Effect of M2-like macrophages of the injured-kidney cortex on kidney cancer progression

Taisuke Ishii, Imari Mimura, Koji Nagaoka, Akihiro Naito, Takehito Sugasawa, Ryohei Kuroda, Daisuke Yamada, Yasuharu Kanki, Haruki Kume, Tetsuo Ushiku, Kazuhiro Kakimi, Tetsuhiro Tanaka, Masaomi Nangaku


1 被引用数 (Scopus)


Chronic kidney disease (CKD) affects kidney cancer patients’ mortality. However, the underlying mechanism remains unknown. M2-like macrophages have pro-tumor functions, also exist in injured kidney, and promote kidney fibrosis. Thus, it is suspected that M2-like macrophages in injured kidney induce the pro-tumor microenvironment leading to kidney cancer progression. We found that M2-like macrophages present in the injured kidney promoted kidney cancer progression and induced resistance to anti-PD1 antibody through its pro-tumor function and inhibition of CD8+ T cell infiltration. RNA-seq revealed Slc7a11 was upregulated in M2-like macrophages. Inhibition of Slc7a11 with sulfasalazine inhibited the pro-tumor function of M2-like macrophages and synergized with anti-PD1 antibody. Moreover, SLC7A11-positive macrophages were associated with poor prognosis among kidney cancer patients. Collectively, this study dissects the characteristic microenvironment in the injured kidney that contributed to kidney cancer progression and anti-PD1 antibody resistance. This insight offers promising combination therapy with anti-PD1 antibody and macrophage targeted therapy.

ジャーナルCell Death Discovery
出版ステータスPublished - 12月 2022

ASJC Scopus subject areas

  • 免疫学
  • 細胞および分子神経科学
  • 細胞生物学
  • 癌研究


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