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Publication : Interleukin-34 drives macrophage polarization to the M2 phenotype in autoimmune hepatitis.

First Author  Liu Y Year  2019
Journal  Pathol Res Pract Volume  215
Issue  8 Pages  152493
PubMed ID  31201067 Mgi Jnum  J:289284
Mgi Id  MGI:6434947 Doi  10.1016/j.prp.2019.152493
Citation  Liu Y, et al. (2019) Interleukin-34 drives macrophage polarization to the M2 phenotype in autoimmune hepatitis. Pathol Res Pract 215(8):152493
abstractText  BACKGROUND: Autoimmune hepatitis is a chronic inflammatory disease, the abnormal immunological function is the main pathogenesis. Interleukin-34 is a newly identified cytokine that shares the same receptor as colony stimulating factor-1. METHODS: We used interleukin-34 knockout and wild-type mice in a Con A-induced hepatitis model and cocultured RAW264.7 macrophage cells with interleukin-34. We then detected associated inflammatory cytokine and chemokine levels to elucidate the role of interleukin-34. RESULTS: In this study, we found that the loss of interleukin-34 resulted in higher sensitivity to Con A-induced hepatitis. RAW264.7 macrophage cells were able to differentiate to the M2 phenotype upon interleukin-34 stimulation. CONCLUSIONS: We conclude that interleukin-34 may protect the liver from Con A-mediated hepatitis by driving M2 macrophage polarization and suppressing inflammation.
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