Eosinophil recruitment and activation: the role of lipid mediators

Luna-Gomes, Tatiana; Bozza, Patrı́cia T.; Bandeira‐Melo, Christianne

doi:10.3389/fphar.2013.00027

Cited by 32 publications

(47 citation statements)

References 80 publications

(89 reference statements)

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“…Early studies of the roles of eosinophils in host responses, immunity and allergic inflammation focused on the potential effects of eosinophil degranulation, with release of the cardinal cationic proteins that are uniquely packaged within eosinophil granules. However, eosinophils are also both sources of and responders to diverse cytokines, as well as many other mediators, including lipids 144 . As discussed above, recent insights into the roles of tissue-dwelling eosinophils in the steady state are mainly based on eosinophil-derived cytokines.…”

Section: Discussionmentioning

confidence: 99%

Functions of tissue-resident eosinophils

2017

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Eosinophils are a prominent cell type in particular host responses such as the response to helminth infection and allergic disease. Their effector functions have been attributed to their capacity to release cationic proteins stored in cytoplasmic granules by degranulation. However, eosinophils are now being recognized for more varied functions in previously underappreciated diverse tissue sites, based on the ability of eosinophils to release cytokines (often preformed) that mediate a broad range of activities into the local environment. In this Review, we consider evolving insights into the tissue distribution of eosinophils and their functional immunobiology, which enable eosinophils to secrete in a selective manner cytokines and other mediators that have diverse, ‘non-effector’ functions in health and disease.

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Section: Discussionmentioning

confidence: 99%

Functions of tissue-resident eosinophils

2017

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“…The above results showed a global decrease in transcriptional V9V2 T cell responses to successive in vivo stimulations by PAg and an activation of the PPAR pathway in macaque V9V2 T cells after a I3 exposure to stimulating PAg. Among the natural ligands of PPAR, various eicosanoids, such as leucotriene B4, are generated during inflammatory responses [20,21]. In addition to these effects of ligand-bound PPAR on NF-B and c-jun, it has also been reported that ligand-free PPAR may inhibit the phosphorylation of p38 [22], a kinase that also promotes IFN transcription downstream of TCR stimulation [23].…”

Section: Resultsmentioning

confidence: 99%

The PPARα pathway in Vγ9Vδ2 T cell anergy

Poupot

Boissard

Bétous

et al. 2014

Cellular and Molecular Biology Letters

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Phosphoantigens (PAgs) activate V9V2 T lymphocytes, inducing their potent and rapid response in vitro and in vivo. However, humans and nonhuman primates that receive repeated injections of PAgs progressively lose their V9V2 T cell response to them. To elucidate the molecular mechanisms of this in vivo desensitization, we analyzed the transcriptome of circulating V9V2 T cells from macaques injected with PAg. We showed that three PAg injections induced the activation of the PPAR pathway in V9V2 T cells. Thus, we analyzed the in vitro response of V9V2 T cells stimulated with a PPAR agonist. We demonstrated that in vitro PPAR pathway activation led to the inhibition of the BrHPP-induced activation and proliferation of human V9V2 T cells. Since the PPAR pathway is involved in the antigen-selective desensitization of human V9V2 T cells, the use of PPAR inhibitors could enhance cancer immunotherapy based on V9V2 T cells.

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“…Complement C5a, platelet activating factor (PAF), the eicosanoids (leukotriene B4 (LTB 4 ) and prostaglandin D2), and the ligands for CC-chemokine receptor 3 (CCR3) (RANTES, MCP-4, and eotaxin 1–3) are the major chemoattractants for eosinophils. 58 Warringa et al compared chemotactism of eosinophils for 2.5 hours toward PAF, LTB 4 , C5a and IL-8 after a short pre-activation (30 min) with increasing concentrations of either GM-CSF or IL-3. 59 Both GM-CSF and IL-3 increased eosinophil chemotactism toward LTB 4 and IL-8, although at different cytokine concentrations.…”

Section: Commonalities and Differences Among Il-3 Il-5 And Gm-cmentioning

confidence: 99%

Essential mechanisms of differential activation of eosinophils by IL-3 compared to GM-CSF and IL-5

Esnault

Kelly

2017

Crit Rev Immunol

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There is compelling evidence that the eosinophils bring negative biological outcomes in several diseases, including eosinophilic asthma and hypereosinophilic syndromes. Eosinophils produce and store a broad range of toxic proteins and other mediators that enhance the inflammatory response and lead to tissue damage. For instance, in asthma, there is a close relationship between increased lung eosinophilia, asthma exacerbation, and loss of lung function. The use of an anti-IL-5 therapy in severe eosinophilic asthmatic patients is efficient to reduce exacerbations. However, anti-IL-5-treated patients still display a relatively high amount of functional lung tissue eosinophils, indicating that supplemental therapies are required to damper the eosinophil functions. Our recent published works, suggest that compared to IL-5, IL-3 can more strongly and differentially affect eosinophil functions. In this review, we will summarize our and other investigations that have compared the effects of the three β-chain receptor cytokines (IL-5, GM-CSF and IL-3) on eosinophil biology. We will focus on how IL-3 differentially activates eosinophils compared to IL-5 or GM-CSF.

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Eosinophil recruitment and activation: the role of lipid mediators

Cited by 32 publications

References 80 publications

Functions of tissue-resident eosinophils

Functions of tissue-resident eosinophils

The PPARα pathway in Vγ9Vδ2 T cell anergy

Essential mechanisms of differential activation of eosinophils by IL-3 compared to GM-CSF and IL-5

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