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The Relationship of Modulation of Major Histocompatibility Complex Class I Antigens to Retrovirus Transformation in Rat Cell Lines¹

Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli [L. R., E. C., M. G., M. T. B., A. F., S. Z.], and Centro di Endocrinologia e Oncologia Sperimentale, CNR [S. F.], 5 via S. Pansini, 80131 Naples; Divisione di Immunoematologia, Ospedale "A. Cardarelli," via A. Cardarelli, 80131 Naples [L. D. V.]; and Istituto Internazionale di Genetica e Biofisica, CNR, 10 via G. Marconi, 80125 Naples [E. B.], Italy

The expression of major histocompatibility complex (MHC) Class I antigens has been studied, by means of monoclonal antibodies directed against nonpolymorphic determinants of MHC Class I molecules, in two epithelial differentiated cell lines (FRTL-5 clone 2 and PC clone 3) and in one fibroblast cell line (FRT Fibro) of Fischer rat thyroid origin, before and after infection with various acute retroviruses carrying the v-ras-Ha, v-mos, v-src, polyoma middle T, and c-myc oncogenes. The results obtained indicate that a single virus does not produce identical changes in MHC Class I molecule expression in all tested lines, but a general increase occurs in lines derived from FRTL-5 clone 2 and a decrease occurs in lines derived from PC clone 3 and from FRT Fibro. Thus the modulation of expression seems to proceed always in the same direction in each cell line regardless of the infecting retrovirus and appears to involve posttranscriptional mechanisms, since no modification of expression of mRNA levels has been observed between normal and transformed cells. Only one line of PC clone 3 origin, transformed by the cooperation of two oncogenes (human c-myc and middle T), almost completely lost MHC Class I antigens on the cell surface and presented a significantly reduced synthesis of Class I mRNA.

¹ Supported in part by CNR Grants [Progetti Finalizzati "Oncologia" (86.00617.44, 87.01490.44) and Ingegneria Genetica e Basi Molecolari delle Malattie Ereditarie (86.00109.51, 87.00876.51)] and by a grant from the Associzione Italiana per la Ricerca sul Cancro.

² Recipient of a Research Fellowship from the Associazione Italiana per la Ricerca sul Cancro.

³ To whom requests for reprints should be addressed.

Received 8/18/87. Revised 2/10/88. Accepted 3/11/88.