We are analyzing https://link.springer.com/article/10.1186/ar1916.

Title:
Interleukin-6: discovery of a pleiotropic cytokine | Arthritis Research & Therapy
Description:
In the late 1960s, the essential role played by T cells in antibody production was reported. This led to our hypothesis that certain molecules would have to be released from T cells to effect the stimulation of B cells. This hypothesis was shown to be true. There were certain factors present in the culture supernatant of T cells that induced proliferation and differentiation of B cells. The factor that induced B cells to produce immunoglobulins was initially named B cell stimulatory factor-2. The cDNA encoding the human B cell stimulatory factor-2 was cloned in 1986. At the same time, IFN-β2 and a 26 kDa protein in the fibroblasts were independently cloned and found to be identical to B cell stimulatory factor-2. Later, a hybridoma/plasmacytoma growth factor and a hepatocyte stimulating factor were also proven to be the same molecule as B cell stimulatory factor-2. Various names were used for this single molecule because of its multiple biological activities, but these have all been unified and the molecule is now known as IL-6. Since the discovery of IL-6, rapid progress has been made in our understanding of IL-6 activities, the IL-6 receptor system and the IL-6 signal transduction mechanism. More importantly, it has been shown to be involved in a number of diseases such as rheumatoid arthritis and Castleman
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Topics {✒️}

granulocyte-macrophage colony-stimulating factor t-cell replacing factor monocyte-derived hepatocyte-stimulating factor granulocyte colony-stimulating factor hybridoma/plasmacytoma growth factor experimental autoimmune encephalomyelitis systemic juvenile arthritis janus activated kinase plasmacytoma/myeloma growth factor il-11-mediated signal transduction jak tyrosine kinase hapten-specific memory cells anti-il-6 receptor antibody anti-interleukin-6 monoclonal antibodies antigen-transformed endothelial cells carrier-specific helper cells type ii collagen anti-il-6 antibody demonstrated including osteoclast formation hepatocyte stimulating factor il-6 knockout mice collagen-induced arthritis acute-phase responses privacy choices/manage cookies antigen-induced arthritis [33–35] antigen-induced arthritis accumulated basic research interleukin-6-deficient mice springer semin immunopathol common receptor component cell stimulatory factor-2 cell stimulatory factor hepatocyte stimulatory factor il-6-deficient mice anti-peptide antibody published research resulting shared signaling pathways article number s2 pristane-treated mice socs-1 deficient mice enhancing soluble factor osteoclastlike cell formation strong stimulatory effect ciliary neurotrophic factor jak-stat pathways cytokines including il-6 cell growth factors anti-il-6 strategies anti-il-6 treatments acute phase response

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         headline:Interleukin-6: discovery of a pleiotropic cytokine
         description:In the late 1960s, the essential role played by T cells in antibody production was reported. This led to our hypothesis that certain molecules would have to be released from T cells to effect the stimulation of B cells. This hypothesis was shown to be true. There were certain factors present in the culture supernatant of T cells that induced proliferation and differentiation of B cells. The factor that induced B cells to produce immunoglobulins was initially named B cell stimulatory factor-2. The cDNA encoding the human B cell stimulatory factor-2 was cloned in 1986. At the same time, IFN-β2 and a 26 kDa protein in the fibroblasts were independently cloned and found to be identical to B cell stimulatory factor-2. Later, a hybridoma/plasmacytoma growth factor and a hepatocyte stimulating factor were also proven to be the same molecule as B cell stimulatory factor-2. Various names were used for this single molecule because of its multiple biological activities, but these have all been unified and the molecule is now known as IL-6. Since the discovery of IL-6, rapid progress has been made in our understanding of IL-6 activities, the IL-6 receptor system and the IL-6 signal transduction mechanism. More importantly, it has been shown to be involved in a number of diseases such as rheumatoid arthritis and Castleman's disease. When taking into account all the accumulated basic research on the various aspects of this molecule, it appeared that blocking the activity of IL-6 was a feasible, new therapeutic approach for chronic inflammatory diseases.
         datePublished:2006-07-28T00:00:00Z
         dateModified:2006-07-28T00:00:00Z
         pageStart:1
         pageEnd:6
         sameAs:https://doi.org/10.1186/ar1916
         keywords:
            Tocilizumab
            Cardiac Myxoma
            Janus Family Tyrosine Kinase
            Systemic Onset Juvenile Arthritis
            Rheumatology
            Orthopedics
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ScholarlyArticle:
      headline:Interleukin-6: discovery of a pleiotropic cytokine
      description:In the late 1960s, the essential role played by T cells in antibody production was reported. This led to our hypothesis that certain molecules would have to be released from T cells to effect the stimulation of B cells. This hypothesis was shown to be true. There were certain factors present in the culture supernatant of T cells that induced proliferation and differentiation of B cells. The factor that induced B cells to produce immunoglobulins was initially named B cell stimulatory factor-2. The cDNA encoding the human B cell stimulatory factor-2 was cloned in 1986. At the same time, IFN-β2 and a 26 kDa protein in the fibroblasts were independently cloned and found to be identical to B cell stimulatory factor-2. Later, a hybridoma/plasmacytoma growth factor and a hepatocyte stimulating factor were also proven to be the same molecule as B cell stimulatory factor-2. Various names were used for this single molecule because of its multiple biological activities, but these have all been unified and the molecule is now known as IL-6. Since the discovery of IL-6, rapid progress has been made in our understanding of IL-6 activities, the IL-6 receptor system and the IL-6 signal transduction mechanism. More importantly, it has been shown to be involved in a number of diseases such as rheumatoid arthritis and Castleman's disease. When taking into account all the accumulated basic research on the various aspects of this molecule, it appeared that blocking the activity of IL-6 was a feasible, new therapeutic approach for chronic inflammatory diseases.
      datePublished:2006-07-28T00:00:00Z
      dateModified:2006-07-28T00:00:00Z
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      pageEnd:6
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         Cardiac Myxoma
         Janus Family Tyrosine Kinase
         Systemic Onset Juvenile Arthritis
         Rheumatology
         Orthopedics
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            name:Tadamitsu Kishimoto
            affiliation:
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      name:Osaka University
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