Type 1 and type 2 cytokine-producing mouse CD4+ and CD8+ T cells in acuteSchistosoma mansoni infection

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

doi:10.1002/(sici)1521-4141(199804)28:04<1408::aid-immu1408>3.0.co;2-h

Cited by 80 publications

(79 citation statements)

References 31 publications

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“…Intracellular Cytokine Analysis-Intracellular detection of IL-4 and IFN-␥ in CD4 ϩ T cells was performed essentially as described (31). All intracellular antibodies and reagents were from Caltag (Burlingame, CA).…”

Section: Methodsmentioning

confidence: 99%

Characterization of Signaling Pathways Activated by the Interleukin 1 (IL-1) Receptor Homologue T1/ST2

Brint

Fitzgerald

Smith

et al. 2002

Journal of Biological Chemistry

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Section: Methodsmentioning

confidence: 99%

Characterization of Signaling Pathways Activated by the Interleukin 1 (IL-1) Receptor Homologue T1/ST2

Brint

Fitzgerald

Smith

et al. 2002

Journal of Biological Chemistry

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“…Surface marker expression and intracellular cytokine phenotyping were assessed by immunofluorescent staining of B cell populations as previously described (25,26). Data were collected on a FACScan flow cytometer (BD Biosciences, San Jose, CA) and were analyzed using CellQuest software (BD Biosciences).…”

Section: Flow Cytometrymentioning

confidence: 99%

Helminth Infection Protects Mice from Anaphylaxis via IL-10-Producing B Cells

Mangan

Fallon

Smith³

et al. 2004

The Journal of Immunology

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247

208

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Modulation of the immune system by infection with helminth parasites, including schistosomes, is proposed to reduce the levels of allergic responses in infected individuals. In this study we investigated whether experimental infection with Schistosoma mansoni could alter the susceptibility of mice to an extreme allergic response, anaphylaxis. We formally demonstrate that S. mansoni infection protects mice from an experimental model of systemic fatal anaphylaxis. The worm stage of infection is shown to mediate this protective effect. In vivo depletion studies demonstrated an imperative role for B cells and IL-10 in worm-mediated protection. Furthermore, worm infection of mice increases the frequency of IL-10-producing B cells compared with that in uninfected mice. However, transfer of B cells from worm-infected mice or in vitro worm-modulated B cells to sensitized recipients exacerbated anaphylaxis, which was attributed to the presence of elevated levels of IL-4-producing B cells. Worm-modulated, IL-10-producing B cells from IL-4-deficient, but not IL-5-, IL-9- or IL-13-deficient, mice conferred complete resistance to anaphylaxis when transferred to naive mice. Therefore, we have dissected a novel immunomodulatory mechanism induced by S. mansoni worms that is dependent on an IL-10-producing B cell population that can protect against allergic hypersensitivity. These data support a role for helminth immune modulation in the hygiene hypothesis and further illustrate the delicate balance between parasite induction of protective regulatory (IL-10) responses and detrimental (IL-4) allergic responses.

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“…The spleen and mesenteric lymph node cells were aseptically removed. Single-cell suspensions were prepared as described (31). Cells (5 ϫ 10 6 /ml) were stimulated with parasite egg Ags (10 g/ml) or Escherichia coli LPS serotype 0127:B8 (1 g/ml; Sigma).…”

Section: Immunological Assaysmentioning

confidence: 99%

Schistosome Infection of Transgenic Mice Defines Distinct and Contrasting Pathogenic Roles for IL-4 and IL-13: IL-13 Is a Profibrotic Agent

Fallon

Richardson

McKenzie

et al. 2000

The Journal of Immunology

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376

373

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Experimental Schistosoma mansoni infections of mice lead to a dynamic type 2 cytokine-mediated pathological process. We have used IL-4-deficient, IL-13-deficient, and IL-4/13-deficient mice to dissect the role of these cytokines in the development of immune response and pathology following S. mansoni infection. We demonstrate that while both of these cytokines are necessary to develop a robust Th2 cell-driven, eosinophil-rich granuloma response, they also perform disparate functions that identify novel sites for therapeutic intervention. IL-13-deficient mice demonstrated significantly enhanced survival following infection, which correlated with reduced hepatic fibrosis. In contrast, increased mortality was manifest in IL-4-deficient and IL-4/13-deficient mice, and this correlated with hepatocyte damage and intestinal pathology. Therefore, we demonstrate that during a dynamic type 2 cytokine disease process IL-13 is detrimental to survival following infection, whereas IL-4 is beneficial.

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Type 1 and type 2 cytokine-producing mouse CD4+ and CD8+ T cells in acuteSchistosoma mansoni infection

Cited by 80 publications

References 31 publications

Characterization of Signaling Pathways Activated by the Interleukin 1 (IL-1) Receptor Homologue T1/ST2

Characterization of Signaling Pathways Activated by the Interleukin 1 (IL-1) Receptor Homologue T1/ST2

Helminth Infection Protects Mice from Anaphylaxis via IL-10-Producing B Cells

Schistosome Infection of Transgenic Mice Defines Distinct and Contrasting Pathogenic Roles for IL-4 and IL-13: IL-13 Is a Profibrotic Agent

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