Novel role for IL-22 in protection during chronic Mycobacterium tuberculosis HN878 infection

[1]  E. Mohammadi,et al.  Barriers and facilitators related to the implementation of a physiological track and trigger system: A systematic review of the qualitative evidence , 2017, International journal for quality in health care : journal of the International Society for Quality in Health Care.

[2]  M. V. D. van den Brink,et al.  Interleukin-22: immunobiology and pathology. , 2015, Annual review of immunology.

[3]  S. Khader,et al.  Chemokines in tuberculosis: the good, the bad and the ugly. , 2014, Seminars in immunology.

[4]  J. Kolls,et al.  Unexpected Role for IL-17 in Protective Immunity against Hypervirulent Mycobacterium tuberculosis HN878 Infection , 2014, PLoS pathogens.

[5]  Xinchun Chen,et al.  Anti-tuberculosis treatment enhances the production of IL-22 through reducing the frequencies of regulatory B cell. , 2014, Tuberculosis.

[6]  P. Barnes,et al.  Interleukin 22 inhibits intracellular growth of Mycobacterium tuberculosis by enhancing calgranulin A expression. , 2014, The Journal of infectious diseases.

[7]  M. Selman,et al.  S100A8/A9 proteins mediate neutrophilic inflammation and lung pathology during tuberculosis. , 2013, American journal of respiratory and critical care medicine.

[8]  Kevin J. McHugh,et al.  IL-22 is essential for lung epithelial repair following influenza infection. , 2013, American Journal of Pathology.

[9]  C. Dye,et al.  Prospects for tuberculosis elimination. , 2013, Annual review of public health.

[10]  M. Kaplan,et al.  Innate Stat3-mediated induction of the antimicrobial protein Reg3γ is required for host defense against MRSA pneumonia , 2013, The Journal of experimental medicine.

[11]  J. Renauld,et al.  IL-22 Is Mainly Produced by IFNγ-Secreting Cells but Is Dispensable for Host Protection against Mycobacterium tuberculosis Infection , 2013, PloS one.

[12]  M. Selman,et al.  CXCR5⁺ T helper cells mediate protective immunity against tuberculosis. , 2013, The Journal of clinical investigation.

[13]  G. Maartens,et al.  Role of the Interleukin 10 Family of Cytokines in Patients With Immune Reconstitution Inflammatory Syndrome Associated With HIV Infection and Tuberculosis , 2013, The Journal of infectious diseases.

[14]  P. Barnes,et al.  NK1.1+ Cells and IL-22 Regulate Vaccine-Induced Protective Immunity against Challenge with Mycobacterium tuberculosis , 2012, The Journal of Immunology.

[15]  W. Ouyang,et al.  IL-22 from conventional NK cells is epithelial regenerative and inflammation protective during influenza infection , 2012, Mucosal Immunology.

[16]  J. Ernst,et al.  Dynamic Roles of Type I and Type II IFNs in Early Infection with Mycobacterium tuberculosis , 2012, The Journal of Immunology.

[17]  S. Pandey,et al.  Comparison of interferon‐γ‐, interleukin (IL)‐17‐ and IL‐22‐expressing CD4 T cells, IL‐22‐expressing granulocytes and proinflammatory cytokines during latent and active tuberculosis infection , 2012, Clinical and experimental immunology.

[18]  N. Scarmeas,et al.  The good, bad, and ugly? , 2012, Neurology.

[19]  A. Diacon,et al.  Predominance of interleukin-22 over interleukin-17 at the site of disease in human tuberculosis , 2011, Tuberculosis.

[20]  J. Blanchard,et al.  Reactivation of latent tuberculosis in rhesus macaques by coinfection with simian immunodeficiency virus , 2011, Journal of medical primatology.

[21]  G. Zeng,et al.  Membrane-Bound IL-22 after De Novo Production in Tuberculosis and Anti-Mycobacterium tuberculosis Effector Function of IL-22+ CD4+ T Cells , 2011, The Journal of Immunology.

[22]  Mingxia Zhang,et al.  An SNP selection strategy identified IL-22 associating with susceptibility to tuberculosis in Chinese , 2011, Scientific reports.

[23]  J. Kolls,et al.  IL-23 Is Required for Long-Term Control of Mycobacterium tuberculosis and B Cell Follicle Formation in the Infected Lung , 2011, The Journal of Immunology.

[24]  J. Kolls,et al.  The role of Th17 cytokines in primary mucosal immunity. , 2010, Cytokine & growth factor reviews.

[25]  D. Artis,et al.  Pathological versus protective functions of IL-22 in airway inflammation are regulated by IL-17A , 2010, The Journal of experimental medicine.

