engleski

Activation of NK and NKT Cells during Experimental Colitis in CD26 Deficient Mice

The CD26 molecule (dipeptidyl peptidase IV, DPP IV, EC 3.4.14.5) is a broadly expressed multifunctional transmembrane glycoprotein involved in different biological processes through its proteolytic activity as well as its role in T-cell activation. Based on recent findings, immunological abnormalities including the overproduction of proinflammatory cytokines and natural killer T cells activation, suggest a potential role of CD26 in the pathogenesis of chronic inflammatory diseases. In order to investigate the role of CD26 in the etiopathogenesis of colitis, an experimental murine model was established. Aim The aim of this study was to investigate the potential role of CD26 in the development and activation of hepatic and splenic natural killer (NK) and NK T (NKT) cells in experimental murine model of colitis induced in C57BL/6 and CD26 deficient mice. Material and methods In this study, male homozygous CD26 deficient mice generated on a C57BL/6 genetic background and wild-type C57BL/6 mice were used. Colitis was induced by administration of 3% (w/v) dextran sulfate sodium dissolved in drinking water with free access during 7 days. Changes in percentages of liver and spleen NK and NKT cells were analyzed by flow-cytometry (FACSCalibur, Becton Dickinson). Data were evaluated using the Sigma Plot Scientific Graphing System, Version 6.10. The statistical significance was tested using Mann-Whitney U-test. Differences were considered statistically significant for p<0.05. Results The results of our study show a decreased percentage of spleen NK and NKT cells in the acute phase of the disease in CD26 deficient and C57BL/6 mice in comparison with healthy mice. In CD26 deficient mice, in the acute phase of the disease, percentages of spleen NK and NKT cells were increased in comparison with C57BL/6 mice. Furthermore, in the acute phase of the disease, in CD26 deficient mice, percentages of NK and NKT cells in liver were statistically significantly increased in comparison to healthy mice. Conclusion Our results suggest a possible modulating role of the CD26 molecule in the regulation of local and systemic innate immune response in the acute phase of colitis, which makes it important in the pathogenesis of inflammatory processes.

CD26 deficient mice; NK cells; NKT cells; experimental colitis

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