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  • Cell Research
    innate and adaptive immune responses Jason R Dunkelberger and Wen Chao Song Institute for Translational Medicine and Therapeutics and Department of Pharmacology University of Pennsylvania School of Medicine 1254 BRB II III 421 Curie Blvd Philadelphia PA 19104 USA Correspondence Wen Chao Song Tel 215 573 6641 E mail Songwe upenn edu The complement system plays a crucial role in the innate defense against common pathogens Activation of complement leads to robust and efficient proteolytic cascades which terminate in opsonization and lysis of the pathogen as well as in the generation of the classical inflammatory response through the production of potent proinflammatory molecules More recently however the role of complement in the immune response has been expanded due to observations that link complement activation to adaptive immune responses It is now appreciated that complement is a functional bridge between innate and adaptive immune responses that allows an integrated host defense to pathogenic challenges As such a study of its functions allows insight into the molecular underpinnings of host pathogen interactions as well as the organization and orchestration of the host immune response This review attempts to summarize the roles that complement plays in both innate and adaptive immune responses and

    Original URL path: http://www.cell-research.com/arts.asp?id=588 (2016-02-14)
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  • Cell Research
    of Chinese Academy of Agricultural Sciences Harbin 150001 China 3 Institute of Microbiology Chinese Academy of Sciences Beijing 100101 China 4 State Key Laboratory for Disease Prevention and Control National Institute for Viral Disease Control and Prevention Chinese Center for Disease Control and Prevention Beijing 100050 China 5 Institute of Medical Sciences University of Tokyo Tokyo 108 8639 Japan Correspondence Yoshihiro Kawaoka E mail kawaokay svm vetmed wisc edu All known subtypes of influenza A viruses are maintained in wild waterfowl the natural reservoir of these viruses Influenza A viruses are isolated from a variety of animal species with varying morbidity and mortality rates More importantly influenza A viruses cause respiratory disease in humans with potentially fatal outcome Local or global outbreaks in humans are typically characterized by excess hospitalizations and deaths In 1997 highly pathogenic avian influenza viruses of the H5N1 subtype emerged in Hong Kong that transmitted to humans resulting in the first documented cases of human death by avian influenza virus infection A new outbreak started in July 2003 in poultry in Vietnam Indonesia and Thailand and highly pathogenic avian H5N1 influenza viruses have since spread throughout Asia and into Europe and Africa These viruses continue to

    Original URL path: http://www.cell-research.com/arts.asp?id=589 (2016-02-14)
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  • Cell Research
    71 IL 23 signaling enhances Th2 polarization and regulates allergic airway inflammation Juan Peng 1 2 3 Xuexian O Yang 1 Seon Hee Chang 1 Jiong Yang 2 3 and Chen Dong 1 1 Department of Immunology MD Anderson Cancer Center Houston TX 77030 USA 2 Department of Respiratory Diseases Renmin Hospital Wuhan University Wuhan 430060 China 3 Department of Respiratory Diseases Zhongnan Hospital Wuhan University Wuhan 430071 China Correspondence Chen Dong Xuexian O Yang Tel 713 563 3263 713 563 8926 E mail cdong mdanderson org xoyang mdanderson org IL 23 IL 17 axis is an important regulator in various inflammatory diseases However the role of IL 23 in allergic airway inflammation is not well understood In this study we show that in an allergen induced asthma model mice with transgenic overexpression of IL 23R exhibited increased airway infiltration of eosinophils and Th2 cytokine production whereas those deficient in IL 23 displayed reduced airway inflammation In vitro IL 23 IL 23R signaling promoted GATA 3 expression and enhanced Th2 cytokine expression Conversely in the absence of this signal Th2 cell differentiation was partially inhibited Therefore IL 23 signaling may regulate allergic asthma through modulation of Th2 cell differentiation Cell

