Expression of IL-4 receptor on non-bone marrow-derived cells is necessary for the timely elimination of Strongyloides venezuelensis in mice, but not for intestinal IL-4 production

Negrão-Corrêa, Déborah; Pinho, Vanessa; Souza, Danielle G.; Pereira, Ana Terezinha M.; Fernandes, André Almeida; Scheuermann, Karina; Souza, Adriano Lopes de; Teixeira, Mauro M.

doi:10.1016/j.ijpara.2006.05.005

Cited by 33 publications

(32 citation statements)

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“…Phenotypic analysis of these cells after primary and secondary infections with S. stercoralis revealed increased expression of Relm-␣ by macrophages, a phenotype associated with AAM. Polarization of AAM in the peritoneal cavities of infected mice was dependent on IL-4 and IL-4R␣, consistent with the importance of IL-4/IL-13 signaling for the development of AAM observed during other parasite infections (39)(40)(41)(42). The presence of AAM in the peritoneal cavity following a subcutaneous injection reflects a systemic immune response likely induced by the highly motile larvae of S. stercoralis (43).…”

Section: Discussionsupporting

confidence: 80%

Human and Mouse Macrophages Collaborate with Neutrophils To Kill Larval Strongyloides stercoralis

et al. 2013

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bMacrophages are multifunctional cells that are active in T H 1-and T H 2-mediated responses. In this study, we demonstrate that human and mouse macrophages collaborate with neutrophils and complement to kill the parasite Strongyloides stercoralis in vitro. Infection of mice with worms resulted in the induction of alternatively activated macrophages (AAM) within the peritoneal cavity. These cells killed the worms in vivo and collaborated with neutrophils and complement during the in vitro killing process. AAM generated in vitro killed larvae more rapidly than naive macrophages, which killed larvae after a longer time period. In contrast, classically activated macrophages were unable to kill larvae either in vitro or in vivo. This study adds macrophages to the armamentarium of immune components that function in elimination of parasitic helminths and demonstrate a novel function by which AAM control large extracellular parasites.

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Section: Discussionsupporting

confidence: 80%

Human and Mouse Macrophages Collaborate with Neutrophils To Kill Larval Strongyloides stercoralis

et al. 2013

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“…This type 2 response is likely helpful in controlling helminth infections as deficiencies of IL-4, IL-4R signaling, and IgE are associated with increased parasite burdens in a number of animal models (1)(2)(3)(4)(5)(6)(7).…”

mentioning

confidence: 99%

Basophils Amplify Type 2 Immune Responses, but Do Not Serve a Protective Role, during Chronic Infection of Mice with the Filarial Nematode Litomosoides sigmodontis

Torrero

Hübner

Larson

et al. 2010

The Journal of Immunology

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“…For the quantitative analysis of mucus area, images covering 81.754 m 2 of lung sections were captured and mucus (red-stained areas) was measured with the software Image Pro-Plus (Media Cybernetics). To estimate eosinophil levels in the lungs, the eosinophil peroxidase (EPO) colorimetric assay was performed as described previously (32).…”

Section: Ova-induced Airway Inflammationmentioning

confidence: 99%

IL-33 Induces Antigen-Specific IL-5+ T Cells and Promotes Allergic-Induced Airway Inflammation Independent of IL-4

Kurowska‐Stolarska

Kewin

Murphy

et al. 2008

The Journal of Immunology

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418

423

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Type 2 cytokines (IL-4, IL-5, and IL-13) play a pivotal role in helminthic infection and allergic disorders. CD4+ T cells which produce type 2 cytokines can be generated via IL-4-dependent and -independent pathways. Although the IL-4-dependent pathway is well documented, factors that drive IL-4-independent Th2 cell differentiation remain obscure. We report here that the new cytokine IL-33, in the presence of Ag, polarizes murine and human naive CD4+ T cells into a population of T cells which produce mainly IL-5 but not IL-4. This polarization requires IL-1R-related molecule and MyD88 but not IL-4 or STAT6. The IL-33-induced T cell differentiation is also dependent on the phosphorylation of MAPKs and NF-κB but not the induction of GATA3 or T-bet. In vivo, ST2−/− mice developed attenuated airway inflammation and IL-5 production in a murine model of asthma. Conversely, IL-33 administration induced the IL-5-producing T cells and exacerbated allergen-induced airway inflammation in wild-type as well as IL-4−/− mice. Finally, adoptive transfer of IL-33-polarized IL-5+IL-4−T cells triggered airway inflammation in naive IL-4−/− mice. Thus, we demonstrate here that, in the presence of Ag, IL-33 induces IL-5-producing T cells and promotes airway inflammation independent of IL-4.

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Expression of IL-4 receptor on non-bone marrow-derived cells is necessary for the timely elimination of Strongyloides venezuelensis in mice, but not for intestinal IL-4 production

Cited by 33 publications

References 50 publications

Human and Mouse Macrophages Collaborate with Neutrophils To Kill Larval Strongyloides stercoralis

Human and Mouse Macrophages Collaborate with Neutrophils To Kill Larval Strongyloides stercoralis

Basophils Amplify Type 2 Immune Responses, but Do Not Serve a Protective Role, during Chronic Infection of Mice with the Filarial Nematode Litomosoides sigmodontis

IL-33 Induces Antigen-Specific IL-5+ T Cells and Promotes Allergic-Induced Airway Inflammation Independent of IL-4

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