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Liver Failure and Defective Hepatocyte Regeneration in Interleukin-6-Deficient Mice
TLDR
Treatment ofIL-6-deficient mice with a single preoperative dose of IL-6 returned STAT3 binding, gene expression, and hepatocyte proliferation to near normal and prevented liver damage, establishing that IL- 6 is a critical component of the regenerative response.
Interleukin 6 Is Required for the Development of Collagen-induced Arthritis
TLDR
It is suggested that IL-6 receptor antagonists might be beneficial for the treatment of RA, accompanied by a reduced antibody response to type II collagen and the absence of inflammatory cells and tissue damage in knee joints.
Interleukin 6 causes growth impairment in transgenic mice through a decrease in insulin-like growth factor-I. A model for stunted growth in children with chronic inflammation.
TLDR
In NSE/hIL-6 transgenic mice, circulating IGF-I levels were significantly lower than those of nontransgenic littermates; on the contrary, the distribution of growth hormone pituitary cells, as well as circulating growth hormone levels, were normal.
Interleukin‐6 deficient mice are protected from bone loss caused by estrogen depletion.
TLDR
It is reported that IL‐6 deficient mice generated by gene targeting are viable and do not present any evident phenotypic abnormality, and analysis of bone metabolism revealed a specific bone phenotype, indicating that IL-6 plays an important role in the local regulation of bone turnover.
The induction of antibody production by IL-6 is indirectly mediated by IL-21 produced by CD4+ T cells
TLDR
It is shown that IL-6 is sufficient and necessary to induce IL-21 production by naive and memory CD4+ T cells upon T cell receptor stimulation and could be a potential coadjuvant to enhance humoral immunity.
Interleukin-6-Induced STAT3 and AP-1 Amplify Hepatocyte Nuclear Factor 1-Mediated Transactivation of Hepatic Genes, an Adaptive Response to Liver Injury
TLDR
The results demonstrate that the two classes of transcription factors, growth induced (STAT3 and AP-1) and tissue specific (HNF-1), can interact as an adaptive response to liver injury to amplify expression of hepatic genes important for the homeostatic response during organ repair.
Elevated levels of interleukin-6 in unstable angina.
TLDR
It is demonstrated that raised levels of interleukin-6 are common in unstable angina, correlate with C-reactive protein, and are associated with prognosis, thus confirming the importance of the cytokine pathway for the production by the liver of acute-phase proteins and strengthening the role of inflammation in this syndrome.
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