Endogenous superantigen expression is controlled by mouse mammary tumor proviral loci

• Published in: The Journal of experimental medicine Vol. 174; no. 5; pp. 1255 - 1258
• Main Authors: WOODLAND, D. L, LUND, F. E, HAPP, M. P, BLACKMAN, M. A, PALMER, E, CORLEY, R. B
• Format: Journal Article
• Language: English
• Published: New York, NY Rockefeller University Press 01-11-1991; The Rockefeller University Press
• Subjects: Animals; Antigens - analysis; Biological and medical sciences; Chromosome Mapping; Fundamental and applied biological sciences. Psychology; Gammaretrovirus - genetics; Mice; Mice, Inbred BALB C; Microbiology; Open Reading Frames; Proviruses - genetics; Receptors, Antigen, T-Cell - analysis; Repetitive Sequences, Nucleic Acid; Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains; T-Lymphocytes - immunology; Transfection; Virology; Cell culture; Oncovirinae; T cell receptor; Variable region; Beta-Peptide chain; Elimination; Retroviridae; Hybridoma; Gene expression; Provirus; Virus; Endogenous; Gene; T-Lymphocyte; Type B oncovirus; LTR sequence; Mouse mammary tumor virus; Clone; Specific relation
• ISSN: 0022-1007; 1540-9538
• DOI: 10.1084/jem.174.5.1255

Superantigens are defined by their ability to stimulate T cells based predominantly on their V beta expression and ability to delete T cells in the thymus when expressed endogenously. We show here that the expression of one endogenous superantigen, Etc-1, is controlled by the expression of the open reading frame region of the 3' long terminal repeat of the mouse mammary tumor proviral gene, Mtv-9. We show that Mtv-8 controls a superantigen with similar specificity, and that both Mtv-8 and Mtv-9 stimulate some V beta 17+ T cells. A third provirus, Mtv-6, controls a superantigen with specificity for V beta 3. Data presented raise the possibility that endogenous superantigens may compete for class II molecules in a single B cell.