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  • 1
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    BAFF inhibition attenuates fibrosis in scleroderma by modulating the regulatory and effector B cell balance (2018)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2018-07-12
    Description: Systemic sclerosis (SSc) is an autoimmune disease characterized by skin and lung fibrosis. More than 90% of patients with SSc are positive for autoantibodies. In addition, serum B cell activating factor (BAFF) level is correlated with SSc severity and activity. Thus, B cells are considered to play a pathogenic role in SSc. However, there are two opposing subsets: regulatory B cells (Bregs) and effector B cells (Beffs). Interleukin-10 (IL-10)–producing Bregs negatively regulate the immune response, while IL-6–producing Beffs positively regulate it. Therefore, a protocol that selectively depletes Beffs would represent a potent therapy for SSc. The aims of this study were to investigate the roles of Bregs and Beffs in SSc and to provide a scientific basis for developing a new treatment strategy targeting B cells. A bleomycin-induced scleroderma model was induced in mice with a B cell–specific deficiency in IL-6 or IL-10. We also examined whether BAFF regulates cytokine-producing B cells and its effects on the scleroderma model. IL-6–producing Beffs increased in number and infiltrated the inflamed skin in the scleroderma model. The skin and lung fibrosis was attenuated in B cell–specific IL-6–deficient mice, whereas B cell–specific IL-10–deficient mice showed more severe fibrosis. In addition, BAFF increased Beffs but suppressed Bregs. Furthermore, BAFF antagonist attenuated skin and lung fibrosis in the scleroderma model with reduction of Beffs but not of Bregs. The current study indicates that Beffs play a pathogenic role in the scleroderma model, while Bregs play a protective role. BAFF inhibition is a potential therapeutic strategy for SSc via alteration of B cell balance.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Induction of inflammatory arthropathy resembling rheumatoid arthritis in mice transgenic for HTLV-I (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-30
    Description: Human T cell leukemia virus type-I (HTLV-I) is the etiologic agent of adult T cell leukemia and has also been suggested to be involved in other diseases such as chronic arthritis or myelopathy. To elucidate pathological roles of the virus in disease, transgenic mice were produced that carry the HTLV-I genome. At 2 to 3 months of age, many of the mice developed chronic arthritis resembling rheumatoid arthritis. Synovial and periarticular inflammation with articular erosion caused by invasion of granulation tissues were marked. These observations suggest a possibility that HTLV-I is one of the etiologic agents of chronic arthritis in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwakura, Y -- Tosu, M -- Yoshida, E -- Takiguchi, M -- Sato, K -- Kitajima, I -- Nishioka, K -- Yamamoto, K -- Takeda, T -- Hatanaka, M -- New York, N.Y. -- Science. 1991 Aug 30;253(5023):1026-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medical Science, University of Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1887217" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/*genetics/pathology/physiopathology ; Genes, Viral ; Human T-lymphotropic virus 1/*genetics ; Inflammation ; Joints/pathology ; Mice ; Mice, Inbred Strains ; Mice, Transgenic ; RNA, Messenger/genetics ; Repetitive Sequences, Nucleic Acid ; Viral Envelope Proteins/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Control of TH17 cells occurs in the small intestine (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-07-19
    Description: Interleukin (IL)-17-producing T helper cells (T(H)17) are a recently identified CD4(+) T cell subset distinct from T helper type 1 (T(H)1) and T helper type 2 (T(H)2) cells. T(H)17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE), the mouse model for multiple sclerosis. The factors that are needed for the generation of T(H)17 cells have been well characterized. However, where and how the immune system controls T(H)17 cells in vivo remains unclear. Here, by using a model of tolerance induced by CD3-specific antibody, a model of sepsis and influenza A viral infection (H1N1), we show that pro-inflammatory T(H)17 cells can be redirected to and controlled in the small intestine. T(H)17-specific IL-17A secretion induced expression of the chemokine CCL20 in the small intestine, facilitating the migration of these cells specifically to the small intestine via the CCR6/CCL20 axis. Moreover, we found that T(H)17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory T(H)17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rT(H)17). These results identify mechanisms limiting T(H)17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of T(H)17 cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148838/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148838/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esplugues, Enric -- Huber, Samuel -- Gagliani, Nicola -- Hauser, Anja E -- Town, Terrence -- Wan, Yisong Y -- O'Connor, William Jr -- Rongvaux, Anthony -- Van Rooijen, Nico -- Haberman, Ann M -- Iwakura, Yoichiro -- Kuchroo, Vijay K -- Kolls, Jay K -- Bluestone, Jeffrey A -- Herold, Kevan C -- Flavell, Richard A -- DK45735/DK/NIDDK NIH HHS/ -- P30 DK045735/DK/NIDDK NIH HHS/ -- P30 DK045735-20/DK/NIDDK NIH HHS/ -- R01 HL061271/HL/NHLBI NIH HHS/ -- R01 HL062052/HL/NHLBI NIH HHS/ -- R21 HL104601/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Jul 17;475(7357):514-8. doi: 10.1038/nature10228.