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      Pathophysiology of T follicular helper cells in humans and mice.

      Author(s): 1 , 2 , 3
      Publication date (Electronic):
      Journal: Nature immunology

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          Abstract

          Follicular helper T cells (TFH cells) compose a heterogeneous subset of CD4(+) T cells that induce the differentiation of B cells into plasma cells and memory cells. They are found within and in proximity to germinal centers in secondary lymphoid organs, and their memory compartment also circulates in the blood. Our knowledge on the biology of TFH cells has increased significantly during the past decade, largely as a result of mouse studies. However, recent studies on human TFH cells isolated from lymphoid organ and blood samples and recent observations on the developmental mechanism of human TFH cells have revealed both similarities and differences between human and mouse TFH cells. Here we present the similarities and differences between mouse and human lymphoid organ-resident TFH cells and discuss the role of TFH cells in response to vaccines and in disease pathogenesis.

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          Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells.

          Hsin-Jung J. Wu, Ivaylo Ivanov, Jaime Darce … (2010)
          Commensal microbes can have a substantial impact on autoimmune disorders, but the underlying molecular and cellular mechanisms remain largely unexplored. We report that autoimmune arthritis was strongly attenuated in the K/BxN mouse model under germ-free (GF) conditions, accompanied by reductions in serum autoantibody titers, splenic autoantibody-secreting cells, germinal centers, and the splenic T helper 17 (Th17) cell population. Neutralization of interleukin-17 prevented arthritis development in specific-pathogen-free K/BxN mice resulting from a direct effect of this cytokine on B cells to inhibit germinal center formation. The systemic deficiencies of the GF animals reflected a loss of Th17 cells from the small intestinal lamina propria. Introduction of a single gut-residing species, segmented filamentous bacteria, into GF animals reinstated the lamina propria Th17 cell compartment and production of autoantibodies, and arthritis rapidly ensued. Thus, a single commensal microbe, via its ability to promote a specific Th cell subset, can drive an autoimmune disease. Copyright 2010 Elsevier Inc. All rights reserved.
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            IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses.

            Thomas Krausgruber, Katrina Blazek, Tim Smallie … (2011)
            Polymorphisms in the gene encoding the transcription factor IRF5 that lead to higher mRNA expression are associated with many autoimmune diseases. Here we show that IRF5 expression in macrophages was reversibly induced by inflammatory stimuli and contributed to the plasticity of macrophage polarization. High expression of IRF5 was characteristic of M1 macrophages, in which it directly activated transcription of the genes encoding interleukin 12 subunit p40 (IL-12p40), IL-12p35 and IL-23p19 and repressed the gene encoding IL-10. Consequently, those macrophages set up the environment for a potent T helper type 1 (T(H)1)-T(H)17 response. Global gene expression analysis demonstrated that exogenous IRF5 upregulated or downregulated expression of established phenotypic markers of M1 or M2 macrophages, respectively. Our data suggest a critical role for IRF5 in M1 macrophage polarization and define a previously unknown function for IRF5 as a transcriptional repressor.
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              Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology.

              Roberta Magliozzi, Owain W Howell, Abhilash Vora … (2007)
              Intrathecal antibody production is a hallmark of multiple sclerosis and humoral immunity is thought to play an important role in the inflammatory response and development of demyelinated lesions. The presence of lymphoid follicle-like structures in the cerebral meninges of some multiple sclerosis patients indicates that B-cell maturation can be sustained locally within the CNS and contribute to the establishment of a compartmentalized humoral immune response. In this study we examined the distribution of ectopic B-cell follicles in multiple sclerosis cases with primary and secondary progressive clinical courses to determine their association with clinical and neuropathological features. A detailed immunohistochemical and morphometric analysis was performed on post-mortem brain tissue samples from 29 secondary progressive (SP) and 7 primary progressive (PP) multiple sclerosis cases. B-cell follicles were detected in the meninges entering the cerebral sulci of 41.4% of the SPMS cases, but not in PPMS cases. The SPMS cases with follicles significantly differed from those without with respect to a younger age at multiple sclerosis onset, irreversible disability and death and more pronounced demyelination, microglia activation and loss of neurites in the cerebral cortex. Cortical demyelination in these SPMS cases was also more severe than in PPMS cases. Notably, all meningeal B-cell follicles were found adjacent to large subpial cortical lesions, suggesting that soluble factors diffusing from these structures have a pathogenic role. These data support an immunopathogenetic mechanism whereby B-cell follicles developing in the multiple sclerosis meninges exacerbate the detrimental effects of humoral immunity with a subsequent major impact on the integrity of the cortical structures.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Nat. Immunol.
                Title: Nature immunology
                ISSN (Electronic): 1529-2916
                ISSN (Print): 1529-2908
                Publication date (Electronic): Feb 2015
                Volume: 16
                Issue: 2
                Affiliations
                [1 ] Baylor Institute for Immunology Research, Dallas, Texas, USA.
                [2 ] Jackson Laboratory for Genomic Medicine, Farmington, Connecticut, USA, and Vaccine Research Institute, INSERM U955, Hopital Henri Mondor, Creteil, France.
                [3 ] Department of Pathogens and Immunity, John Curtin School of Medical Research, Australian National University, Canberra, Australia.
                Article
                Publisher Item ID: ni.3054 Mid ID: NIHMS687796
                DOI: 10.1038/ni.3054
                PMC ID: 4459756
                PubMed ID: 25594465
                SO-VID: 622a726e-6f2c-4dae-b5e6-6aa480f30c1a
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