@article{oai:nagasaki-u.repo.nii.ac.jp:00001535,
 author = {Miyakoda, Mana and Bayarsaikhan, Ganchimeg and Kimura, Daisuke and Akbari, Masoud and Udono, Heiichiro and Yui, Katsuyuki},
 journal = {Frontiers in Immunology},
 month = {Dec},
 note = {Adaptive immune responses are critical for protection against infection with Plasmodium parasites. The metabolic state dramatically changes in T cells during activation and the memory phase. Recent findings suggest that metformin, a medication for treating type-II diabetes, enhances T-cell immune responses
 by modulating lymphocyte metabolism. In this study, we investigated whether metformin could enhance anti-malaria immunity. Mice were infected with Plasmodium yoelii and administered metformin. Levels of parasitemia were reduced in treated mice compared with those in untreated mice, starting at ~2 weeks post-infection. The number of γδ T cells dramatically increased 
in the spleens of treated mice compared with that in untreated mice during the later phase of infection, while that of αβ T cells did not. The proportions of Vγ1+ and Vγ2+ γδ T cells increased, suggesting that activated cells were selectively expanded. However, these γδ T cells expressed inhibitory receptors and had severe defects in cytokine production, suggesting that they were in a state of exhaustion. Metformin was unable to rescue the cells from exhaustion at this stage.Depletion of γδ T cells with antibody treatment did not affect the reduction of parasitemia in metformin-treated mice, 
suggesting that the effect of metformin on the reduction of parasitemia was independent of γδ T cells., Frontiers in immunology, 9, 2942; 2018},
 title = {Metformin Promotes the Protection of Mice Infected With Plasmodium yoelii Independently of γδ T Cell Expansion},
 volume = {9},
 year = {2018}
}