scholarly journals IL-13 Induces Disease-Promoting Type 2 Cytokines, Alternatively Activated Macrophages and Allergic Inflammation during Pulmonary Infection of Mice withCryptococcus neoformans

2007 ◽  
Vol 179 (8) ◽  
pp. 5367-5377 ◽  
Author(s):  
Uwe Müller ◽  
Werner Stenzel ◽  
Gabriele Köhler ◽  
Christoph Werner ◽  
Tobias Polte ◽  
...  
Keyword(s):  
Pulmonary Infection ◽  
Allergic Inflammation ◽  
Activated Macrophages ◽  
Alternatively Activated Macrophages ◽  
Type 2 Cytokines ◽  
Alternatively Activated

scholarly journals Group-2 innate lymphoid cell-dependent regulation of tissue neutrophil migration by alternatively activated macrophage-secreted Ear11

2020 ◽  
Vol 14 (1) ◽  
pp. 26-37 ◽  
Author(s):  
Veera Panova ◽  
Mayuri Gogoi ◽  
Noe Rodriguez-Rodriguez ◽  
Meera Sivasubramaniam ◽  
Helen E. Jolin ◽  
...  
Keyword(s):  
Neutrophil Migration ◽  
Neutrophil Infiltration ◽  
Rnase A ◽  
Activated Macrophages ◽  
Mucus Production ◽  
Alternatively Activated Macrophages ◽  
Group 2 ◽  
Classically Activated Macrophages ◽  
Alternatively Activated

AbstractType-2 immunity is characterised by interleukin (IL)-4, IL-5 and IL-13, eosinophilia, mucus production, IgE, and alternatively activated macrophages (AAM). However, despite the lack of neutrophil chemoattractants such as CXCL1, neutrophils, a feature of type-1 immunity, are observed in type-2 responses. Consequently, alternative mechanisms must exist to ensure that neutrophils can contribute to type-2 immune reactions without escalation of deleterious inflammation. We now demonstrate that type-2 immune-associated neutrophil infiltration is regulated by the mouse RNase A homologue, eosinophil-associated ribonuclease 11 (Ear11), which is secreted by AAM downstream of IL-25-stimulated ILC2. Transgenic overexpression of Ear11 resulted in tissue neutrophilia, whereas Ear11-deficient mice have fewer resting tissue neutrophils, whilst other type-2 immune responses are not impaired. Notably, administration of recombinant mouse Ear11 increases neutrophil motility and recruitment. Thus, Ear11 helps maintain tissue neutrophils at homoeostasis and during type-2 reactions when chemokine-producing classically activated macrophages are infrequently elicited.

scholarly journals Ablation of NK Cell Function During Tumor Growth Favors Type 2-Associated Macrophages, Leading to Suppressed CTL Generation

2003 ◽  
Vol 10 (2-4) ◽  
pp. 71-81 ◽  
Author(s):  
Anja B. Geldhof ◽  
Jo A. van Ginderachter ◽  
Yuanqing Liu ◽  
Wim Noël ◽  
Patrick de Baetselier
Keyword(s):  
Nk Cells ◽  
Cell Function ◽  
Nk Cell ◽  
Activated Macrophages ◽  
Alternatively Activated Macrophages ◽  
Accessory Function ◽  
Alternatively Activated

Several reports describe regulatory interactions between NK cells and CTLs. We addressed the issue of NK participation in the early anti-tumor defense by inoculating α-ASGM-1 treated mice with BW-Sp3 T lymphoma. Rejection of BW-Sp3 depends on strong CTL responses. Our results demonstrated that (i) NK cells are a prerequisite for efficient CTL generation and (ii) the absence of NK cells favors the outgrowth of alternatively activated macrophages that can suppress CTL restimulation.In vitrostudies demonstrate that in splenic cultures from NK-deficient, tumor-bearing mice, the presence of alternatively activated macrophages correlates with a lack of Type 1 cytokines, while the production of Type 2 cytokines is promoted. Provision of the Type 1 cytokine, IFN-γ can boost overall CTL activity but does not revert the dominance of arginase producing adherent cells in the NK-deficient CTL cultures. The role of NK effector functions in the efficient switch of the immune system towards Type 1 activation was evaluated in cytotoxicity assays. The results indicate that the accessory function of NK can depend at least partially on their ability to preferentially engage arginase-producing cells, suggesting that NK/macrophage lytic interactions might be involved in the switch from Type 2 to Type 1-dependent immune responses.

