| Summary: | 碩士 === 國立交通大學 === 生化工程研究所 === 96 === H. pylori is a common gastrointestinal bacterium that causes chronic inflammation for lifelong. Many factors were investigated to see their functions on immune suppression. However, these factors may not be strong enough to help every stain escape from immune responses. According to the literature research, some members of heat shock proteins play a dual role in immune responses. For example, Mycobacterium tuberculosis hsp60 (Mt hsp60) protects the rat from arthritis by inducing Treg. Thus, we hypothesized that H. pylori heat shock protein 60 (Hp hsp60) might also induce Treg generation to suppress almost every population of immune cells. In our study, we used PBMC and CD3+ T cells as targets to investigate whether Hp hsp60 increases the percentage of Treg in CD4+ T cells. At first, we demonstrated the effect of Hp hsp60 on cell proliferation which is a character for immune cell activation. We found that Hp hsp60 has a strong suppressive ability for PBMC proliferation and a slight effect on Jurkat cells, which is a T lymphoma cell line. In addition, the proliferation inhibition was caused by cell arrest. The proliferation inhibition caused by Hp hsp60 might be due to the cell arrest. Furthermore, we intended to see whether this inhibition was associated with Treg. The CD4/CD25 double staining and foxp3 mRNA expression level showed that the Treg were increased after treated with Hp hsp60. Taken together, we found that Hp hsp60 could increase Treg cell generation and may help H. pylori escape from the immune system.
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