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      Friend or Foe: The Protective and Pathological Roles of Inducible Bronchus-Associated Lymphoid Tissue in Pulmonary Diseases

      Author(s): , , ,
      Publication date Created:
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      Journal: The Journal of Immunology
      Publisher: The American Association of Immunologists

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          Abstract

          Inducible bronchus associated lymphoid tissue (iBALT) is a tertiary lymphoid structure (TLOs) that resembles secondary lymphoid organs (SLOs). iBALT is induced in the lung in response to antigen exposure. In some cases, such as infection with Mycobacterium tuberculosis (Mtb) , the formation of iBALT structure is indicative of an effective, protective immune response. However, with persistent exposure to antigen during chronic inflammation, allergy, or autoimmune diseases, iBALT may be associated with exacerbation of inflammation. iBALT is characterized by well-organized T and B areas enmeshed with conventional dendritic cells (cDCs), follicular dendritic cells (FDCs) and stromal cells, usually located surrounding airways or blood vessels. Several of the molecular signals and cellular contributors that mediate formation of iBALT structures have been recently identified. This review will outline the recent findings associated with the formation and maintenance of iBALT, and their contributions toward a protective or pathogenic function in pulmonary disease outcome.

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          IL-23 and IL-17 in the establishment of protective pulmonary CD4+ T cell responses after vaccination and during Mycobacterium tuberculosis challenge.

          Susan Swain, Andrea Cooper, Troy D. Randall … (2007)
          Interferon-gamma is key in limiting Mycobacterium tuberculosis infection. Here we show that vaccination triggered an accelerated interferon-gamma response by CD4(+) T cells in the lung during subsequent M. tuberculosis infection. Interleukin 23 (IL-23) was essential for the accelerated response, for early cessation of bacterial growth and for establishment of an IL-17-producing CD4(+) T cell population in the lung. The recall response of the IL-17-producing CD4(+) T cell population occurred concurrently with expression of the chemokines CXCL9, CXCL10 and CXCL11. Depletion of IL-17 during challenge reduced the chemokine expression and accumulation of CD4(+) T cells producing interferon-gamma in the lung. We propose that vaccination induces IL-17-producing CD4(+) T cells that populate the lung and, after challenge, trigger the production of chemokines that recruit CD4(+) T cells producing interferon-gamma, which ultimately restrict bacterial growth.
          Article 0 comments Cited 433 times – based on 0 reviews     Review now
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            Requirement of Interleukin 17 Receptor Signaling for Lung Cxc Chemokine and Granulocyte Colony-Stimulating Factor Expression, Neutrophil Recruitment, and Host Defense

            Lu-peng Ye, Fred H. Rodriguez, Suzanne Kanaly … (2001)
            Bacterial pneumonia is an increasing complication of HIV infection and inversely correlates with the CD4+ lymphocyte count. Interleukin (IL)-17 is a cytokine produced principally by CD4+ T cells, which induces granulopoiesis via granulocyte colony-stimulating factor (G-CSF) production and induces CXC chemokines. We hypothesized that IL-17 receptor (IL-17R) signaling is critical for G-CSF and CXC chemokine production and lung host defenses. To test this, we used a model of Klebsiella pneumoniae lung infection in mice genetically deficient in IL-17R or in mice overexpressing a soluble IL-17R. IL-17R–deficient mice were exquisitely sensitive to intranasal K. pneumoniae with 100% mortality after 48 h compared with only 40% mortality in controls. IL-17R knockout (KO) mice displayed a significant delay in neutrophil recruitment into the alveolar space, and had greater dissemination of K. pneumoniae compared with control mice. This defect was associated with a significant reduction in steady-state levels of G-CSF and macrophage inflammatory protein (MIP)-2 mRNA and protein in the lung in response to the K. pneumoniae challenge in IL-17R KO mice. Thus, IL-17R signaling is critical for optimal production of G-CSF and MIP-2 and local control of pulmonary K. pneumoniae infection. These data support impaired IL-17R signaling as a potential mechanism by which deficiency of CD4 lymphocytes predisposes to bacterial pneumonia.
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              Th17 cells at the crossroads of innate and adaptive immunity against infectious diseases at the mucosa.

              S A Khader, S L Gaffen, J K Kolls (2009)
              T helper type 17 (Th17) cells are a distinct lineage of T cells that produce the effector molecules IL-17, IL-17F, IL-21, and IL-22. Although the role of Th17 cells in autoimmunity is well documented, there is growing evidence that the Th17 lineage and other interleukin (IL)-17-producing cells are critical for host defense against bacterial, fungal, and viral infections at mucosal surfaces. Here we summarize recent progress in our understanding of the function of IL-17-producing cells as a bridge between innate and adaptive immunity against infectious diseases at the mucosa.
              Article 0 comments Cited 139 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: The Journal of Immunology
                Abbreviated Title: J.I.
                Publisher: The American Association of Immunologists
                ISSN (Print): 0022-1767
                ISSN (Electronic): 1550-6606
                Publication date Created: April 22 2019
                Publication date Created: May 01 2019
                Publication date (Electronic): April 22 2019
                Publication date (Print): May 01 2019
                Volume: 202
                Issue: 9
                Pages: 2519-2526
                Article
                DOI: 10.4049/jimmunol.1801135
                PMC ID: 6481307
                PubMed ID: 31010841
                SO-VID: 423dcfc5-7e7a-43a8-bae7-71ec9aa34619
                Copyright © © 2019
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