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IL-33 Promotes the Development of Colorectal Cancer Through Inducing
Tumor-Infiltrating ST2L(+) Regulatory T Cells in Mice
#MMPMID29950152
Zhou Y
; Ji Y
; Wang H
; Zhang H
; Zhou H
Technol Cancer Res Treat
2018[Jan]; 17
(?): 1533033818780091
PMID29950152
show ga
Colorectal cancer, one of the most commonly diagnosed and lethal cancers
worldwide, is accompanied by the disorders of immune system. However, the
underlying mechanism is still not fully understood. In this study, our goal was
to determine whether interleukin 33 promotes tumorigenesis and progression of
colorectal cancer through increased recruitment of tumor-infiltrating ST2(+)
regulatory T cells in CT26 tumor-bearing mice. We found that the mRNA or protein
levels of interleukin 33, soluble ST2, and membrane ST2 were elevated in the
serum of tumor-bearing mice when compared to WT mice. The mRNA levels of
interleukin 33, soluble ST2, and membrane ST2 were also elevated in the tissue of
tumor-bearing mice when compared to surrounding nontumor muscular tissues. In
addition, the frequency of ST2L(+) regulatory T cells was significantly increased
in both tumor tissue and spleen of tumor-bearing mice. Higher protein levels of
interleukin-4, -10, and -13 were also observed in the serum or the tumor
homogenates of tumor-bearing mice. We found exogenously administered recombinant
mouse interleukin 33 promoted tumor size and induced tumor-infiltrating ST2L(+)
regulatory T cells in tumor-bearing mice while neutralizing interleukin-33 or
ST2L inhibited tumor size and decreased ST2L(+) regulatory T cells. Furthermore,
ST2L(+) regulatory T cells from tumor tissue were also able to suppress
CD4(+)CD25(-)T cell proliferation and interferon ? production. Altogether, our
findings demonstrate the critical roles of interleukin 33 in promoting colorectal
cancer development through inducing tumor-infiltrating ST2L(+) regulatory T
cells, and inhibition of interleukin-33/ST2L signaling maybe a potential target
for the prevention of colorectal cancer.
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