File Name: diversity and dialogue in immunity to helminths .zip
The vertebrate immune system has evolved in concert with a broad range of infectious agents, including ubiquitous helminth worm parasites. The constant pressure of helminth infections has been a powerful force in shaping not only how immunity is initiated and maintained, but also how the body self-regulates and controls untoward immune responses to minimize overall harm. In this Review, we discuss recent advances in defining the immune cell types and molecules that are mobilized in response to helminth infection. Finally, we more broadly consider how these immunological players are blended and regulated in order to accommodate persistent infection or to mount a vigorous protective response and achieve sterile immunity.
The vertebrate immune system has evolved in concert with a broad range of infectious agents, including ubiquitous helminth worm parasites. The constant pressure of helminth infections has been a powerful force in shaping not only how immunity is initiated and maintained, but also how the body self-regulates and controls untoward immune responses to minimize overall harm.
In this Review, we discuss recent advances in defining the immune cell types and molecules that are mobilized in response to helminth infection. Finally, we more broadly consider how these immunological players are blended and regulated in order to accommodate persistent infection or to mount a vigorous protective response and achieve sterile immunity.
Anthelmintics or antihelminthics are a group of antiparasitic drugs that expel parasitic worms helminths and other internal parasites from the body by either stunning or killing them and without causing significant damage to the host.
Discover the latest research on anthelmintics here. Nature Reviews. Get PDF. Understanding chronic nematode infections: evolutionary considerations, current hypotheses and the way forward. Immunity after treatment of human schistosomiasis: association between IgE antibodies to adult worm antigens and resistance to reinfection. The function of allergy: immunological defense against toxins. Fc epsilon receptor II-positive macrophages and platelets: potent effector cells in allergy and defence against helminth parasites.
Immunoglobulin E and effector cells in schistosomiasis. Schistosoma mansoni egg-induced early IL-4 production is dependent upon IL-5 and eosinophils. Depression of antigen-specific interleukin-5 and interferon-gamma responses in human lymphatic filariasis as a function of clinical status and age.
Studies on schistosomiasis in western Kenya: I. Evidence for immune-facilitated excretion of schistosome eggs from patients with Schistosoma mansoni and human immunodeficiency virus coinfections. IL, IL-4Ralpha, and Stat6 are required for the expulsion of the gastrointestinal nematode parasite Nippostrongylus brasiliensis.
Antigen-specific proliferation and interferon-gamma and interleukin-5 production are down-regulated during Schistosoma haematobium infection. Protection in lambs vaccinated with Haemonchus contortus antigens is age related, and correlates with IgE rather than IgG1 antibody. A new mechanism for ILdependent helminth control: neutrophil accumulation and neutrophil-mediated worm encapsulation in murine filariasis are abolished in the absence of IL Analysis of type 2 immunity in vivo with a bicistronic IL-4 reporter.
Cutting edge: polarized Th cell response induction by transferred antigen-pulsed dendritic cells is dependent on IL-4 or IL production by recipient cells. IL-4 dependent alternatively-activated macrophages have a distinctive in vivo gene expression phenotype. Microbial recognition via Toll-like receptor-dependent and -independent pathways determines the cytokine response of murine dendritic cell subsets to CD40 triggering. A novel host-parasite lipid cross-talk.
Schistosomal lyso-phosphatidylserine activates toll-like receptor 2 and affects immune polarization. Alternative activation of macrophages. Cytokine-mediated host responses during schistosome infections; walking the fine line between immunological control and immunopathology.
His electrogram alternans reveal dual atrioventricular nodal pathway conduction during atrial fibrillation: the role of slow-pathway modification.
Mast cells disrupt epithelial barrier function during enteric nematode infection. Contrasting roles for IL in protective immunity to different life cycle stages of intestinal nematode parasites. Immune regulation by helminth parasites: cellular and molecular mechanisms. Both free-living and parasitic nematodes induce a characteristic Th2 response that is dependent on the presence of intact glycans.
Immunoglobulin E and eosinophil-dependent protective immunity to larval Onchocerca volvulus in mice immunized with irradiated larvae. Cutting edge: dendritic cells copulsed with microbial and helminth antigens undergo modified maturation, segregate the antigens to distinct intracellular compartments, and concurrently induce microbe-specific Th1 and helminth-specific Th2 responses.
