We have previously shown that while IVIG-IL protected mice against lethal doses of WNV, the low exposure to the virus of US donors resulted in no effect of IVIG produced from the plasma of US donors (IVIG-US) [ 13, 18].
As a control, IL-6 involvement in cell resistance was only observed in two cases in our study: 1) IL-6 protected U937 cells from radiations; this protection was non-significantly decreased by an anti-IL-6 (Figure S4A); 2) anti-IL-6 antibody was able to increase dexamethasone-induced cytotoxic effects on Daudi cells, alone or in association with doxorubicin (Figure S4B).
IL-3 protected against 8-Cl-cAMP induced cytotoxicity suggesting that IL-3 can activate p210 bcr/abl independent survival pathways.
In contrast, following schistosome infection, IL-13 induces a detrimental hepatic fibrosis, while IL-4 protects against endotoxemia.
Supporting the concept that IL-1 drives cartilage destruction are the findings of a recent study by Schett's group in which crossing the arthritic human TNF transgenic (hTNFtg) mice with mice deficient in IL-1α and IL-1β protected against cartilage erosion without affecting synovial inflammation [ 75].
The column heater was set at 30 °C and a GenesisLightn C18 column (100×2.1 mm, 4 μm) (Grace, IL, USA) protected by an Acquity-LC column in-line filter unit (0.2 μm in-line frit) was used for separation of metabolites.
In vitro, IL-6 protects M1 myeloid leukemia cells against apoptosis induced by cytotoxic drugs [18], but also renal carcinoma cells (RCC), erythro-leukemic cells and myeloid leukemia cells against the effects of cisplatin [16], [19], [20].
Specifically, IL-6 protects against Fas-induced apoptosis in IPF fibroblasts, and yet it enhances the apoptotic effect of Fas in normal fibroblasts.
Furthermore and as first demonstrated for hepatocytes/the liver by the research group of Bin Gao, IL-22 protects IL-22R1-carrying cells from damage [ 3].
Polarized Th-2 immune activation associated with helminthic infection modifies cytokine profiles, whereby anti-inflammatory IL-4, IL-10 and IL-13 protect vessel walls from oxidized LDL-induced monocyte injury in the endothelium, and downregulate fibrinogen synthesis [58].
In vitro experiments showed that IL-2 protected Foxp3+ but not Foxp3− cells cells from apoptosis by increasing the expression of Bcl-2, which was mediated by STAT5.
