Anti-CD132 Monoclonal Antibodies Inducing T Cells Apoptosis after Alloantigen Stimulation and Its Possible Clinical Applications

Abstract

Abstract: Aim To investigate the mechanism of anti-CD132 monoclonal antibodies (mAbs) inhibiting T cells proliferation in vitro, and their potential values for clinical use. Methods BALB/c and C57BL/6 mice splenocytes were harvested for two-ways mixed lymphocyte culture (MLC). Anti-CD132 mAbs (final concentration 100 mg·L^-1) were added in MLC on day 0 (group 1) or day 3 (group 2). Fluorescence activated cell sorting (FACS) was used to measure the proliferation (carboxy-fluorescein dia cetate, succinimidyl ester,CFSE), apoptosis of T cells (PE-CD3, FITC-annexin-v), and cell cycle (propidium iodide stain). The expression of survivin in T cells was detected by immunochemical stai- ning. Results Multi-generation CFSE-labeled splenocytes were found dividing and their fluorescent strength decreased in MLC. There was no noticeable change in fluorescent intensity in group 1 and group 2. On day 3, apoptosis induced by anti-CD132 mAbs was detected in part of T cells, but was not detected in the former two days in group 1. In group 2, the number of cells in M phase (activated T cells) decreased and apoptotic cells increased on day 4. The phenomena were not observed in control group (P<0.01). Expression of survivin in T cells was detected in control group but not in groups 1 and 2. Conclusion Blockade of CD132 signaling pathway inhibits T cell proliferation in vitro by means of inducing activated alloreactive T cell apoptosis but not the resting T cells. Anti-CD132 mAbs may be candidates for clinical applications.

Key words: CD132, CD132, apoptosis, apoptosis, two-ways mixed lymphocyte culture, two-ways mixed lymphocyte culture

CLC Number:

R392.4

R392.12

Supporting:

CHEN Bi-cheng, CHANG Sheng, TANG Li, ZHANG Xin, Xiang Fu-li, GUO Hui, CHEN Zhong-hua Klaus^*. Anti-CD132 Monoclonal Antibodies Inducing T Cells Apoptosis after Alloantigen Stimulation and Its Possible Clinical Applications[J]. .

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