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. enric.esplugues@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21765430" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology/pharmacology ; Antigens, CD3/immunology ; CD4-Positive T-Lymphocytes/immunology/transplantation ; Cell Movement/drug effects ; Chemokine CCL20/immunology ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Female ; Gene Expression Profiling ; Gene Expression Regulation/immunology ; Influenza A virus/immunology ; Interleukin-17/immunology ; Intestine, Small/cytology/*immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Orthomyxoviridae Infections/immunology ; Receptors, CCR6/immunology ; Sepsis/immunology ; Staphylococcal Infections/immunology ; Th17 Cells/*immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Obesity-induced gut microbial metabolite promotes liver cancer through senescence secretome (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-06-28
    Description: Obesity has become more prevalent in most developed countries over the past few decades, and is increasingly recognized as a major risk factor for several common types of cancer. As the worldwide obesity epidemic has shown no signs of abating, better understanding of the mechanisms underlying obesity-associated cancer is urgently needed. Although several events were proposed to be involved in obesity-associated cancer, the exact molecular mechanisms that integrate these events have remained largely unclear. Here we show that senescence-associated secretory phenotype (SASP) has crucial roles in promoting obesity-associated hepatocellular carcinoma (HCC) development in mice. Dietary or genetic obesity induces alterations of gut microbiota, thereby increasing the levels of deoxycholic acid (DCA), a gut bacterial metabolite known to cause DNA damage. The enterohepatic circulation of DCA provokes SASP phenotype in hepatic stellate cells (HSCs), which in turn secretes various inflammatory and tumour-promoting factors in the liver, thus facilitating HCC development in mice after exposure to chemical carcinogen. Notably, blocking DCA production or reducing gut bacteria efficiently prevents HCC development in obese mice. Similar results were also observed in mice lacking an SASP inducer or depleted of senescent HSCs, indicating that the DCA-SASP axis in HSCs has key roles in obesity-associated HCC development. Moreover, signs of SASP were also observed in the HSCs in the area of HCC arising in patients with non-alcoholic steatohepatitis, indicating that a similar pathway may contribute to at least certain aspects of obesity-associated HCC development in humans as well. These findings provide valuable new insights into the development of obesity-associated cancer and open up new possibilities for its control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshimoto, Shin -- Loo, Tze Mun -- Atarashi, Koji -- Kanda, Hiroaki -- Sato, Seidai -- Oyadomari, Seiichi -- Iwakura, Yoichiro -- Oshima, Kenshiro -- Morita, Hidetoshi -- Hattori, Masahira -- Honda, Kenya -- Ishikawa, Yuichi -- Hara, Eiji -- Ohtani, Naoko -- England -- Nature. 2013 Jul 4;499(7456):97-101. doi: 10.1038/nature12347. Epub 2013 Jun 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cancer Biology, Cancer Institute, Japanese Foundation for Cancer Research, Koto-ku, Tokyo 135-8550, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23803760" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Bacteria/metabolism ; Bile Acids and Salts/metabolism ; Carcinoma, Hepatocellular/complications/etiology/metabolism/prevention & control ; *Cell Aging/drug effects ; Cells, Cultured ; Cytokines/metabolism/secretion ; DNA Damage/drug effects ; Deoxycholic Acid/blood/*metabolism ; Dietary Fats/adverse effects/pharmacology ; Disease Models, Animal ; Fatty Liver/complications/pathology ; Gastrointestinal Tract/drug effects/*metabolism/*microbiology ; Hepatic Stellate Cells/cytology/drug effects/metabolism/*secretion ; Humans ; Interleukin-1beta/deficiency ; Liver Neoplasms/complications/etiology/*metabolism/prevention & control ; Male ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease ; Obesity/chemically induced/*metabolism ; Phenotype ; Risk Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    RIP1-driven autoinflammation targets IL-1alpha independently of inflammasomes and RIP3 (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-05-28
    Description: The protein-tyrosine phosphatase SHP-1 has critical roles in immune signalling, but how mutations in SHP-1 cause inflammatory disease in humans remains poorly defined. Mice homozygous for the Tyr208Asn amino acid substitution in the carboxy terminus of SHP-1 (referred to as Ptpn6(spin) mice) spontaneously develop a severe inflammatory syndrome that resembles neutrophilic dermatosis in humans and is characterized by persistent footpad swelling and suppurative inflammation. Here we report that receptor-interacting protein 1 (RIP1)-regulated interleukin (IL)-1alpha production by haematopoietic cells critically mediates chronic inflammatory disease in Ptpn6(spin) mice, whereas inflammasome signalling and IL-1beta-mediated events are dispensable. IL-1alpha was also crucial for exacerbated inflammatory responses and unremitting tissue damage upon footpad microabrasion of Ptpn6(spin) mice. Notably, pharmacological and genetic blockade of the kinase RIP1 protected against wound-induced inflammation and tissue damage in Ptpn6(spin) mice, whereas RIP3 deletion