Immunology and Immunodiagnosis of Cystic Echinococcosis: An Update

Cystic echinococcosis (CE) is a cosmopolitan zoonosis caused by the larval cystic stage of the dog tapewormEchinococcus granulosus. This complex multicellular pathogen produces various antigens which modulate the host immune response and promote parasite survival and development. The recent application of modern molecular and immunological approaches has revealed novel insights on the nature of the immune responses generated during the course of a hydatid infection, although many aspects of theEchinococcus-host interplay remain unexplored. This paper summarizes recent developments in our understanding of the immunology and diagnosis of echinococcosis, indicates areas where information is lacking, and suggests possible new strategies to improve serodiagnosis for practical application.

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The role of chemokines and their receptors during protist parasite infections

Parasitology ◽

10.1017/s0031182016001694 ◽

2016 ◽

Vol 143 (14) ◽

pp. 1890-1901 ◽

Cited By ~ 4

Author(s):

FIONA M. MENZIES ◽

DAVID MACPHAIL ◽

FIONA L. HENRIQUEZ

Keyword(s):

Immune Response ◽

Immune Responses ◽

Chemokine Receptors ◽

Drug Targeting ◽

Scientific Literature ◽

Parasite Survival ◽

Recent Developments ◽

Parasite Infections ◽

Eukaryotic Organisms

SUMMARYProtists are a diverse collection of eukaryotic organisms that account for a significant global infection burden. Often, the immune responses mounted against these parasites cause excessive inflammation and therefore pathology in the host. Elucidating the mechanisms of both protective and harmful immune responses is complex, and often relies of the use of animal models. In any immune response, leucocyte trafficking to the site of infection, or inflammation, is paramount, and this involves the production of chemokines, small chemotactic cytokines of approximately 8–10 kDa in size, which bind to specific chemokine receptors to induce leucocyte movement. Herein, the scientific literature investigating the role of chemokines in the propagation of immune responses against key protist infections will be reviewed, focussing onPlasmodiumspecies,Toxoplasma gondii, Leishmaniaspecies andCryptosporidiumspecies. Interestingly, many studies find that chemokines can in fact, promote parasite survival in the host, by drawing in leucocytes for spread and further replication. Recent developments in drug targeting against chemokine receptors highlights the need for further understanding of the role played by these proteins and their receptors in many different diseases.

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Response patterns in adventitial layer of Echinococcus granulosus sensu stricto cysts from naturally infected cattle and sheep

Veterinary Research ◽

10.1186/s13567-021-00936-8 ◽

2021 ◽

Vol 52 (1) ◽

Author(s):

Christian Hidalgo ◽

Caroll Stoore ◽

María Soledad Baquedano ◽

Ismael Pereira ◽

Carmen Franco ◽

...

Keyword(s):

Immune Response ◽

Echinococcus Granulosus ◽

Cystic Echinococcosis ◽

Direct Contact ◽

Sensu Stricto ◽

Response Patterns ◽

Granulomatous Reaction ◽

Adventitial Layer ◽

Laminated Layer ◽

Cattle And Sheep

AbstractCystic echinococcosis is a zoonotic disease caused by the metacestode of Echinococcus granulosus sensu lato. The disease is characterized by the development of cystic structures inside viscera of the intermediate host, mainly liver and lungs. These cysts are formed by three layers: germinal, laminated, and adventitial layer, the latter being the local host immune response. Metacestodes that develop protoscoleces, the infective stage to the definitive host, are termed fertile, whereas cysts that do not produce protoscoleces are termed non-fertile. Sheep usually harbor fertile cysts while cattle usually harbor non-fertile cysts. Adventitial layers with fibrotic resolution are associated to fertile cysts, whereas a granulomatous reaction is associated with non-fertile cysts. The aim of this study was to analyze cellular distribution in the adventitial layer of fertile and non-fertile E. granulosus sensu stricto cysts found in liver and lungs of cattle and sheep. A total of 418 cysts were analyzed, 203 from cattle (8 fertile and 195 non-fertile) and 215 from sheep (64 fertile and 151 non-fertile). Fertile cysts from cattle showed mixed patterns of response, with fibrotic resolution and presence of granulomatous response in direct contact with the laminated layer, while sheep fertile cysts always displayed fibrotic resolution next to the laminated layer. Cattle non-fertile cysts display a granulomatous reaction in direct contact with the laminated layer, whereas sheep non-fertile cysts display a granulomatous reaction, but in direct contact with the fibrotic resolution. This shows that cattle and sheep cystic echinococcosis cysts have distinct local immune response patterns, which are associated to metacestode fertility.

