TY - JOUR
T1 - Interleukin-33 augments Treg cell levels
T2 - A flaw mechanism in atherosclerosis
AU - Wasserman, Asaf
AU - Ben-Shoshan, Jeremy
AU - Entin-Meer, Michal
AU - Maysel-Auslender, Sofia
AU - Guzner-Gur, Hanan
AU - Keren, Gad
PY - 2012/10
Y1 - 2012/10
N2 - Background: Atherosclerosis is a well-established inflammatory disease in which T helper 1 (Th1) cells play a key role. Regulatory T (Treg) cells drive a shift from Th1 to Th2 response and were shown to be reduced in atherosclerosis. ST2/interleukin (IL)-33 signal was found to promote Th2 response, attenuating atherosclerotic plaque progression. Objectives: To evaluate the effect of IL-33 on Treg cell number. Methods: We employed flow cytometry to determine Treg cell number, as well as ST2 levels, among splenocytes of C57BL/6J vs ApoE-/- mice. Soluble ST2 (sST2) levels were detected by enzyme-linked immunosorbent assay. Results: IL-33 contributed to an increase in Treg cells, but this association was attenuated in ApoE knockout (ApoE-/-) atherosclerotic mice. As a possible mechanism we demonstrated a reduction in the levels of CD4+ST2+ cells by flow cytometry, which is cotemporary to the previously described decrease in Treg cells in ApoE-/- mice. Additionally, the serum level of the soluble ST2 (sST2) decoy receptor was higher in ApoE-/- mice than in control animals. Conclusions: Our results suggest that a repressed ST2/IL-33 signaling may contribute to the decrease in Treg cells observed in atherosclerosis.
AB - Background: Atherosclerosis is a well-established inflammatory disease in which T helper 1 (Th1) cells play a key role. Regulatory T (Treg) cells drive a shift from Th1 to Th2 response and were shown to be reduced in atherosclerosis. ST2/interleukin (IL)-33 signal was found to promote Th2 response, attenuating atherosclerotic plaque progression. Objectives: To evaluate the effect of IL-33 on Treg cell number. Methods: We employed flow cytometry to determine Treg cell number, as well as ST2 levels, among splenocytes of C57BL/6J vs ApoE-/- mice. Soluble ST2 (sST2) levels were detected by enzyme-linked immunosorbent assay. Results: IL-33 contributed to an increase in Treg cells, but this association was attenuated in ApoE knockout (ApoE-/-) atherosclerotic mice. As a possible mechanism we demonstrated a reduction in the levels of CD4+ST2+ cells by flow cytometry, which is cotemporary to the previously described decrease in Treg cells in ApoE-/- mice. Additionally, the serum level of the soluble ST2 (sST2) decoy receptor was higher in ApoE-/- mice than in control animals. Conclusions: Our results suggest that a repressed ST2/IL-33 signaling may contribute to the decrease in Treg cells observed in atherosclerosis.
KW - Apolipoprotein E (ApoE)
KW - Inflammation
KW - Interleukin-33 (IL-33)
KW - ST2
KW - Treg cells
UR - http://www.scopus.com/inward/record.url?scp=84868216186&partnerID=8YFLogxK
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AN - SCOPUS:84868216186
SN - 1565-1088
VL - 14
SP - 620
EP - 623
JO - Israel Medical Association Journal
JF - Israel Medical Association Journal
IS - 10
ER -