Regular ArticleTumor Necrosis Factor-α Plays a Central Role in Interleukin-2-Induced Pulmonary Vascular Leak and Lymphocyte Accumulation
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Induction of vascular leak syndrome by tumor necrosis factor-alpha alone
2015, Biomedicine and PharmacotherapyCitation Excerpt :Also, TNF-α has been regarded as one of the important factors in IL-2-induced VLS [17]. IL-2 induced TNF-α expression was observed in immune cells [11,21], tissues [22], and serum [10,23,24]. Moreover, anti-TNF-α monoclonal antibodies (mAb) treated group survived longer but eventually died in mice treated with high-dose-IL-2 [25].
Increased ICAM-1 expression causes endothelial cell leakiness, cytoskeletal reorganization and junctional alterations
2007, Journal of Investigative DermatologyCitation Excerpt :Intradermal injection of TNF causes adhesion molecule expression and local extravasation of leukocytes (Munro et al., 1989). TNF is also sufficient to produce vascular leak in vivo, for example during cytokine-based immunotherapy (Cotran et al., 1988; Lo et al., 1992; Dubinett et al., 1994; Thom et al., 1995). In cell culture, TNF causes EC to undergo cytoskeletal and junctional rearrangements and shape changes (Stolpen et al., 1986; Blum et al., 1997).
Capillary leak syndrome in children with C4A-deficiency undergoing cardiac surgery with cardiopulmonary bypass: A double-blind, randomised controlled study
2005, LancetCitation Excerpt :Patients with capillary leak syndrome had significantly decreased plasma protein concentrations and developed postoperative generalised oedema, which were also the criteria used to define the syndrome in other studies.13–15 IL6, IL8, and TNFα are important inflammatory mediators,19,25,26 and have been reported to increase microvascular permeability.27–29 The amounts of these inflammatory mediators in the C4A-rich group in the present study are similar to those reported by Tassani and colleagues,8 who suggested that the inflammatory response induced by these concentrations of inflammatory mediators is not sufficient to induce capillary leak syndrome.
Transplantation of IL-2-transduced murine bone marrow is associated with dose-dependent toxicity
2000, Experimental HematologyModulation of lung local immune responses by oral administration of a herbal medicine Sho-saiko-to
2000, International Journal of ImmunopharmacologyCitation Excerpt :Various studies demonstrate pro-inflammatory effect of TNF-α and anti-inflammatory one by IL-6. In some acute lung injury models, the neutralization of intrinsic IL-6 activity [9,50,60,65] or administration of recombinant TNF-α [16,22,60] was noted here to exacerbate lung injury and neutralization of TNF-α activity [1,10,18,43,49,61] or administration of recombinant IL-6 [9,60] to ameliorate injury. In the present study, SST which increases IL-6 levels ameliorated the later phase of lung injury induced by intranasal administration of LPS.