This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Sugiyama, M. Articles by Epstein, L. B. Search for Related Content PubMed PubMed Citation Articles by Sugiyama, M. Articles by Epstein, L. B.

Effect of Corynebacterium parvum on Human T-Lymphocyte Interferon Production and T-Lymphocyte Proliferation in Vitro¹

Cancer Research Institute and Department of Pediatrics, University of California, San Francisco, California 94143

Heat-killed, preservative-free preparations of strain CN 6134 Corynebacterium parvum have been demonstrated to induce interferon in cultures of normal adult human T-lymphocytes. C. parvum was also shown to induce human T-lymphocytes to proliferate in vitro. The maximum interferon and proliferative response was observed 7 days after initiation of culture at a final C. parvum concentration of 140 µg/ml. Human monocyte-derived macrophages did not produce interferon in response to C. parvum or in response to products of C. parvum-stimulated T-lymphocytes. The addition of macrophages to cultures of T-lymphocytes did not significantly enhance the production of interferon by the T-lymphocytes; however, it did significantly enhance the proliferative response to C. parvum. C. parvum can also enhance the production of interferon by T-lymphocytes stimulated with phytohemagglutinin in the presence of macrophages, and the amount of interferon produced in the presence of both agents was greater than the sum of the amounts of interferon stimulated by each agent acting alone. The type of interferon produced by T-lymphocytes in response to C. parvum is similar to type II or immune interferon, because it was labile to low pH and heat. Thus, a link has been found between two agents, C. parvum and interferon, both of which have in common antitumor properties and the ability to modulate the immune response.

¹ This work was supported by Grants AI 12481 and CA 14508 from NIH and by a grant from the Burroughs Wellcome Company. A portion of the work was presented at the Oncology section of the annual meeting of the American Society for Clinical Investigation, May 2, 1977 (11).

² This work was performed when Dr. Sugiyama was on leave from the Department of Otolaryngology, Osaka City University Medical School, Osaka, Japan.

³ To whom requests for reprints should be addressed, at Cancer Research Institute, Moffitt 1282, University of California, San Francisco, Calif. 94143.

Received 4/28/78. Accepted 9/ 7/78.