The Experts below are selected from a list of 24741 Experts worldwide ranked by ideXlab platform
William A Sewell - One of the best experts on this subject based on the ideXlab platform.
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protection against nippostrongylus brasiliensis infection in mice is independent of gm csf
Immunology and Cell Biology, 2012Co-Authors: Doris Shim, Heidi C Schilter, Michelle L Knott, Ranni A Almeida, Robert P Short, Charles R Mackay, Lindsay A Dent, William A SewellAbstract:Granulocyte macrophage-colony stimulating factor (GM-CSF) is a cytokine with the capacity to promote inflammation in a wide variety of infectious and inflammatory diseases. These conditions include allergic airway inflammation, which is driven by T-helper 2 (Th2) cells. Because of the importance of Th2 cells in Parasite infections, we have investigated the role of GM-CSF in mice infected with the nematode Nippostrongylus brasiliensis. The effect of primary and secondary infection was investigated in mice lacking functional genes for GM-CSF (CSF2 genes) (ΔGM-CSF mice), and in mice lacking the cytokine receptor common β chain (Δβ mice), the latter being unable to signal in response to GM-CSF and interleukin (IL)-5. ΔGM-CSF mice showed no significant defect in Parasite Immunity, measured by larval numbers in the lungs, worm numbers in the intestine or egg numbers in the faeces, in either primary or secondary infection. By contrast, the Δβ mice showed increased Parasite burden, with higher numbers of lung larvae after secondary infection and higher numbers of intestinal worms and faecal eggs after both primary and secondary infection. Unexpectedly, there were increased numbers of circulating eosinophils in the ΔGM-CSF mice, associated with significantly reduced larval numbers in the lungs. These results indicate that GM-CSF is redundant in protection against N. brasiliensis infection, and that the increased susceptibility of Δβ mice to infection is likely to be attributed to the lack of IL-5 signalling in these mice. The results suggest that clinical use of agents that neutralise GM-CSF may not be associated with increased risk of Parasite infection.
Martin J. Holland - One of the best experts on this subject based on the ideXlab platform.
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Parasite Immunity: Pathways for expelling intestinal helminths
Current biology : CB, 1998Co-Authors: Rick M. Maizels, Martin J. HollandAbstract:Helminth Parasites induce strong immune responses that are initiated by cytokines, in the first instance interleukin-4 and interleukin-13. Recent studies of knockout mice deficient in these mediators or their shared receptor have revealed discrete pathways required for expulsion of different gut Parasites.
E. Olguín-martínez - One of the best experts on this subject based on the ideXlab platform.
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IL-9 and Th9 in Parasite Immunity
Seminars in Immunopathology, 2017Co-Authors: P. Licona-limón, A. Arias-rojas, E. Olguín-martínezAbstract:Interleukin-9 is a cytokine classically related to type 2 immune responses whose cellular identity has been recently reevaluated to identify a new specialized T helper subset called Th9 and an innate source referred as innate lymphoid cell type 2. Over the past years, IL-9 has been associated with allergic responses, tumor immunology, and autoImmunity; however, in this review, we will specifically focus on the role of IL-9 and Th9 cells in the context of parasitic infections. We will summarize and discuss all the evidence relating IL-9 expression and function in parasitic infections with a particular emphasis in helminth infections, an important health issue in developing countries; we will also provide a general description and classification of Parasites, the immune response and cellular compartments activated in this context, and its implications and future directions towards a complete understanding of this interesting new T helper subset and its potential therapeutic use.
Alan J. Husband - One of the best experts on this subject based on the ideXlab platform.
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Interleukin-6 expression in gut of Parasite challenged sheep.
Veterinary Immunology and Immunopathology, 2000Co-Authors: Jie Shen, Shisan Bao, S.j. Mcclure, David Emery, Alan J. HusbandAbstract:Following challenge with Trichosirongylus colubrifonizis, increased numbers of T-cells and immunoglobulin responses are seen in the intestine of sheep immunised by repeated infection with live worms. IL-6 mRNA expression in the small intestine from T. colubriformis-immunised and naive sheep was determined by in situ hybridisation, whereas CD4(+), IgA(+), IgG(+) cells in the gut were evaluated by immunohistochemistry. There was constitutive expression of IL-6 mRNA by cells in the naive gut, and the number of these cells was increased by Parasite challenge. There were corresponding increases in numbers of CD4(+) and TCR gamma/delta(+) T-cells and IgG(+) B-cells. Our data are consistent with a role for IL-6, perhaps produced by CD4(+) and/or TCR gamma/delta(+) T-cells or B-cells, in B-cell terminal differentiation. Infiltration of B-cells, particularly IgG(+) B-cells, may reflect Parasite Immunity in the host.
