BACKGROUND: CD52 monoclonal antibody (mAb) has been used therapeutically in lymphocytic leukemia, autoimmune disease, and organ transplantation. But the effect of CD52 mAb on intestinal intraepithelial lymphocytes (IELs) was unknown. The aim of this study was to assess the influence of anti-mouse CD52 mAb on IELs. METHODS: Twenty male C57BL/6 mice were randomly assigned to a treatment or a control group. The treatment group received anti-mouse CD52 mAb (20 mug, subcutaneously), whereas the control group received the same volume of phosphate-buffered solution. On the seventh day after treatment, mice were killed, and ileum and colon were obtained for histopathology and immunohistochemistry examination, IELs were isolated for flow cytometric analysis and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide analysis. Furthermore, the intestinal permeability was measured by lactulose-mannitol test. RESULTS: The number and viability of IELs were decreased significantly in treatment compared with the control group. There were significant differences between the two groups considering IELs phenotypes. In addition, the proportion of apoptotic IELs in CD52 mAb treatment group was significantly higher than the control group (19.59%+/-3.13% and 2.02%+/-0.33%, respectively; P<0.05). Furthermore, lactulose-mannitol test showed a marked increase intestinal permeability after CD52 treatment (90.38%+/-5.96% and 46.02%+/-6.40%, respectively; P<0.05). CONCLUSION: Anti-mouse CD52 mAb could induce more IELs to apoptosis and result in reducing the number of IELs, which may disrupt intestinal barrier function.
BACKGROUND:CD52 monoclonal antibody (mAb) has been used therapeutically in lymphocytic leukemia, autoimmune disease, and organ transplantation. But the effect of CD52 mAb on intestinal intraepithelial lymphocytes (IELs) was unknown. The aim of this study was to assess the influence of anti-mouseCD52 mAb on IELs. METHODS: Twenty male C57BL/6 mice were randomly assigned to a treatment or a control group. The treatment group received anti-mouseCD52 mAb (20 mug, subcutaneously), whereas the control group received the same volume of phosphate-buffered solution. On the seventh day after treatment, mice were killed, and ileum and colon were obtained for histopathology and immunohistochemistry examination, IELs were isolated for flow cytometric analysis and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide analysis. Furthermore, the intestinal permeability was measured by lactulose-mannitol test. RESULTS: The number and viability of IELs were decreased significantly in treatment compared with the control group. There were significant differences between the two groups considering IELs phenotypes. In addition, the proportion of apoptotic IELs in CD52 mAb treatment group was significantly higher than the control group (19.59%+/-3.13% and 2.02%+/-0.33%, respectively; P<0.05). Furthermore, lactulose-mannitol test showed a marked increase intestinal permeability after CD52 treatment (90.38%+/-5.96% and 46.02%+/-6.40%, respectively; P<0.05). CONCLUSION: Anti-mouseCD52 mAb could induce more IELs to apoptosis and result in reducing the number of IELs, which may disrupt intestinal barrier function.