    Original URL path: http://www.cell-research.com/arts.asp?id=590 (2016-02-14)
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  • Cell Research
    D Arkwright 1 2 Francesca Luchetti 2 3 Julien Tour 2 Charlotte Roberts 2 Rahna Ayub 2 Ana P Morales 2 José J Rodríguez 2 Andrew Gilmore 2 Barbara Canonico 3 Stefano Papa 3 and Mauro Degli Esposti 2 1 University of Manchester Royal Manchester Children s Hospital Manchester 2 Faculty of Life Sciences University of Manchester Oxford Road Manchester M13 9PT United Kingdom 3 Department of Human Environmental and Nature Science University of Urbino Italy Correspondence Mauro Degli Esposti Tel 44 1612755447 E mail mauro esposti manchester ac uk The Fas CD95 surface receptor mediates rapid death of various cell types including autoreactive T cells with the potential for triggering autoimmunity Here we present novel aspects of Fas signalling that define a social dimension to receptor induced apoptosis Fas stimulation rapidly induces extensive membrane nanotube formation between neighbouring T cells This is critically dependent on Rho GTPases but not on caspase activation Bidirectional transfer of membrane and cytosolic elements including active caspases can be observed to occur via these nanotubes Nanotube formation and intercellular exchanges of death signals are defective in T lymphocytes from patients with autoimmune lymphoproliferative syndrome harbouring mutations in the Fas receptor We conclude that nanotube

    Original URL path: http://www.cell-research.com/arts.asp?id=591 (2016-02-14)
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  • Cell Research
    College of Medicine Temple TX 76504 USA 3 Department of Medicine Division of Gastroenterology Hepatology and Nutrition Stritch School of Medicine Loyola University Chicago Maywood IL 60153 USA 4 Hines Veterans Affairs Medical Center Hines IL 60141 USA Correspondence Ajay Rana Tel 1 708 216 5761 E mail arana lumc edu Mixed lineage kinase 3 MLK3 is a mitogen activated protein kinase kinase kinase that is activated by tumor necrosis factor α TNF α and specifically activates c Jun N terminal kinase JNK on TNF α stimulation The mechanism by which TNF α activates MLK3 is still not known TNF receptor associated factors TRAFs are adapter molecules that are recruited to cytoplasmic end of TNF receptor and mediate the downstream signaling including activation of JNK Here we report that MLK3 associates with TRAF2 TRAF5 and TRAF6 however only TRAF2 can significantly induce the kinase activity of MLK3 The interaction domain of TRAF2 maps to the TRAF domain and for MLK3 to its C terminal half amino acids 511 847 Endogenous TRAF2 and MLK3 associate with each other in response to TNF α treatment in a time dependent manner The association between MLK3 and TRAF2 mediates MLK3 activation and competition with

    Original URL path: http://www.cell-research.com/arts.asp?id=592 (2016-02-14)
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  • Cell Research
    Li Haifeng Liu Chao Zheng Hongbin Ji and Xiaolong Liu Laboratory of Molecular Cell Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China Correspondence Xiaolong Liu Tel 86 21 54921176 E mail liux sibs ac cn LKB1 is a serine threonine kinase that directly activates the energy sensor AMP activated protein kinase AMPK in response to bioenergetic stress and mainly acts as a tumor suppressor that controls cell polarity and proliferation Although LKB1 is expressed in multiple tissues including the thymus and the spleen its roles in T cell development and function remain unknown Here we show that T cell specific deletion of LKB1 resulted in reduced survival of double positive DP thymocytes and impaired generation of both CD4 and CD8 single positive thymocytes Disruption of LKB1 not only prevented the activation of AMPK but also impaired the expression of anti apoptotic protein Bcl XL Importantly ectopic expression of either Bcl XL or the constitutively active AMPK mutant significantly rescued DP thymocytes from LKB1 deficiency induced cell death Moreover ectopic expression of the constitutively active AMPK mutant was found to restore the expression of Bcl XL in LKB1 deficient DP

    Original URL path: http://www.cell-research.com/arts.asp?id=593 (2016-02-14)
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  • Cell Research
    109 112 Evidence for the involvement of ActA in maturation of the Listeria monocytogenes phagosome Mathilde A Poussin 1 2 and Howard Goldfine 1 1 Department of Microbiology University of Pennsylvania School of Medicine Philadelphia PA 19104 6076 USA 2 Current address Ovarian Cancer Research Center 421 Curie Boulevard Room 1326 1328A BRB II III University of Pennsylvania School of Medicine Philadelphia PA 19104 USA Correspondence Howard Goldfine Tel 1

    Original URL path: http://www.cell-research.com/arts.asp?id=594 (2016-02-14)
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  • Cell Research

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    Original URL path: /artsmore1.asp?id=41 (2016-02-14)




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