Recruitment of Neutrophils Mediated by Vγ2 γδ T Cells Deteriorates Liver Fibrosis Induced by Schistosoma japonicum Infection in C57BL/6 Mice

Zheng, Li; Hu, Yuan; Wang, Yanjuan; Huang, Xi-Bao; Xu, Yaobo; Shen, Yujuan; Cao, Jianping

doi:10.1128/iai.01020-16

Cited by 30 publications

(36 citation statements)

References 44 publications

(59 reference statements)

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“…However, an earlier study investigating the relative roles of αβ and γδ T cells in the immunopathology of schistosomiasis found that mutant mice lacking γδ T cells display vigorous formation of egg granulomas similar to normal mice, which demonstrates that granuloma formation is not dependent on γδT cells (127). In contrast with this study, another study identified two different γδ T cell subsets, including the Vγ1 γδ T cells that secrete IFN-γ only and the Vγ2 γδ T cells that secrete both IL-17A and IFN-γ (74). During S. japonicum infection, Vγ2 γδ T cells prevent hepatic fibrosis by recruiting neutrophils and secreting IL-17A (74).…”

Section: Innate γδ T Cells In Schistosomiasiscontrasting

confidence: 72%

“…In contrast with this study, another study identified two different γδ T cell subsets, including the Vγ1 γδ T cells that secrete IFN-γ only and the Vγ2 γδ T cells that secrete both IL-17A and IFN-γ (74). During S. japonicum infection, Vγ2 γδ T cells prevent hepatic fibrosis by recruiting neutrophils and secreting IL-17A (74). Thus, the role of innate γδ T cells in the pathology of schistosomiasis requires further investigation.…”

Section: Innate γδ T Cells In Schistosomiasiscontrasting

confidence: 56%

“…Some researchers ignore the source of IL-17, and others found that Th17 cells are the major IL-17-producing cell population that contributes to pulmonary granuloma induced by S. japonicum (72). However, some studies showed that innate γδ T cells are the major IL-17-producing cells that contribute to the formation of granuloma in murine schistosomiasis (73,74). The above discrepant findings may result from the different granuloma models.…”

Section: Th17/il-17 Exacerbate the Egg-induced Liver Immunopathologymentioning

confidence: 99%

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T Lymphocyte-Mediated Liver Immunopathology of Schistosomiasis

et al. 2020

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The parasitic worms, Schistosoma mansoni and Schistosoma japonicum, reside in the mesenteric veins, where they release eggs that induce a dramatic granulomatous response in the liver and intestines. Subsequently, infection may further develop into significant fibrosis and portal hypertension. Over the past several years, uncovering the mechanism of immunopathology in schistosomiasis has become a major research objective. It is known that T lymphocytes, especially CD4 + T cells, are essential for immune responses against Schistosoma species. However, obtaining a clear understanding of how T lymphocytes regulate the pathological process is proving to be a daunting challenge. To date, CD4 + T cell subsets have been classified into several distinct T helper (Th) phenotypes including Th1, Th2, Th17, T follicular helper cells (Tfh), Th9, and regulatory T cells (Tregs). In the case of schistosomiasis, the granulomatous inflammation and the chronic liver pathology are critically regulated by the Th1/Th2 responses. Animal studies suggest that there is a moderate Th1 response to parasite antigens during the acute stage, but then, egg-derived antigens induce a sustained and dominant Th2 response that mediates granuloma formation and liver fibrosis. In addition, the newly discovered Th17 cells also play a critical role in the hepatic immunopathology of schistosomiasis. Within the liver, Tregs are recruited to hepatic granulomas and exert an immunosuppressive role to limit the granulomatous inflammation and fibrosis. Moreover, recent studies have shown that Tfh and Th9 cells might also promote liver granulomas and fibrogenesis in the murine schistosomiasis. Thus, during infection, T-cell subsets undergo complicated cross-talk with antigen presenting cells that then defines their various roles in the local microenvironment for regulating the pathological progression of schistosomiasis. This current review summarizes a vast body of literature to elucidate the contribution of T lymphocytes and their associated cytokines in the immunopathology of schistosomiasis.

