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Dihydroartemisinin regulates splenic immune cell heterogeneity through SOD3-JNK-AP-1 axis

DHA stimulates normal T cell proliferation (green), interferon-γ + cytotoxic CD8 + T cells (red), and MHCIIlow follicular (Fo) B cells (blue) in mice (left ventricles) by injection and superoxide dismutase 3 (SOD3) expression, increased phosphorylation of c-Jun N-terminal kinases and low-affinity activated protein 1 transcription factors (right ventricle). Credit: Science China Press

Dihydroartemisinin (DHA), an active metabolite of artemisinin and the most potent anti-malarial drug, is also used to treat autoimmune diseases such as lupus erythematosus (SLE) and psoriasis. Since the first report of the immunomodulatory effects of DHA in the 1990s, there has been additional evidence that DHA is effective in regulating the immune system of the host after administration. However, the potential of the system remains to be seen. Professor Qijun Chen’s team built the first single cell of the DHA-specific virus cell and explained, using a single RNA system with cellular and historical methods, that DHA regulates the immune system of splenic by SOD3-JNK-AP. – 1 axis.

The group found that improved T cells (Tregs) and interferon-γ (IFN-γ) + CD8+ Cytotoxic T cells were aggregated in treatment after DHA of the mouse. The expression of antibodies to CD73, CD274 and IL-10 was normalized in the Tregs, while the key expression of granzyme A and granzyme B was reduced in IFN-γ.+CD8+ Cytotoxic T. cells+ T cells and reduced Tregs immune function are routinely observed in patients with SLE. “Our results may explain the effect of DHA in patients with SLE,” said Professor Qijun Chen.

In a humorous immune system, the team also found that the appearance of MHCII in follicular B cells (FOB) was reduced after-DHA treatment regimens. Furthermore, several key molecules associated with activating cell B, including CD79a, CD79b, and Ms4a1, have also been reduced in Fo B. cells These results suggest that DHA exerts a different effect on immunity jokes and cellular.

Through research on genes expressed differently after DHA treatment, the team found that c-Jun N-terminal kinases (JNK) phosphorylation and activated protein-1 (AP-1) in a wide range of bacterial cells are related to DHA treatment. . The researchers further confirmed that the changes in the AP-1 expression and kinase JNK above were due to the use of DHA. cytometry flow, Western Blot and other testing strategies. Studies continue to show that increased expression of superoxide dismutase 3 (SOD3), as a growth factor, may induce AP-1 activation. The team of Professor Qijun Chen confirmed that DHA induced by the immune cells and activated the JNK-AP-1 axis was inhibited in SOD3-knockout mice.

“Here, we found that the enhancement of SOD3 is associated with the activation of JNK and AP-1 phosphorylation and the immune system in response to DHA treatment. Together, our data suggest that the immune function of DHA intervenes by activating the SOD3-JNK-AP-1 axis, “said Professor Qijun Chen.

Finally, their study compares the natural state of the splenic immune system in response to DHA treatment which forms the basis for a deeper understanding of the DHA immune system.

The article was published in Chinese Life Sciences.


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Learn more:
Yiwei Zhang et al, Dihydroartemisinin is effective in regulating the immune system of cells through the SOD3-JNK-AP-1 axis, Chinese Life Sciences (2022). DOI: 10.1007 / s11427-021-2061-7

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