A novel anti-Thy-1 (CD90) monoclonal antibody induces apoptosis in mouse malignant T-lymphoma cells in spite of inducing bcl-2 expression
✍ Scribed by Naoya Fujita; Yukinari Kato; Mikihiko Naito; Takashi Tsuruo
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- French
- Weight
- 856 KB
- Volume
- 66
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
Mouse malignant T-lymphoma CS-21 cells can survive and proliferate in vitro when co-cultured with CA-I 2 stromal cells isolated from lymph nodes, but CS-2 I cells undergo apoptotic cell death with DNA fragmentation when cultured alone. We immunized rats with CS-2 I cells and raised monoclonal antibodies (MAbs) that recognized Thy-I (CD90) or CD45 protein. The majority of these MAbs were able to inhibit the adhesion and apoptosis of CS-2 I cells. When anti-Thy-I MAbs were examined for their recognition site on Thy-I glycoprotein, one of them, MCS-34, was found to recognize both Thy-I. I and Thy-I .2. In addition, MCS-34, just like the anti-Thy-I MAb G7, recognized the Thy-I A epitope. 6 7 was known to induce apoptosis in some T-cell hybridomas and in thymocytes. In CS-21 cells, however, 6 7 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 apoptosisinducing mechanisms of MCS-34, we found that it promoted a sustained increase in cytoplasmic-free calcium in CS-2 I cells. Calcium ionophore A23 I87 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-2 I cells in spite of bcl-2 protein expression.