To survey whether galectin-7 is associated with acute rejection and the function of galectin-7 in acute allograft rejection.

In this study, the allografts and isografts were detected immunohistologically and analysed by quantitative Western blot analysis for galectin-7 protein. The expression of galectin-7 in T lymphocytes from draining lymph nodes in the recipient mice was examined by flow cytometry. Further, purified T cells of BALB/c mice had been cultured with anti-CD3 and anti-CD28 antibody in the presence or absence of recombined mouse galectin-7 for 5 days. The proliferation of T lymphocytes was detected using flow cytometry.

We found that galectin-7 in the allografts gradually increased with time and was significantly higher than in the isografts at days 3, 5, and 7 post-operation (0·85 ± 0·03 vs. 0·69 ± 0·05, 1·15 ± 0·11 vs. 0·81 ± 0·02, and 2·02 ± 0·12 vs. 0·81 ± 0·05; P < 0·05). The majority of galectin-7 was located in the infiltrating lymphocytes and vascular endothelial cells in the allografts. Furthermore, the percentage of CD4+galectin-7+ and CD8+galectin-7+ T-cells from draining lymph nodes in the allograft group was higher than that in the isograft group (28·0 ± 1·0% vs. 1·2 ± 0·2%; 12·4 ± 0·8% vs. 0·4 ± 0·1%, P < 0·01) (figure1). The proliferation index of T lymphocytes cultured with anti-CD3 and anti-CD28 antibody in the presence of recombined galectin-7 was significantly higher than in absence of recombined galectin-7 (5·26 ± 0·35 vs. 1·71 ± 0·12, p<0·05).

In conclusion, galectin-7 is related to the acute allograft rejection and T-cell response and play important roles in accelerating rejection response.

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