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Human Cystic Echinococcosis: Old Problems and New Perspectives

Interdisciplinary Perspectives on Infectious Diseases ◽

10.1155/2009/474368 ◽

2009 ◽

Vol 2009 ◽

pp. 1-7 ◽

Cited By ~ 35

Author(s):

Alessandra Siracusano ◽

Antonella Teggi ◽

Elena Ortona

Keyword(s):

Molecular Biology ◽

Inflammatory Response ◽

Immune Responses ◽

Cystic Echinococcosis ◽

Clinical Management ◽

Host Immune Responses ◽

New Concepts ◽

Immune Mediated ◽

Parasite Survival ◽

Human Cystic Echinococcosis

Cystic echinococcosis (CE) is a widespread chronic endemic helminthic disease caused by infection with metacestodes of the tapewormEchinococcus granulosus. CE affects humans and has a worldwide prevalence of approximately six million. In this review, we discuss current findings in diagnosis and clinical management of CE and new concepts relating toE. granulosusmolecules that directly modulate the host immune responses favouring a strong anti-inflammatory response and perpetuating parasite survival in the host. New insights into the molecular biology ofE. granulosuswill improve considerably our knowledge of the disease and will provide new potential therapeutic applications to treat or prevent inflammatory immune-mediated disease.

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Trypanosoma cruzi Immune Response Modulation Decreases Microbiota in Rhodnius prolixus Gut and Is Crucial for Parasite Survival and Development

PLoS ONE ◽

10.1371/journal.pone.0036591 ◽

2012 ◽

Vol 7 (5) ◽

pp. e36591 ◽

Cited By ~ 67

Author(s):

Daniele P. Castro ◽

Caroline S. Moraes ◽

Marcelo S. Gonzalez ◽

Norman A. Ratcliffe ◽

Patrícia Azambuja ◽

...

Keyword(s):

Immune Response ◽

Trypanosoma Cruzi ◽

Rhodnius Prolixus ◽

Response Modulation ◽

Parasite Survival ◽

Survival And Development ◽

Immune Response Modulation

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Th9/IL-9 Profile in Human Echinococcosis: Their Involvement in Immune Response during Infection byEchinococcus granulosus

Mediators of Inflammation ◽

10.1155/2014/781649 ◽

2014 ◽

Vol 2014 ◽

pp. 1-11 ◽

Cited By ~ 22

Author(s):

Nannan Pang ◽

Fengbo Zhang ◽

Xiumin Ma ◽

Zhaoxia Zhang ◽

Hui Zhao ◽

...

Keyword(s):