[26]  M. Pillay,et al.  Adhesion to and invasion of pulmonary epithelial cells by the F15/LAM4/KZN and Beijing strains of Mycobacterium tuberculosis. , 2010, Journal of medical microbiology.

[27]  A. Sher,et al.  Redundant and Pathogenic Roles for IL-22 in Mycobacterial, Protozoan, and Helminth Infections , 2010, The Journal of Immunology.

[28]  G. Zeng,et al.  Differentiation, distribution and {gamma}{delta} T cell-driven regulation of IL-22-producing T cells in tuberculosis , 2010 .

[29]  G. Zeng,et al.  Differentiation, Distribution and γδ T Cell-Driven Regulation of IL-22-Producing T Cells in Tuberculosis , 2010, PLoS pathogens.

[30]  R. Vankayalapati,et al.  IL-22 Produced by Human NK Cells Inhibits Growth of Mycobacterium tuberculosis by Enhancing Phagolysosomal Fusion1 , 2009, The Journal of Immunology.

[31]  S. Khader,et al.  The role of cytokines in the initiation, expansion, and control of cellular immunity to tuberculosis , 2008, Immunological reviews.

[32]  S. Sa,et al.  Interleukin-22 mediates early host defense against attaching and effacing bacterial pathogens , 2008, Nature Medicine.

[33]  J. Farrar,et al.  The Influence of Host and Bacterial Genotype on the Development of Disseminated Disease with Mycobacterium tuberculosis , 2008, PLoS pathogens.

[34]  M. Fei,et al.  IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia , 2008, Nature Medicine.

[35]  R. Wilkinson,et al.  Distinct, Specific IL-17- and IL-22-Producing CD4+ T Cell Subsets Contribute to the Human Anti-Mycobacterial Immune Response1 , 2008, The Journal of Immunology.

[36]  A. Cooper.  Faculty Opinions recommendation of Distinct, specific IL-17- and IL-22-producing CD4+ T cell subsets contribute to the human anti-mycobacterial immune response. , 2008 .

[37]  I. Orme,et al.  The Hypervirulent Mycobacterium tuberculosis Strain HN878 Induces a Potent TH1 Response followed by Rapid Down-Regulation1 , 2007, The Journal of Immunology.

[38]  G. Kaplan,et al.  Hypervirulent M. tuberculosis W/Beijing strains upregulate type I IFNs and increase expression of negative regulators of the Jak-Stat pathway. , 2005, Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research.

[39]  G. Nau.  Faculty Opinions recommendation of IL-23 compensates for the absence of IL-12p70 and is essential for the IL-17 response during tuberculosis but is dispensable for protection and antigen-specific IFN-gamma responses if IL-12p70 is available. , 2005 .

[40]  S. Khader,et al.  IL-23 Compensates for the Absence of IL-12p70 and Is Essential for the IL-17 Response during Tuberculosis but Is Dispensable for Protection and Antigen-Specific IFN-γ Responses if IL-12p70 Is Available1 , 2005, The Journal of Immunology.

[41]  M. Reed,et al.  A glycolipid of hypervirulent tuberculosis strains that inhibits the innate immune response , 2004, Nature.

[42]  Stefan Niemann,et al.  Definition of the Beijing/W Lineage of Mycobacterium tuberculosis on the Basis of Genetic Markers , 2004, Journal of Clinical Microbiology.

[43]  L. Armstrong,et al.  Interleukin-22: a potential immunomodulatory molecule in the lung. , 2004, American journal of respiratory cell and molecular biology.

[44]  D. van Soolingen,et al.  Worldwide Occurrence of Beijing/W Strains of Mycobacterium tuberculosis: A Systematic Review , 2002, Emerging infectious diseases.

[45]  S. Svenson,et al.  Spread of Drug-Resistant Pulmonary Tuberculosis in Estonia , 2001, Journal of Clinical Microbiology.

[46]  G. Kaplan,et al.  Virulence of a Mycobacterium tuberculosis clinical isolate in mice is determined by failure to induce Th1 type immunity and is associated with induction of IFN-α/β , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[47]  P. Haslett,et al.  Mycobacterium tuberculosis CDC1551 induces a more vigorous host response in vivo and in vitro, but is not more virulent than other clinical isolates. , 1999, Journal of immunology.

[48]  Barun Mathema,et al.  Global dissemination of the Mycobacterium tuberculosis W-Beijing family strains. , 2002, Trends in microbiology.

[49]  M. Fingerman,et al.  Immunobiology and pathology , 2000 .