Pulmonary Interleukin-17-Positive Lymphocytes Increase during Pneumocystis murina Infection but Are Not Required for Clearance of Pneumocystis

Ripamonti, Carla; Bishop, Lisa R.; Kovacs, Joseph A.

doi:10.1128/iai.00434-16

Cited by 15 publications

(16 citation statements)

References 44 publications

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“…Though there is robust evidence from both mouse and human studies that strongly suggest that CD4 T‐cell responses are required for clearance of Pneumocystis infection, the exact CD4 T‐cell phenotype(s) required for protection remains a subject of open debate. Numerous groups have suggested a role for IL‐17A and Th17 cells in host protection against Pneumocystis . Interleukin‐17A‐producing CD4 T cells are recruited to the lungs of infected animals, and neutralization of IL‐17A or the Th17‐promoting cytokine IL‐23 both significantly increase lung fungal burden at later time‐points .…”

Section: Type 1 Responses To Pulmonary Mycosesmentioning

confidence: 99%

“…Numerous groups have suggested a role for IL‐17A and Th17 cells in host protection against Pneumocystis . Interleukin‐17A‐producing CD4 T cells are recruited to the lungs of infected animals, and neutralization of IL‐17A or the Th17‐promoting cytokine IL‐23 both significantly increase lung fungal burden at later time‐points . Furthermore, impaired fungal clearance was associated with significantly reduced IL‐17 + CD4 T‐cell numbers in the lungs of IKK ∆LEC mice (which lack NF‐ κ B signalling specifically within the lung epithelium), suggesting a potential mechanism by which the lung epithelium marshals protective immunity to Pneumocystis .…”

Section: Type 1 Responses To Pulmonary Mycosesmentioning

confidence: 99%

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Helper T‐cell responses and pulmonary fungal infections

McDermott

Klein

2018

Immunology

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The mucosal surface of the respiratory tract encounters microbes, such as fungal particles, with every inhaled breath. When pathogenic fungi breach the physical barrier and innate immune system within the lung to establish an infection, adaptive immunity is engaged, often in the form of helper CD4 T-cell responses. Type 1 responses, characterized by interferon-γ production from CD4 cells, promote clearance of Histoplasma capsulatum and Cryptococcus neoformans infection. Likewise, interleukin-17A (IL-17A) production from Th17 cells promotes immunity to Blastomyces dermatitidis and Coccidioides species infection by recruiting neutrophils. In contrast the development of T helper type 2 responses, characterized by IL-5 production from T cells and eosinophil influx into the lungs, drives allergic bronchopulmonary aspergillosis and poor outcomes during C. neoformans infection. Experimental vaccines against several endemic mycoses, including Histoplasma capsulatum, Coccidioides, Cryptococcus and Blastomyces dermatitidis, induce protective T-cell responses and foreshadow the development of vaccines against pulmonary fungal infections for use in humans. Additionally, recent work using antifungal T cells as immunotherapy to protect immune-compromised patients from opportunist fungal infections also shows great promise. This review covers the role of T-cell responses in driving protection and pathology in response to pulmonary fungal infections, and highlights promising therapeutic applications of antifungal T cells.

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Section: Type 1 Responses To Pulmonary Mycosesmentioning

confidence: 99%

Section: Type 1 Responses To Pulmonary Mycosesmentioning

confidence: 99%

Helper T‐cell responses and pulmonary fungal infections

McDermott

Klein

2018

Immunology

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“…Th1, Th2 and Th17 responses have each been implicated in protective responses during infection. However, it remains unclear if any Th subset is absolutely necessary in controlling PCP ( 14 ).…”

Section: Discussionmentioning

confidence: 99%

“…Pneumocystis quantification was performed by TaqMan quantitative PCR as previously described ( 31 ) using the right inferior mouse lungs (see below). The left lungs were harvested and minced into pieces, then digested and filtered to get isolated leukocytes ( 14 ) for further flow cytometry analysis and cell counting.…”

