozygous for RT1.Aa and another class I MHC allele, RT1.Ac, only the RT1.Aa protein is subject to slow transport. The cim gene product therefore shows class I allele specificity in its action, cim appears to be a polymorphic locus whose product is directly involved in the processes of class I MHC assembly and/or intracellular transport.