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Section: Innate γδ T Cells In Schistosomiasiscontrasting

confidence: 72%

Section: Innate γδ T Cells In Schistosomiasiscontrasting

confidence: 56%

Section: Th17/il-17 Exacerbate the Egg-induced Liver Immunopathologymentioning

confidence: 99%

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T Lymphocyte-Mediated Liver Immunopathology of Schistosomiasis

et al. 2020

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“…Leishmania and Toxoplasma gondii also induce expression of IL‐17A, the role of which is still unclear because both protective and non‐protective roles have been reported. Schistosoma helminths, which cause liver granulomas and fibrosis, also induce IL‐17A production by Th17 and γδ T cells . Lack of IL‐17A or IL‐23 results in decreased granuloma formation and suppression of liver fibrosis, indicating that IL‐17A can exacerbate clinical symptoms of schistosomiasis.…”

Section: Role Of Hematopoietic Cell‐derived Il‐17a In Infectionsmentioning

confidence: 99%

Interleukin‐17 family cytokines in protective immunity against infections: role of hematopoietic cell‐derived and non‐hematopoietic cell‐derived interleukin‐17s

Matsuzaki

Umemura

2018

Microbiology and Immunology

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Interleukin-17 family cytokines, consisting of six members, participate in immune response in infections and autoimmune and inflammatory diseases. The prototype cytokine of the family, IL-17A, was originally identified from CD4þ T cells which are now termed Th17 cells. Later, IL-17A-producing cells were expanded to include various hematopoietic cells, namely CD8þ T cells (Tc17), invariant NKT cells, gd T cells, non-T non-B lymphocytes (termed type 3 innate lymphoid cells) and neutrophils. Some IL-17 family cytokines other than IL-17A are also expressed by CD4þ T cells: IL-17E by Th2 cells and IL-17F by Th17 cells. IL-17A and IL-17F induce expression of pro-inflammatory cytokines to induce inflammation and anti-microbial peptides to kill pathogens, whereas IL-17E induces allergic inflammation. However, the functions of other IL-17 family cytokines have been unclear. Recent studies have shown that IL-17B and IL-17C are expressed by epithelial rather than hematopoietic cells. Interestingly, expression of IL-17E and IL-17F by epithelial cells has also been reported and epithelial cell-derived IL-17 family cytokines shown to play important roles in immune responses to infections at epithelial sites. In this review, we summarize current information on hematopoietic cell-derived IL-17A and non-hematopoietic cell-derived IL-17B, IL-17C, IL-17D, IL-17E and IL-17F in infections and propose functional differences between these two categories of IL-17 family cytokines.

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“…Hepatic γδ T cells are often Vγ4 cells and secrete the cytokine IL-17 and/or IL-10 [13]. Studies in mice indicate a role for IL-17 producing γδ T cells in liver fibrosis and immune pathology during infection with Schistosoma japonicum [14][15][16][17] and SM [18]. They can either be pathogenic as in the case of S. japonicum, or protective in the case of Listeria monocytogenes [13].…”

Section: Introductionmentioning

confidence: 99%

Adults from Kisumu, Kenya have robust γδ T cell responses to Schistosoma mansoni, which are modulated by tuberculosis

et al. 2020

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Schistosoma mansoni (SM) is a parasitic helminth that infects over 200 million people and causes severe morbidity. It undergoes a multi-stage life cycle in human hosts and as such stimulates a stage-specific immune response. The human T cell response to SM is complex and varies throughout the life cycle of SM. Relative to the wealth of information regarding the immune response to SM eggs, little is known about the immune response to the adult worm. In addition, while a great deal of research has uncovered mechanisms by which coinfection with helminths modulates immunity to other pathogens, there is a paucity of data on the effect of pathogens on immunity to helminths. As such, we sought to characterize the breadth of the T cell response to SM and determine whether co-infection with Mycobacterium tuberculosis (Mtb) modifies SM-specific T cell responses in a cohort of HIV-uninfected adults in Kisumu, Kenya. SM-infected individuals were categorized into three groups by Mtb infection status: active TB (TB), Interferon-γ Release Assay positive (IGRA+), and Interferon-γ Release Assay negative (IGRA-). U.S. adults that were seronegative for SM antibodies served as naïve controls. We utilized flow cytometry to characterize the T cell repertoire to SM egg and worm antigens. We found that T cells had significantly higher proliferation and cytokine production in response to worm antigen than to egg antigen. The T cell response to SM was dominated by γδ T cells that produced TNFα and IFNγ. Furthermore, we found that in individuals infected with Mtb, γδ T cells proliferated less in response to SM worm antigens and had higher IL-4 production compared to naïve controls. Together these data demonstrate that γδ T cells respond robustly to SM worm antigens and that Mtb infection modifies the γδ T cell response to SM.

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Recruitment of Neutrophils Mediated by Vγ2 γδ T Cells Deteriorates Liver Fibrosis Induced by Schistosoma japonicum Infection in C57BL/6 Mice

Cited by 30 publications

References 44 publications

T Lymphocyte-Mediated Liver Immunopathology of Schistosomiasis

T Lymphocyte-Mediated Liver Immunopathology of Schistosomiasis

Interleukin‐17 family cytokines in protective immunity against infections: role of hematopoietic cell‐derived and non‐hematopoietic cell‐derived interleukin‐17s

Adults from Kisumu, Kenya have robust γδ T cell responses to Schistosoma mansoni, which are modulated by tuberculosis

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