Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Science 28 October 1988:
Vol. 242. no. 4878, pp. 569 - 571
DOI: 10.1126/science.2902689
Prev | Table of Contents | Next

Articles

Science, Vol 242, Issue 4878, 569-571
Copyright © 1988 by American Association for the Advancement of Science

articles

In vivo administration of anti-CD3 prevents malignant progressor tumor growth

JD Ellenhorn, R Hirsch, H Schreiber, and JA Bluestone

University of Chicago, IL 60637.

Malignant progressor tumors are only weakly immunogenic and can evade host recognition and rejection. One approach to therapy involves activation of the host antitumor cellular effector mechanisms. Since monoclonal antibodies to CD3 (anti-CD3) can activate T cells in vitro, an attempt was made to determine if tumor immunity could be achieved by the administration of anti-CD3 in vivo. T lymphocytes from mice injected with anti-CD3 showed increased interleukin-2 receptor (IL-2R) expression, increased proliferation to recombinant IL-2 (rIL-2), and enhanced reactivity in both an allogeneic mixed lymphocyte reaction and a mixed lymphocyte tumor culture. Malignant tumor growth in treated mice was also examined. The anti-CD3 treatment prevented tumor outgrowth that would have killed untreated animals and also stimulated an in vivo response against a malignant progressor tumor providing lasting tumor immunity.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Anti-CD3 induces bi-phasic apoptosis in murine intestinal epithelial cells: possible involvement of the Fas/Fas ligand system in different T cell compartments.
N. Miura, M. Yamamoto, M. Fukutake, N. Ohtake, S. Iizuka, A. Ishige, H. Sasaki, K. Fukuda, T. Yamamoto, and S. Hayakawa (2005)
Int. Immunol. 17, 513-522
   Abstract »    Full Text »    PDF »
A Single-Chain Class II MHC-IgG3 Fusion Protein Inhibits Autoimmune Arthritis by Induction of Antigen-Specific Hyporesponsiveness.
L. Zuo, C. M. Cullen, M. L. DeLay, S. Thornton, L. K. Myers, E. F. Rosloniec, G. P. Boivin, and R. Hirsch (2002)
J. Immunol. 168, 2554-2559
   Abstract »    Full Text »    PDF »
Phase I Evaluation of Humanized OKT3: Toxicity and Immunomodulatory Effects of hOKT3{{gamma}}4.
J. Richards, J. Auger, D. Peace, D. Gale, J. Michel, A. Koons, T. Haverty, R. Zivin, L. Jolliffe, and J. A. Bluestone (1999)
Cancer Res. 59, 2096-2101
   Abstract »    Full Text »    PDF »
A lymphocyte-activating monoclonal antibody induces regression of human tumors in severe combined immunodeficient mice.
B. Hardy, R. Kovjazin, A. Raiter, N. Ganor, and A. Novogrodsky (1997)
PNAS 94, 5756-5760
   Abstract »    Full Text »    PDF »
Hematopoietic Changes Induced by a Single Injection of Anti-CD3 Monoclonal Antibody into Normal Mice.
E. Schneider, V. Salaün, A. Ben Amor, and M. Dy (1997)
Stem Cells 15, 154-160
   Abstract »    Full Text »
Successful Combination Immunotherapy for the Generation In Vivo of Antitumor Activity With Anti-CD3, Interleukin 2, and Tumor Necrosis Factor {alpha}.
S. C. Yang, K. D. Fry, E. A. Grimm, and J. A. Roth (1990)
Arch Surg 125, 220-225
   Abstract »    PDF »
CD3-mediated activation of tumor-reactive lymphocytes from patients with advanced cancer.
I. Hellstrom, J. A. Ledbetter, N. Scholler, Y. Yang, Z. Ye, G. Goodman, J. Pullman, M. Hayden-Ledbetter, and K. E. Hellstrom (2001)
PNAS 98, 6783-6788
   Abstract »    Full Text »    PDF »


To Advertise     Find Products

Science. ISSN 0036-8075 (print), 1095-9203 (online)