Parasite antigen-driven basophils are a major source of IL-4 in human filarial infections. Mechanisms of tolerance to inhalant allergens: the relevance of a modified Th2 response to allergens from domestic animals.
FIZZ1 stimulation of myofibroblast differentiation. Schistosoma mansoni worms induce anergy of T cells via selective up-regulation of programmed death ligand 1 on macrophages. Basophils produce IL-4 and accumulate in tissues after infection with a Th2-inducing parasite. Interleukin and interleukinmediated host protection against intestinal nematode parasites. Interleukin in the skin and interferon-gamma in the liver are key players in immune protection in human schistosomiasis.
A critical role for eosinophils in allergic airways remodeling. Selective maturation of dendritic cells by Nippostrongylus brasiliensis-secreted proteins drives Th2 immune responses. Helminth infection protects mice from anaphylaxis via ILproducing B cells. Opposing roles for IL and IL receptor alpha 2 in health and disease.
Arginase I is constitutively expressed in human granulocytes and participates in fungicidal activity. Chitinase and Fizz family members are a generalized feature of nematode infection with selective upregulation of Ym1 and Fizz1 by antigen-presenting cells.
Removal of regulatory T cell activity reverses hyporesponsiveness and leads to filarial parasite clearance in vivo. Accelerated intestinal epithelial cell turnover: a new mechanism of parasite expulsion. Role of the programmed Death-1 pathway in the suppressive activity of alternatively activated macrophages in experimental cysticercosis. IL with IL-2 protects against Strongyloides venezuelensis infection by activating mucosal mast cell-dependent type 2 innate immunity.
Infections and allergy - helminths, hygiene and host immune regulation. Activation of invariant NKT cells by the helminth parasite schistosoma mansoni.
Simvastatin promotes Th2-type responses through the induction of the chitinase family member Ym1 in dendritic cells. Memory T H 2 cells induce alternatively activated macrophages to mediate protection against nematode parasites.
Innate immune responses to lung-stage helminth infection induce alternatively activated alveolar macrophages. Lack of eosinophil peroxidase or major basic protein impairs defense against murine filarial infection.
Disruption-induced mucus secretion: repair and protection. Cutting edge: TREM-2 attenuates macrophage activation. Delayed goblet cell hyperplasia, acetylcholine receptor expression, and worm expulsion in SMC-specific IL-4Ralpha-deficient mice. Schistosoma mansoni soluble egg antigens are internalized by human dendritic cells through multiple C-type lectins and suppress TLR-induced dendritic cell activation.
Signaling through Galphai2 protein is required for recruitment of neutrophils for antibody-mediated elimination of larval Strongyloides stercoralis in mice.
Inflammation in wound repair: molecular and cellular mechanisms. Helminths as governors of immune-mediated inflammation. The hygiene hypothesis and multiple sclerosis. Suppression of TH2-type allergic reactions by helminth infection. Impaired resistance in early secondary Nippostrongylus brasiliensis infections in mice with defective eosinophilopoeisis.
Impairment of dendritic cell function by excretory-secretory products: a potential mechanism for nematode-induced immunosuppression. Immunopathology in schistosomiasis is controlled by antigen-specific regulatory T cells primed in the presence of TLR2. Protective effect of Schistosoma mansoni infection on allergic airway inflammation depends on the intensity and chronicity of infection. Alternatively activated macrophages in helminth infections.
Mapping immune response profiles: the emerging scenario from helminth immunology. Protective immune mechanisms in helminth infection. Alarming dendritic cells for Th2 induction. IL is required for the development of severe egg-induced immunopathology in schistosomiasis and for lesional expression of IL Functional analysis of effector and regulatory T cells in a parasitic nematode infection.
Immunity to varicella zoster virus among young adults: a decline prior to widespread uptake of varicella vaccines. Intensity of intestinal infection with multiple worm species is related to regulatory cytokine output and immune hyporesponsiveness. Helminth infections associated with multiple sclerosis induce regulatory B cells.