Immune Response ◽

Immune Responses ◽

Echinococcus Granulosus ◽

Th2 Cells ◽

Mrna Levels ◽

Flow Cytometry Analysis ◽

Qrt Pcr ◽

Th9 Cells ◽

Human Echinococcosis

Th9 cells have been reported to contribute to immune responses; however, the role of Th9 cells inEchinococcus granulosusinfection is unknown. This study is to determine whether Th9 cells and IL-9 are involved in humanEchinococcus granulosusinfection. Compared with healthy controls (HC group), the mRNA levels of PU.1, IL-9, and GATA-3 were significantly increased in patients before therapy (CE group), as revealed by qRT-PCR. Flow cytometry analysis showed that the percentages of Th9 and Th2 cells in CE group were significantly higher. The levels of IL-9, IL-4, IL-10, and TGF-βin CE group were also significantly increased, as detected by CBA assay. The percentages of Th9 and Th2 cells in CE group were positively correlated. After treatments of surgery in combination with albendazole, the PU.1 and GATA-3 mRNA levels were significantly decreased in patients after therapy (PCE group) compared with CE group. The numbers of Th9 and Th2 cells and levels of IL-9, IL-4, IL-10, and TGF-βwere also significantly decreased in PCE group. In conclusion, the ratios of Th9 cells and IL-9 levels were significantly decreased after treatment, suggesting that Th9/IL-9 may be involved in immune response induced byEchinococcus granulosusinfection.

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Oral Immune Activation by Disgust and Disease-Related Pictures

Journal of Psychophysiology ◽

10.1027/0269-8803/a000143 ◽

2015 ◽

Vol 29 (3) ◽

pp. 119-129 ◽

Cited By ~ 4

Author(s):

Richard J. Stevenson ◽

Deborah Hodgson ◽

Megan J. Oaten ◽

Luba Sominsky ◽

Mehmet Mahmut ◽

...

Keyword(s):

Immune Response ◽

Immune Responses ◽

Innate Immune Response ◽

Negative Control ◽

Innate Immune ◽

Innate Immune Responses ◽

Immune Markers ◽

Before And After ◽

Secondary Analyses ◽

Image Set

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.

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Coupled complementation of immune response genes controlling responsiveness to the H-2.2 alloantigen.

Journal of Experimental Medicine ◽

10.1084/jem.146.2.571 ◽

1977 ◽

Vol 146 (2) ◽

pp. 571-578 ◽

Cited By ~ 16

Author(s):

M E Dorf ◽

J H Stimpfling

Keyword(s):

Immune Response ◽

Immune Responses ◽

Humoral Response ◽

Mixed Lymphocyte Culture ◽

Lymphocyte Culture ◽

F1 Hybrids ◽

Gene Control ◽

Low Responder ◽

Resistant Strains ◽

High Level

The ability of various B10 congenic resistant strains to respond to the alloantigen H-2.2 was tested. High and low antibody-producing strains were distinguished by their anti-H-2.2 hemagglutinating respones. However, these strains do not differ in their ability to respond to these antigenic differences in the mixed lymphocyte culture. The humoral response to the H-2.2 alloantigen was shown to be controlled by two interacting genes localized within the H-2 complex. Thus, F1 hybrids prepared between parental low responder strains could yield high level immune responses. In addition, strains bearing recombinant H-2 haplotypes were used to map the two distinct genes controlling the immune response. The alleles at each locus were shown to be highly polymorphic as evidenced by the asymmetric complementation patterns observed. The restricted interactions of specific alleles was termed coupled complementation. The significance of the results in the terms of mechanisms of Ir gene control are discussed.

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Maintenance of Type 2 Response by CXCR6-Deficient ILC2 in Papain-Induced Lung Inflammation

International Journal of Molecular Sciences ◽

10.3390/ijms20215493 ◽

2019 ◽

Vol 20 (21) ◽

pp. 5493 ◽

Cited By ~ 1

Author(s):

Meunier ◽

Chea ◽

Garrido ◽

Perchet ◽

Petit ◽

...

Keyword(s):

Immune Response ◽

Immune Responses ◽

Nk Cell ◽

Lymphoid Cells ◽

Inflammatory Conditions ◽

Airway Diseases ◽

Type 2 Cytokines ◽

Lymphoid Organogenesis ◽

Deficient Mice

Innate lymphoid cells (ILC) are important players of early immune defenses in situations like lymphoid organogenesis or in case of immune response to inflammation, infection and cancer. Th1 and Th2 antagonism is crucial for the regulation of immune responses, however mechanisms are still unclear for ILC functions. ILC2 and NK cells were reported to be both involved in allergic airway diseases and were shown to be able to interplay in the regulation of the immune response. CXCR6 is a common chemokine receptor expressed by all ILC, and its deficiency affects ILC2 and ILC1/NK cell numbers and functions in lungs in both steady-state and inflammatory conditions. We determined that the absence of a specific ILC2 KLRG1+ST2– subset in CXCR6-deficient mice is probably dependent on CXCR6 for its recruitment to the lung under inflammation. We show that despite their decreased numbers, lung CXCR6-deficient ILC2 are even more activated cells producing large amount of type 2 cytokines that could drive eosinophilia. This is strongly associated to the decrease of the lung Th1 response in CXCR6-deficient mice.

