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GP73 was upregulated in PBMC stimulated with ConA but failed to promote lymphocyte proliferation
Fang Wang1, Zhaotao Li, Leike Li
1State Key Laboratory of Respiratory Disease, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China.
Golgi protein 73-kD (GP73), a type II Golgi transmembrane glycoprotein, is highly expressed in a variety of human diseases, but its physiology and pathology remain unknown. In examining the function of GP73 in the immune system, treatment of human PBMC with ConA significantly increased the intracellular expression of GP73 and its secretion into the culture medium. Two-way MLR and the ConA stimulation assay showed that treatment with purified GP73 protein barely affected the proliferation of PBMC. These results suggest that lymphocyte-secreted GP73 might partially contribute to higher serum GP73 in patients, and secreted GP73 exerts an extremely weak effect on the proliferation of PBMC ex vivo.
Golgi protein 73-kD (GP73), a type II Golgi transmembrane glycoprotein, is highly expressed in a variety of human diseases, but its physiology and pathology remain unknown. In examining the function of GP73 in the immune system, treatment of human PBMC with ConA significantly increased the intracellular expression of GP73 and its secretion into the culture medium. Two-way MLR and the ConA stimulation assay showed that treatment with purified GP73 protein barely affected the proliferation of PBMC. These results suggest that lymphocyte-secreted GP73 might partially contribute to higher serum GP73 in patients, and secreted GP73 exerts an extremely weak effect on the proliferation of PBMC ex vivo.
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