Global analysis of host-pathogen interactions that regulate early-stage HIV-1 replication. Polyclonal and specific antibodies mediate protective immunity against enteric helminth infection.
Two ways to survive infection: what resistance and tolerance can teach us about treating infectious diseases. Transforming growth factor-beta 'reprograms' the differentiation of T helper 2 cells and promotes an interleukin 9-producing subset. Local and systemic gene expression responses of Atlantic salmon Salmo salar L.
Differential impact of L-arginine deprivation on the activation and effector functions of T cells and macrophages. Efficient colonic mucosal wound repair requires Trem2 signaling. Eosinophil deficiency compromises parasite survival in chronic nematode infection. Welcome to the neighborhood: epithelial cell-derived cytokines license innate and adaptive immune responses at mucosal sites.
Regulatory T cells: a role in the control of helminth-driven intestinal pathology and worm survival. Alternatively activated macrophages elicited by helminth infection can be reprogrammed to enable microbial killing. Cytokine-producing effector B cells regulate type 2 immunity to H. Th2 cell hyporesponsiveness during chronic murine schistosomiasis is cell intrinsic and linked to GRAIL expression.
TSLP regulates intestinal immunity and inflammation in mouse models of helminth infection and colitis. Schistosoma mansoni egg antigens induce Treg that participate in diabetes prevention in NOD mice. Arginaseexpressing macrophages suppress Th2 cytokine-driven inflammation and fibrosis. T follicular helper cells differentiate from Th2 cells in response to helminth antigens. Filarial lymphedema is characterized by antigen-specific Th1 and th17 proinflammatory responses and a lack of regulatory T cells.
Parasitic worms helminths developed various immunoregulatory mechanisms to counteract the immune system of their host. The increasing identification and characterization of helminth-derived factors with strong immune modulatory activity provides novel insights into immune escape strategies of helminths. Such factors might be good targets to enhance anti-helminthic immune responses. In addition, immunosuppressive helminth-derived factors could be useful to develop new therapeutic strategies for treatment of chronic inflammatory conditions. This review will take an in depth look at the effects of immunomodulatory molecules produced by different helminths with a focus on schistosomes and mouse models of hookworm infections.
Key words:. Helminth infections: the great neglected tropical diseases. J Clin Invest. Cox F. History of human parasitology. Clin Microbiol Rev.
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Here, Judith Allen and Rick Maizels discuss how these responses are generated and provide protective immunity during helminth infection.
Publications - A, Allen, J. Parasitology : Hewitson, J. Journal of Immunology Hewitson, J. J, Grainger, J.
Helminths are master regulators of host immune responses utilising complex mechanisms to dampen host protective Th2-type responses and favour long-term persistence. Such evasion mechanisms ensure mutual survival of both the parasite and the host. In this paper, we present recent findings on the cells that are targeted by helminths and the molecules and mechanisms that are induced during infection. We discuss the impact of these factors on the host response as well as their effect in preventing the development of aberrant allergic inflammation. We also examine recent findings on helminth-derived molecules that can be used as tools to pinpoint the underlying mechanisms of immune regulation or to determine new anti-inflammatory therapeutics. These pathogens induce very different immune responses in comparison to bacteria, fungi, viruses, or protozoa.
Helminth parasites are complex metazoans that belong to different taxonomic families but that collectively share the capacity to downregulate the host immune response directed toward themselves parasite-specific immunoregulation. Helminth-induced immunoregulation occurs through the induction of regulatory T cells or Th2-type cells or both. However, secreted or excreted parasite metabolites, proteins, or extracellular vesicles or a combination of these may also directly induce signaling pathways in host cells. Helminth parasites belong to a diverse group of complex metazoans from different taxonomic families. Collectively, helminth infections are a major public health problem worldwide, and recent estimates suggest that 1. There is no development of adult worms in humans.
А теперь все по порядку, - произнесла она вслух. К Хейлу можно вернуться чуть позже. Сосредоточившись, Сьюзан перезагрузила Следопыта и нажала клавишу ВВОД.
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С того места, где он стоял, казалось, что голова сотрудника лаборатории систем безопасности лишилась тела и осталась лежать на полу шифровалки.
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