1994
DOI: 10.1016/1043-4666(94)90058-2
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Soluble interleukin 2 receptors abrogate IL-2 induced activation of peripheral mononuclear cells

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Cited by 32 publications
(21 citation statements)
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“…Elevated sCD25 levels in the ascites of ovarian cancer patients and in the serum of breast cancer patients correlated with a low frequency of TILs, suggesting that sCD25 could inhibit antitumor immunosurveillance [52]. sCD25 suppresses IL-2-induced surface CD25 expression and T cell responses in vitro [30,31,[53][54][55]. Russell et al [56] reported that sCD25 can exacerbate experimental autoimmune encephalitis by acting as a decoy receptor that sequesters IL-2, eventually altering the balance between Th1/Th17 and Tregs.…”
Section: -Test) (F)mentioning
confidence: 99%
“…Elevated sCD25 levels in the ascites of ovarian cancer patients and in the serum of breast cancer patients correlated with a low frequency of TILs, suggesting that sCD25 could inhibit antitumor immunosurveillance [52]. sCD25 suppresses IL-2-induced surface CD25 expression and T cell responses in vitro [30,31,[53][54][55]. Russell et al [56] reported that sCD25 can exacerbate experimental autoimmune encephalitis by acting as a decoy receptor that sequesters IL-2, eventually altering the balance between Th1/Th17 and Tregs.…”
Section: -Test) (F)mentioning
confidence: 99%
“…20,22 Ourselves 19,23 and other investigators 24 previously demonstrated a marked increase of serum-soluble IL-2R (sIL-2R) in IL-2Ra þ leukemia. As sIL-2R competes with IL-2R on normal lymphocytes for the ligand, 25 IL2Ra on the cell surface of leukemia cells coupled to the increased sIL-2R could enhance leukemia progression by suppressing host antitumor immunity, [26][27][28] and this may be one possible explanation for the leukocytosis (leukemic cell proliferation) and the dismal clinical course of IL-2Ra þ ALL.…”
Section: Discussionmentioning
confidence: 99%
“…Whereas the plasma level of soluble IL-2R has been deemed to be a marker for T cell activation in ischemic heart disease (Simon et al, 2001), high levels of sIL-2R paradoxically reduce the relative risk of lesion instability, which is known to be associated with increased inflammatory activity in the plaque (Blum et al, 1995;Takeshita et al, 1997;Simon et al, 2001). Moreover, in vitro studies have evidenced the inhibition of IL-2-induced activation of peripheral mononuclear cells by sIL-2R (Zorn et al, 1994). Soluble IL-4-binding proteins are known to occur in mice (Fernandez-Botran and Vitetta, 1990) and humans (Fanslow et al, 1993).…”
Section: Neutralization Of Proinflammatory Interleukinsmentioning
confidence: 99%