Section: Methodsmentioning

confidence: 99%

“…Th17 cells are clearly distinct from Th1 and Th2 cells and numerous studies have demonstrated that Th17 cells and its signature cytokine IL-17A are important for host defense against various fungal pathogens ( 10 ) including Pneumocystis ( 11 – 14 ). As reported, IL-17A production during Pneumocystis infection is increased ( 14 ), and blockage of IL-17 caused a 10,000-fold increase in Pneumocystis murina load in the lung of mice compared with wide-type mice ( 12 ). Furthermore, Th17 immunity is required for the formation of inducible bronchus-associated lymphoid tissue during Pneumocystis infection in mice ( 13 ).…”

Section: Introductionmentioning

confidence: 99%

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IL-9 Deficiency Promotes Pulmonary Th17 Response in Murine Model of Pneumocystis Infection

Rong

Zhang

et al. 2018

Front. Immunol.

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IntroductionPneumocystis pneumonia (PCP) remains a severe complication with high mortality in immunocompromised patients. It has been well accepted that CD4+ T cells play a major role in controlling Pneumocystis infection. Th9 cells were the main source of IL-9 with multifaced roles depending on specific diseases. It is unclear whether IL-9/Th9 contributes to the immune response against PCP. The current study aims to explore the role of IL-9 and the effect of IL-9 on Th17 cells in murine model of PCP.Materials and methodsMice were intratracheally injected with 1 × 106 Pneumocystis organisms to establish the murine model of Pneumocystis infection. Pneumocystis burden was detected by TaqMan real-time PCR. Using IL-9-deficient (IL-9−/−) mice, flow cytometry, real-time PCR and enzyme-linked immunosorbent assay (ELISA) were conducted to investigate the immune function related to Th17 response in defense against Pneumocystis infection.ResultsReduced Pneumocystis burden was observed in lungs in IL-9−/− mice compared with WT mice at 3-week postinfection. IL-9−/−mice exhibited stronger Th17 immune responses than WT PCP mice through flow cytometer and real-time PCR. ELISA revealed higher levels of IL-17 and IL-23 in bronchoalveolar lavage fluid from IL-9−/− mice than WT mice. And IL-9 deficiency promoted Th17 differentiation from CD4+ naive T cells. IL-17A neutralization increased Pneumocystis burden in IL-9−/− mice.ConclusionAlthough similar basic clearance of Pneumocystis organisms was achieved in both WT and IL-9−/− PCP mice, IL-9 deficiency could lower Pneumocystis organism burden and promote pulmonary Th17 cells response in the early stage of infection.

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Evolved to protect, designed to destroy: IL‐17‐producing γδ T cells in infection, inflammation, and cancer

Agerholm

Bekiaris

2021

Eur J Immunol

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T cells of the gamma delta (γδ) lineage are evolutionary conserved from jawless to cartilaginous and bony fish to mammals and represent the "swiss army knife" of the immune system capable of antigen-dependent or independent responses, memory, antigen presentation, regulation of other lymphocytes, tissue homeostasis, and mucosal barrier maintenance, to list a few. Over the last 10 years, γδ T cells that produce the cytokine IL-17 (γδT17) have taken a leading position in our understanding of how our immune system battles infection, inflicts tissue damage during inflammation, and gets rewired by the tumor microenvironment. A lot of what we know about γδT17 cells stems from mouse models, however, increasing evidence implicates these cells in numerous human diseases. Herein, we aim to give an overview of the most common mouse models that have been used to study the role of γδT17 cells in infection, inflammation, and cancer, while at the same time we will evaluate evidence for their importance in humans. We hope and believe that in the next 10 years, means to take advantage of the protective and destructive properties of γδ T and in particular γδT17 cells will be part of our standard immunotherapy toolkit.

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Pulmonary Interleukin-17-Positive Lymphocytes Increase during Pneumocystis murina Infection but Are Not Required for Clearance of Pneumocystis

Cited by 15 publications

References 44 publications

Helper T‐cell responses and pulmonary fungal infections

Helper T‐cell responses and pulmonary fungal infections

IL-9 Deficiency Promotes Pulmonary Th17 Response in Murine Model of Pneumocystis Infection

Evolved to protect, designed to destroy: IL‐17‐producing γδ T cells in infection, inflammation, and cancer

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