failed to do so. Moreover, RIP1-mediated inflammatory cytokine production was attenuated by NF-kappaB and ERK inhibition. Together, our results indicate that wound-induced tissue damage and chronic inflammation in Ptpn6(spin) mice are critically dependent on RIP1-mediated IL-1alpha production, whereas inflammasome signalling and RIP3-mediated necroptosis are dispensable. Thus, we have unravelled a novel inflammatory circuit in which RIP1-mediated IL-1alpha secretion in response to deregulated SHP-1 activity triggers an inflammatory destructive disease that proceeds independently of inflammasomes and programmed necrosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3683390/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3683390/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lukens, John R -- Vogel, Peter -- Johnson, Gordon R -- Kelliher, Michelle A -- Iwakura, Yoichiro -- Lamkanfi, Mohamed -- Kanneganti, Thirumala-Devi -- AI101935/AI/NIAID NIH HHS/ -- AR056296/AR/NIAMS NIH HHS/ -- CA163507/CA/NCI NIH HHS/ -- R01 AI075118/AI/NIAID NIH HHS/ -- R01 AI101935/AI/NIAID NIH HHS/ -- R01 AR056296/AR/NIAMS NIH HHS/ -- R01 CA163507/CA/NCI NIH HHS/ -- England -- Nature. 2013 Jun 13;498(7453):224-7. doi: 10.1038/nature12174. Epub 2013 May 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23708968" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death ; Dermatitis/immunology/metabolism/pathology ; Disease Models, Animal ; Extremities/pathology ; Female ; Gene Deletion ; Humans ; *Inflammasomes/metabolism ; Inflammation/immunology/metabolism/pathology ; Interleukin-1alpha/deficiency/genetics/*metabolism/secretion ; Interleukin-1beta/metabolism ; Male ; Mice ; NF-kappa B/metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/deficiency/genetics/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/*metabolism ; Signal Transduction ; Wound Healing ; Wounds and Injuries/immunology/pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    The muscle protein Dok-7 is essential for neuromuscular synaptogenesis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-24
    Description: The formation of the neuromuscular synapse requires muscle-specific receptor kinase (MuSK) to orchestrate postsynaptic differentiation, including the clustering of receptors for the neurotransmitter acetylcholine. Upon innervation, neural agrin activates MuSK to establish the postsynaptic apparatus, although agrin-independent formation of neuromuscular synapses can also occur experimentally in the absence of neurotransmission. Dok-7, a MuSK-interacting cytoplasmic protein, is essential for MuSK activation in cultured myotubes; in particular, the Dok-7 phosphotyrosine-binding domain and its target in MuSK are indispensable. Mice lacking Dok-7 formed neither acetylcholine receptor clusters nor neuromuscular synapses. Thus, Dok-7 is essential for neuromuscular synaptogenesis through its interaction with MuSK.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada, Kumiko -- Inoue, Akane -- Okada, Momoko -- Murata, Yoji -- Kakuta, Shigeru -- Jigami, Takafumi -- Kubo, Sachiko -- Shiraishi, Hirokazu -- Eguchi, Katsumi -- Motomura, Masakatsu -- Akiyama, Tetsu -- Iwakura, Yoichiro -- Higuchi, Osamu -- Yamanashi, Yuji -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1802-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Regulation, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794080" target="_blank"〉PubMed〈/a〉
    Keywords: Agrin/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cell Differentiation ; Cell Line ; Down-Regulation ; Enzyme Activation ; Humans ; In Situ Hybridization ; Mice ; Molecular Sequence Data ; Motor Endplate/embryology/metabolism ; Muscle Denervation ; Muscle Fibers, Skeletal/cytology/metabolism ; Muscle Proteins/chemistry/genetics/*metabolism ; Muscle, Skeletal/embryology/*innervation/metabolism ; Mutation ; Neuromuscular Junction/*physiology ; Phosphorylation ; Protein Binding ; Protein Structure, Tertiary ; Receptor Aggregation ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Cholinergic/genetics/*metabolism ; Synapses/*physiology ; Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    TNF-  from inflammatory dendritic cells (DCs) regulates lung IL-17A/IL-5 levels and neutrophilia versus eosinophilia during persistent fungal infection (2011)
    National Academy of Sciences
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    Publication Date: 2011-03-14
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 8
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    Identification and functional characterization of paxillin as a target of protein tyrosine phosphatase receptor T (2010)
    National Academy of Sciences
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    Publication Date: 2010-01-21
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 9
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    Interleukin 18 together with interleukin 12 inhibits IgE production by induction of interferon-  production from activated B cells (1997)
    National Academy of Sciences
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    Publication Date: 1997-04-15
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 10
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    Pituitary adenylate cyclase-activating polypeptide (PACAP) decreases ischemic neuronal cell death in association with IL-6 (2006)
    National Academy of Sciences
    Details
    Publication Date: 2006-05-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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