Interleukin-6 and chronic inflammation

[1]  J. Scheller,et al.  IL-6 transsignaling: the in vivo consequences. , 2005, Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research.

[2]  S. Rose-John,et al.  Soluble IL-6 Receptor Governs IL-6 Activity in Experimental Arthritis: Blockade of Arthritis Severity by Soluble Glycoprotein 130 , 2003, The Journal of Immunology.

[3]  A. Mantovani,et al.  IL-6: a regulator of the transition from neutrophil to monocyte recruitment during inflammation. , 2003, Trends in immunology.

[4]  Takafumi Yoshida,et al.  Induction of the cytokine signal regulator SOCS3/CIS3 as a therapeutic strategy for treating inflammatory arthritis. , 2001, The Journal of clinical investigation.

[5]  P. Bongrand,et al.  The IL-6-Soluble IL-6Rα Autocrine Loop of Endothelial Activation as an Intermediate Between Acute and Chronic Inflammation: an Experimental Model Involving Thrombin , 2001, The Journal of Immunology.

[6]  T. S. Wilkinson,et al.  Il-6 and its soluble receptor orchestrate a temporal switch in the pattern of leukocyte recruitment seen during acute inflammation. , 2001, Immunity.

[7]  J. Lord,et al.  Fibroblasts regulate the switch from acute resolving to chronic persistent inflammation. , 2001, Trends in immunology.

[8]  S. Akira,et al.  Cis3/Socs3/Ssi3 Plays a Negative Regulatory Role in Stat3 Activation and Intestinal Inflammation , 2001, The Journal of experimental medicine.

[9]  鈴木 飛鳥 CIS3/SOCS3/SSI3 plays a negative regulatory role in STAT3 activation and intestinal inflammation , 2001 .

[10]  T. Kishimoto,et al.  IL-6 Is Required for the Development of Th1 Cell-Mediated Murine Colitis1 , 2000, The Journal of Immunology.

[11]  M. Neurath,et al.  Blockade of interleukin 6 trans signaling suppresses T-cell resistance against apoptosis in chronic intestinal inflammation: Evidence in Crohn disease and experimental colitis in vivo , 2000, Nature Medicine.

[12]  T. Yoshimura,et al.  MCP‐1 is selectively expressed in the late phase by cytokine‐stimulated human neutrophils: TNF‐α plays a role in maximal MCP‐1 mRNA expression , 1999, Journal of leukocyte biology.

[13]  I. Kushner,et al.  Acute-phase proteins and other systemic responses to inflammation. , 1999, The New England journal of medicine.

[14]  T. Kishimoto,et al.  Blockage of interleukin-6 receptor ameliorates joint disease in murine collagen-induced arthritis. , 1998, Arthritis and rheumatism.

[15]  R. Steinman,et al.  Differentiation of monocytes into dendritic cells in a model of transendothelial trafficking. , 1998, Science.

[16]  Y. Saeki,et al.  Interleukin 6 plays a key role in the development of antigen-induced arthritis. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[17]  G. Kollias,et al.  Interleukin 6 Is Required for the Development of Collagen-induced Arthritis , 1998, The Journal of experimental medicine.

[18]  M. Jordana,et al.  IL-6 is an antiinflammatory cytokine required for controlling local or systemic acute inflammatory responses. , 1998, The Journal of clinical investigation.

[19]  J. Ross,et al.  Interleukin-8 can mediate acute-phase protein production by isolated human hepatocytes. , 1997, American journal of physiology. Endocrinology and metabolism.

[20]  T. Vischer,et al.  Concentrations and origins of soluble interleukin 6 receptor-alpha in serum and synovial fluid. , 1997, The Journal of rheumatology.

[21]  C. Gabay,et al.  Interleukin 1 receptor antagonist (IL-1Ra) is an acute-phase protein. , 1997, The Journal of clinical investigation.

[22]  Y. Suzuki,et al.  Impaired resistance to the development of toxoplasmic encephalitis in interleukin-6-deficient mice , 1997, Infection and immunity.

[23]  S. Opal,et al.  Characterization of Early Cytokine Responses and an Interleukin (IL)-6–dependent Pathway of Endogenous Glucocorticoid Induction during Murine Cytomegalovirus Infection , 1997, The Journal of experimental medicine.

[24]  G. Ciliberto,et al.  Role of IL-6 and its soluble receptor in induction of chemokines and leukocyte recruitment. , 1997, Immunity.

[25]  J. Ross,et al.  Interleukin-8 can mediate acute-phase protein production by isolated human hepatocytes. , 1997, American journal of physiology. Endocrinology and metabolism.

[26]  C. Haslett,et al.  In vivo fate of the inflammatory macrophage during the resolution of inflammation: inflammatory macrophages do not die locally, but emigrate to the draining lymph nodes. , 1996, Journal of immunology.

[27]  V. Poli,et al.  Impaired neutrophil response and CD4+ T helper cell 1 development in interleukin 6-deficient mice infected with Candida albicans , 1996, The Journal of experimental medicine.

[28]  S. Dalrymple,et al.  Interleukin-6-deficient mice are highly susceptible to Listeria monocytogenes infection: correlation with inefficient neutrophilia , 1995, Infection and immunity.

[29]  M. Jordana,et al.  Adenovirus-mediated cytokine gene transfer at tissue sites. Overexpression of IL-6 induces lymphocytic hyperplasia in the lung. , 1994, Journal of immunology.

[30]  G. Fantuzzi,et al.  Defective inflammatory response in interleukin 6-deficient mice , 1994, The Journal of experimental medicine.

[31]  A. Husband,et al.  The role of interleukin-6 in mucosal IgA antibody responses in vivo. , 1994, Science.

[32]  R. Zinkernagel,et al.  Impaired immune and acute-phase responses in interleukin-6-deficient mice , 1994, Nature.

[33]  I. Kushner Regulation of the Acute Phase Response by Cytokines , 2015, Perspectives in biology and medicine.

[34]  W. Travis,et al.  Cellular mechanisms of the antitumor activity of recombinant IL-6 in mice. , 1992, Journal of immunology.

[35]  P. Horan,et al.  Kinetics of changes in peritoneal cell populations following acute inflammation. , 1989, Cellular immunology.

[36]  G. Downey,et al.  Monocyte retention and migration in pulmonary inflammation. Requirement for neutrophils. , 1988, Laboratory investigation; a journal of technical methods and pathology.

[37]  P. Lansdorp,et al.  Interferon beta 2/B-cell stimulatory factor type 2 shares identity with monocyte-derived hepatocyte-stimulating factor and regulates the major acute phase protein response in liver cells. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[38]  H. Colten,et al.  Molecular Biology of the Acute Phase Plasma Proteins , 1987 .

[39]  G. Majno,et al.  Acute inflammation. A review. , 1977, The American journal of pathology.

[40]  Marta C. Cohen,et al.  Acute Inflammation , 2018, Pathology of the Placenta.