scholarly journals β2-Adrenergic Receptor Enhances the Alternatively Activated Macrophages and Promotes Biliary Injuries Caused by Helminth Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Stephane Koda ◽  
Beibei Zhang ◽  
Qian-Yang Zhou ◽  
Na Xu ◽  
Jing Li ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Adrenergic Receptors ◽  
M2 Macrophages ◽  
Activated Macrophages ◽  
Alternatively Activated Macrophages ◽  
Mtorc1 Signaling ◽  
Β2 Adrenergic Receptor ◽  
Alternatively Activated

The autonomic nervous system has been studied for its involvement in the control of macrophages; however, the mechanisms underlying the interaction between the adrenergic receptors and alternatively activated macrophages (M2) remain obscure. Using FVB wild-type and beta 2 adrenergic receptors knockout, we found that β2-AR deficiency alleviates hepatobiliary damage in mice infected with C. sinensis. Moreover, β2-AR-deficient mice decrease the activation and infiltration of M2 macrophages and decrease the production of type 2 cytokines, which are associated with a significant decrease in liver fibrosis in infected mice. Our in vitro results on bone marrow–derived macrophages revealed that macrophages from Adrb2−/− mice significantly decrease M2 markers and the phosphorylation of ERK/mTORC1 induced by IL-4 compared to that observed in M2 macrophages from Adrb2+/+. This study provides a better understanding of the mechanisms by which the β2-AR enhances type 2 immune response through the ERK/mTORC1 signaling pathway in macrophages and their role in liver fibrosis.

scholarly journals Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages

2013 ◽  
Vol 210 (3) ◽  
pp. 535-549 ◽  
Author(s):  
Ari B. Molofsky ◽  
Jesse C. Nussbaum ◽  
Hong-Erh Liang ◽  
Steven J. Van Dyken ◽  
Laurence E. Cheng ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Cytokine Production ◽  
Activated Macrophages ◽  
Metabolic Homeostasis ◽  
Alternatively Activated Macrophages ◽  
Visceral Adipose ◽  
Alternatively Activated

Eosinophils in visceral adipose tissue (VAT) have been implicated in metabolic homeostasis and the maintenance of alternatively activated macrophages (AAMs). The absence of eosinophils can lead to adiposity and systemic insulin resistance in experimental animals, but what maintains eosinophils in adipose tissue is unknown. We show that interleukin-5 (IL-5) deficiency profoundly impairs VAT eosinophil accumulation and results in increased adiposity and insulin resistance when animals are placed on a high-fat diet. Innate lymphoid type 2 cells (ILC2s) are resident in VAT and are the major source of IL-5 and IL-13, which promote the accumulation of eosinophils and AAM. Deletion of ILC2s causes significant reductions in VAT eosinophils and AAMs, and also impairs the expansion of VAT eosinophils after infection with Nippostrongylus brasiliensis, an intestinal parasite associated with increased adipose ILC2 cytokine production and enhanced insulin sensitivity. Further, IL-33, a cytokine previously shown to promote cytokine production by ILC2s, leads to rapid ILC2-dependent increases in VAT eosinophils and AAMs. Thus, ILC2s are resident in VAT and promote eosinophils and AAM implicated in metabolic homeostasis, and this axis is enhanced during Th2-associated immune stimulation.

Sign in / Sign up

Export Citation Format

Share Document