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Combining Oncolytic Viruses and Small Molecule Therapeutics: Mutual Benefits

Cancers ◽

10.3390/cancers13143386 ◽

2021 ◽

Vol 13 (14) ◽

pp. 3386

Author(s):

Bart Spiesschaert ◽

Katharina Angerer ◽

John Park ◽

Guido Wollmann

Keyword(s):

Immune Response ◽

Immune Responses ◽

Tumor Cells ◽

Small Molecule ◽

Antiviral Immunity ◽

Oncolytic Viruses ◽

Antitumor Immune Response ◽

Antiviral Responses ◽

Small Molecule Therapeutics ◽

Immunosuppressive Factors

The focus of treating cancer with oncolytic viruses (OVs) has increasingly shifted towards achieving efficacy through the induction and augmentation of an antitumor immune response. However, innate antiviral responses can limit the activity of many OVs within the tumor and several immunosuppressive factors can hamper any subsequent antitumor immune responses. In recent decades, numerous small molecule compounds that either inhibit the immunosuppressive features of tumor cells or antagonize antiviral immunity have been developed and tested for. Here we comprehensively review small molecule compounds that can achieve therapeutic synergy with OVs. We also elaborate on the mechanisms by which these treatments elicit anti-tumor effects as monotherapies and how these complement OV treatment.

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The immune response of T cells and therapeutic targets related to regulating the levels of T helper cells after ischaemic stroke

Journal of Neuroinflammation ◽

10.1186/s12974-020-02057-z ◽

2021 ◽

Vol 18 (1) ◽

Author(s):

Tian-Yu Lei ◽

Ying-Ze Ye ◽

Xi-Qun Zhu ◽

Daniel Smerin ◽

Li-Juan Gu ◽

...

Keyword(s):

Immune Response ◽

T Cells ◽

Immune System ◽

Immune Responses ◽

Ischaemic Stroke ◽

Immune Cells ◽

Tissue Injury ◽

Recovery Period ◽

Vital Functions ◽

Anti Inflammatory

AbstractThrough considerable effort in research and clinical studies, the immune system has been identified as a participant in the onset and progression of brain injury after ischaemic stroke. Due to the involvement of all types of immune cells, the roles of the immune system in stroke pathology and associated effects are complicated. Past research concentrated on the functions of monocytes and neutrophils in the pathogenesis of ischaemic stroke and tried to demonstrate the mechanisms of tissue injury and protection involving these immune cells. Within the past several years, an increasing number of studies have elucidated the vital functions of T cells in the innate and adaptive immune responses in both the acute and chronic phases of ischaemic stroke. Recently, the phenotypes of T cells with proinflammatory or anti-inflammatory function have been demonstrated in detail. T cells with distinctive phenotypes can also influence cerebral inflammation through various pathways, such as regulating the immune response, interacting with brain-resident immune cells and modulating neurogenesis and angiogenesis during different phases following stroke. In view of the limited treatment options available following stroke other than tissue plasminogen activator therapy, understanding the function of immune responses, especially T cell responses, in the post-stroke recovery period can provide a new therapeutic direction. Here, we discuss the different functions and temporal evolution of T cells with different phenotypes during the acute and chronic phases of ischaemic stroke. We suggest that modulating the balance between the proinflammatory and anti-inflammatory functions of T cells with distinct phenotypes may become a potential therapeutic approach that reduces the mortality and improves the functional outcomes and prognosis of patients suffering from ischaemic stroke.

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