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differential expression of interleukin 5 mrna cells and eosinophils in nippostrongylus brasiliensis infection in resistant and susceptible strains of mice
European Journal of Immunology, 1996Co-Authors: Yafen Zhou, Shisan Bao, Terence L W Rothwell, Alan J. HusbandAbstract:Interleukin (IL)-5 is produced by both T cells and eosinophils and has been implicated in lymphocyte and eosinophil differentiation and maturation. The extent to which differences in IL-5 expression contribute to genetic variability in Parasite Immunity was investigated by comparing eosinophilia, IgE production, mastocytosis and IL-5 mRNA+ cells following Nippostrongylus brasiliensis infection of resistant (BALB/c) and susceptible (C57BL/6) mice. In uninfected mice, IL-5 mRNA+ cells detected by in situ hybridization were distributed throughout the lamina propria and crypt regions of the small intestine in both strains, but were 1.5-fold higher in BALB/c than in C57BL/6 mice. Following N. brasiliensis infection, the numbers of IL-5 mRNA+ cells in BALB/c mice continued to increase until day 11 post-infection at which time they were more than 4-fold more numerous than in uninfected control mice of the same strain. In C57BL/6 mice, IL-5 mRNA+ cells reached peak numbers on day 7 post-infection, only 1.5-fold higher than uninfected controls, but the numbers began to decline thereafter. At all time points after day 5, the numbers of IL-5 mRNA+ cells in the gut of C57BL/6 mice were significantly lower than BALB/c mice. The differences in numbers of IL-5 mRNA+ cells induced by infection in each strain of mice correlated with changes in blood and intestinal eosinophilia, mastocytosis and IgE production and was reflected in differences in worm expulsion and egg counts. Although numbers of intestinal IgA-containing cells increased in both strains after infection, there was no difference between strains except at day 11 when there were significantly higher numbers in BALB/c mice than in C57BL/6 mice. These results suggest that IL-5 is an important regulatory factor determining host Immunity to Parasite infection and that differential regulation of IL-5 expression explains in part the observed strain differences with respect to Parasite resistance.
João A. N. Filipe - One of the best experts on this subject based on the ideXlab platform.
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loss of population levels of Immunity to malaria as a result of exposure reducing interventions consequences for interpretation of disease trends
PLOS ONE, 2009Co-Authors: João A. N. Filipe, Eleanor M. Riley, Chris Drakeley, Colin J. Sutherland, Azra C. Ghani, Jamie T Griffin, Roly GoslingAbstract:BACKGROUND: The persistence of malaria as an endemic infection and one of the major causes of childhood death in most parts of Africa has lead to a radical new call for a global effort towards eradication. With the deployment of a highly effective vaccine still some years away, there has been an increased focus on interventions which reduce exposure to infection in the individual and -by reducing onward transmission-at the population level. The development of appropriate monitoring of these interventions requires an understanding of the timescales of their effect. METHODS & FINDINGS: Using a mathematical model for malaria transmission which incorporates the acquisition and loss of both clinical and Parasite Immunity, we explore the impact of the trade-off between reduction in exposure and decreased development of Immunity on the dynamics of disease following a transmission-reducing intervention such as insecticide-treated nets. Our model predicts that initially rapid reductions in clinical disease incidence will be observed as transmission is reduced in a highly immune population. However, these benefits in the first 5-10 years after the intervention may be offset by a greater burden of disease decades later as Immunity at the population level is gradually lost. The negative impact of having fewer immune individuals in the population can be counterbalanced either by the implementation of highly-effective transmission-reducing interventions (such as the combined use of insecticide-treated nets and insecticide residual sprays) for an indefinite period or the concurrent use of a pre-erythrocytic stage vaccine or prophylactic therapy in children to protect those at risk from disease as Immunity is lost in the population. CONCLUSIONS: Effective interventions will result in rapid decreases in clinical disease across all transmission settings while population-level Immunity is maintained but may subsequently result in increases in clinical disease many years later as population-level Immunity is lost. A dynamic, evolving intervention programme will therefore be necessary to secure substantial, stable reductions in malaria transmission.
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Determination of the processes driving the acquisition of Immunity to malaria using a mathematical transmission model.
PLoS computational biology, 2007Co-Authors: João A. N. Filipe, Eleanor M. Riley, Chris Drakeley, Colin J. Sutherland, Azra C. GhaniAbstract:Acquisition of partially protective Immunity is a dominant feature of the epidemiology of malaria among exposed individuals. The processes that determine the acquisition of Immunity to clinical disease and to asymptomatic carriage of malaria Parasites are poorly understood, in part because of a lack of validated immunological markers of protection. Using mathematical models, we seek to better understand the processes that determine observed epidemiological patterns. We have developed an age-structured mathematical model of malaria transmission in which acquired Immunity can act in three ways ("Immunity functions"): reducing the probability of clinical disease, speeding the clearance of Parasites, and increasing tolerance to subpatent infections. Each Immunity function was allowed to vary in efficacy depending on both age and malaria transmission intensity. The results were compared to age patterns of Parasite prevalence and clinical disease in endemic settings in northeastern Tanzania and The Gambia. Two types of immune function were required to reproduce the epidemiological age-prevalence curves seen in the empirical data; a form of clinical Immunity that reduces susceptibility to clinical disease and develops with age and exposure (with half-life of the order of five years or more) and a form of anti-Parasite Immunity which results in more rapid clearance of parasitaemia, is acquired later in life and is longer lasting (half-life of >20 y). The development of anti-Parasite Immunity better reproduced observed epidemiological patterns if it was dominated by age-dependent physiological processes rather than by the magnitude of exposure (provided some exposure occurs). Tolerance to subpatent infections was not required to explain the empirical data. The model comprising Immunity to clinical disease which develops early in life and is exposure-dependent, and anti-Parasite Immunity which develops later in life and is not dependent on the magnitude of exposure, appears to best reproduce the pattern of Parasite prevalence and clinical disease by age in different malaria transmission settings. Understanding the effector mechanisms underlying these two immune functions will assist in the design of transmission-reducing interventions against malaria.
