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Your search keyword '"Fallon, Padraic G."' showing total 12 results
Start Over Author "Fallon, Padraic G." Journal european journal of immunology
12 results on '"Fallon, Padraic G."'

5. Ligation of TLR7 on CD19+CD1dhi B cells suppresses allergic lung inflammation via regulatory T cells.

Author

Khan, Adnan R., Amu, Sylvie, Saunders, Sean P., Hams, Emily, Blackshields, Gordon, Leonard, Martin O., Weaver, Casey T., Sparwasser, Tim, Sheils, Orla, and Fallon, Padraic G.

Abstract

B cells have been described as having the capacity to regulate cellular immune responses and suppress inflammatory processes. One such regulatory B-cell population is defined as IL-10-producing CD19+CD1dhi cells. Previous work has identified an expansion of these cells in mice infected with the helminth, Schistosoma mansoni. Here, microarray analysis of CD19+CD1dhi B cells from mice infected with S. mansoni demonstrated significantly increased Tlr7 expression, while CD19+CD1dhi B cells from uninfected mice also demonstrated elevated Tlr7 expression. Using IL-10 reporter, Il10−/− and Tlr7−/- mice, we formally demonstrate that TLR7 ligation of CD19+CD1dhi B cells increases their capacity to produce IL-10. In a mouse model of allergic lung inflammation, the adoptive transfer of TLR7-elicited CD19+CD1dhi B cells reduced airway inflammation and associated airway hyperresponsiveness. Using DEREG mice to deplete FoxP3+ T regulatory cells in allergen-sensitized mice, we show that that TLR7-elicited CD19+CD1dhi B cells suppress airway hyperresponsiveness via a T regulatory cell dependent mechanism. These studies identify that TLR7 stimulation leads to the expansion of IL-10-producing CD19+CD1dhi B cells, which can suppress allergic lung inflammation via T regulatory cells. [ABSTRACT FROM AUTHOR]

Published
2015
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10. Defective in vivoinduction of functional type 2 cytokine responses in aged mice

Author

Smith, Philip, Dunne, David W., and Fallon, Padraic G.

Abstract

Aged mice have various defects in their immune system. We report that following in vivochallenge with type 2 cytokine‐inducing Schistosoma mansonieggs, aged mice fail to produce type 2 cytokines and also have impaired antigen‐specific antibody production. Using two separate type 2 cytokine‐dependent in vivomodels, the synchronous pulmonary schistosome egg granuloma model and infection with the gastro‐intestinal nematode Nippostrongylus brasiliensis, aged mice were shown to have a dramatically impaired capacity to elicit a functional type 2 response, i. e.respectively, impaired pulmonary granulomas and delayed rejection of intestinal worms. Aged mice did not develop eosinophilia and had impaired production of antigen specific IgE. Defective induction of type 2 responses was associated with negligible IL‐2 and elevated IFN‐γ production by cells from aged mice. Naive aged mice had increased numbers of Th1, Th2 and Tc1 cells compared to young animals. In vivotype 2 challenge increased the frequencies of Th1 and Tc1 cells and reducing Th2 cell numbers in aged mice. These data demonstrate that a consequence of ageing is a profound in vivodefect in the capacity to elicit type 2 cytokine responses and such an impairment in type 2 responsiveness may account for the increased incidence of various type 1 cytokine‐mediated diseases in aged individuals.

Published
2001
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11. Type 1 and type 2 cytokine-producing mouse CD4<SUP>+</SUP> and CD8<SUP>+</SUP> T cells in acute Schistosoma mansoni infection

Author

Fallon, Padraic G., Smith, Philip, and Dunne, David W.

Abstract

CD4+ and CD8+ T cells can be divided based on the cytokines that they secrete into type 1 (Th1, Tc1) and type 2 (Th2, Tc2) subsets. Schistosoma mansoni infection in mice is characterized by a type 2-dominated response. We have used intracellular cytokine staining to demonstrate dramatic changes in the relative numbers of Tc1 and Th2 cells in the spleens of mice during acute schistosome infection. In infected mice prior to egg laying a generalized type 1 response dominated, and was associated with an expansion in the frequency of Tc1 and Th1 cells. By week 7 after infection the cytokine response was of type 2, with an increase in the numbers of Th2 cells and a dramatic reduction in the frequency of Tc1 cells. Following the onset of egg laying there was apoptosis of cells in the spleens of mice, with CD4+ and in particular CD8+ T cells undergoing apoptosis. The loss of CD8+ T cells may in part be attributable to the development of a type 2 environment, following egg laying, with type 2 responses mediating the apoptosis of Tc1 cells. Schistosome regulation of Tc1 during egg laying may be required to prevent type 1 inflammatory responses from exacerbating egg-induced pathology.

Published
1998
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12. Ligation of TLR7 on CD19(+) CD1d(hi) B cells suppresses allergic lung inflammation via regulatory T cells.

Author

Khan AR, Amu S, Saunders SP, Hams E, Blackshields G, Leonard MO, Weaver CT, Sparwasser T, Sheils O, and Fallon PG

Subjects
Animals, Antigens, CD19 metabolism, Antigens, CD1d metabolism, Disease Models, Animal, Humans, Hypersensitivity immunology, Hypersensitivity metabolism, Interleukin-10 biosynthesis, Mice, Mice, Knockout, Ovalbumin adverse effects, Pneumonia parasitology, Protein Binding, Respiratory Hypersensitivity immunology, Respiratory Hypersensitivity metabolism, Respiratory Hypersensitivity parasitology, Schistosoma mansoni immunology, Schistosomiasis mansoni immunology, Schistosomiasis mansoni metabolism, Up-Regulation, B-Lymphocytes immunology, B-Lymphocytes metabolism, Pneumonia immunology, Pneumonia metabolism, T-Lymphocytes, Regulatory immunology, T-Lymphocytes, Regulatory metabolism, Toll-Like Receptor 7 metabolism
Abstract

B cells have been described as having the capacity to regulate cellular immune responses and suppress inflammatory processes. One such regulatory B-cell population is defined as IL-10-producing CD19(+) CD1d(hi) cells. Previous work has identified an expansion of these cells in mice infected with the helminth, Schistosoma mansoni. Here, microarray analysis of CD19(+) CD1d(hi) B cells from mice infected with S. mansoni demonstrated significantly increased Tlr7 expression, while CD19(+) CD1d(hi) B cells from uninfected mice also demonstrated elevated Tlr7 expression. Using IL-10 reporter, Il10(-/-) and Tlr7(-/-) mice, we formally demonstrate that TLR7 ligation of CD19(+) CD1d(hi) B cells increases their capacity to produce IL-10. In a mouse model of allergic lung inflammation, the adoptive transfer of TLR7-elicited CD19(+) CD1d(hi) B cells reduced airway inflammation and associated airway hyperresponsiveness. Using DEREG mice to deplete FoxP3(+) T regulatory cells in allergen-sensitized mice, we show that that TLR7-elicited CD19(+) CD1d(hi) B cells suppress airway hyperresponsiveness via a T regulatory cell dependent mechanism. These studies identify that TLR7 stimulation leads to the expansion of IL-10-producing CD19(+) CD1d(hi) B cells, which can suppress allergic lung inflammation via T regulatory cells., (© 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Published
2015
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