A novel anti-Thy-1 (CD90) monoclonal antibody induces apoptosis in mouse malignant T-lymphoma cells in spite of inducing bcl-2 expression

Naoya Fujita, Yukinari Kato, Mikihiko Naito, Takashi Tsuruo

Research output: Contribution to journalArticlepeer-review

20 Citations (Scopus)

Abstract

Mouse malignant T-lymphoma CS-21 cells can survive and proliferate in vitro when co-cultured with CA-12 stromal cells isolated from lymph nodes, but CS-21 cells undergo apoptotic cell death with DNA fragmentation when cultured alone. We immunized vats with CS-21 cells and raised monoclonal antibodies (MAbs) that recognized Thy-1 (CD90) or CD45 protein. The majority of these MAbs were able to inhibit the adhesion and apoptosis of CS-21 cells. When anti-Thy-1 MAbs were examined for their recognition site on Thy-1 glycoprotein, one of them, MCS-34, was found to recognize both Thy-1.1 and Thy-1.2. In addition, MCS-34, just like the anti-Thy-1 MAb G7, recognized the Thy-1A epitope. G7 was known to induce apoptosis in some T-cell hybridomas and in thymocytes. In CS-21 cells, however, G7 could not induce apoptosis, but MCS-34 could. Interestingly, MCS-34 enhanced the expression of bcl-2 protein, in spite of its ability to induce apoptosis. Upon examining the apoptosis-inducing mechanisms of MCS-34, we found that it promoted a sustained increase in cytoplasmic-free calcium in CS-21 cells. Calcium ionophore A23187 was also found to induce apoptosis in a dose-dependent manner. These results indicate that a sustained increase in cytoplasmic-free calcium by MCS-34 induces apoptosis in CS-21 cells in spite of bcl-2 protein expression.

Original languageEnglish
Pages (from-to)544-550
Number of pages7
JournalInternational Journal of Cancer
Volume66
Issue number4
DOIs
Publication statusPublished - 1996 May 16
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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