The Nomenclature of Chemokines

Prieschl, Eva E.; Kulmburg, P; Baumruker, Thomas

doi:10.1159/000237089

Cited by 43 publications

(28 citation statements)

References 2 publications

(2 reference statements)

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“…We next addressed the involvement of PI3-kinase in gene in duction in our cell line using transient transfection assays. As a readout system, we used the recently characterized mast cell-specific chemokine MARC [30,39], which al ready served as a reporter for our investigations regarding ras/raf in allergic signaling [29], In addition, we used a hu man TNFa reporter gene construct as a readout. This in flammatory mediator was chosen because a corresponding, sensitive mouse TN Fa ELISA is available which allows the verification of the transient transfection data on the protein level.…”

Section: Pi3-kinase Inhibition By Dmv Does Not Influence Gene Inductimentioning

confidence: 99%

Effects of Phosphatidylinositol-3-Kinase Inhibitors on Degranulation and Gene Induction in Allergically Triggered Mouse Mast Cells

Pendl¹,

Prieschl²,

Thumb³

et al. 1997

Int Arch Allergy Immunol

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Background: Phosphatidylinositol-3-kinase (PI3-kinase) comprises an essential component in a number of signaling cascades, primarily of the growth factor type. Two specific inhibitors, wortmannin and demethoxyviridin (DMV), are widely used to block signaling via this molecule and link certain receptors to the PI3-kinase pathway Methods: We have studied the extent of involvement of PI3-kinase in signaling events by Fc_εRI in mast cells using a mouse mast cell line as a model system. This was done using β-hexosaminidase release assays, a leukotriene ELISA, transient transfections with reporter gene constructs of TNFα and MARC, and in addition a TNFα ELISA. Results: Consistent with previously published data in the rat basophilic cell line RBL-2H3, we find that wortmannin as well as DMV prevent the degranulation reaction in the mouse mast cell line CPU. DMV also inhibits the release of leukotrienes, leading to the conclusion that Fc_εRI activates PI3-kinase which then mediates these reactions. On the contrary, however, lymphokine and chemokine induction at the gene and protein level is not inhibited, suggesting that the activation of this gene set in mast cells is independent of PI3-kinase. Conclusion: PI3-kinase is activated in our mast cell model system via cross-linking of the FcεRI. This reaction is clearly necessary for the degranulation process and the release of leukotrienes. Activation of lymphokine and chemokine genes as well as secretion of their gene products are not triggered along the PI3-kinase signaling pathway. This is in agreement with our previous findings, showing that the MAP kinase pathway and Ca²⁺ influx are both involved in gene activation in this cell type.

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Section: Pi3-kinase Inhibition By Dmv Does Not Influence Gene Inductimentioning

confidence: 99%

Effects of Phosphatidylinositol-3-Kinase Inhibitors on Degranulation and Gene Induction in Allergically Triggered Mouse Mast Cells

Pendl¹,

Prieschl²,

Thumb³

et al. 1997

Int Arch Allergy Immunol

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“…1 Upon binding to its corresponding cell surface receptor, a chemoattractant induces intracellular Ca ϩϩ mobilization, cytoskeletal rearrangements, exocytosis, histamine release, receptor induction, adhesion, the production of bioactive lipids, and the activation of the respiratory burst system via NADPH oxidase activation. 1,8,9 With this important role of chemoattractants for monocyte function in mind, the identification of new chemoattractants and the characterization of their mechanisms of action are very much needed.…”

Section: Introductionmentioning

confidence: 99%

Identification of novel chemoattractant peptides for human leukocytes

Bae

Kim

et al. 2001

Blood

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“…18). Members of the chemokine superfamily are subdivided into four families based on the position of the first two cysteines at the N terminus: CXC, CC, C, CX3C (19,20). Chemokines are ligands for seven transmembrane-spanning receptors that induce signaling though a G i -protein linked pathway (21).…”

mentioning

confidence: 99%

CC Chemokine Ligand 2 and Its Receptor Regulate Mucosal Production of IL-12 and TGF-β in High Dose Oral Tolerance

DePaolo

Rollins

Kuziel

et al. 2003

The Journal of Immunology

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Oral tolerance is the result of a complex immunoregulatory strategy used by the gut and its associated lymphoid tissues to render the peripheral immune system unresponsive to nonpathogenic proteins, such as food or commensal bacteria. The mechanism of oral tolerance induction and maintenance is not well understood. We have previously shown that the chemokine, CC chemokine ligand 2 (CCL2), is important for the induction and maintenance of oral tolerance. To address the role CCL2 plays in oral tolerance, we used both CCL2−/− and CCR2−/− mice. Cells from the spleen, mesenteric lymph nodes, and peripheral lymph nodes of CCL2−/− and CCR2−/− mice fed high doses of OVA showed robust proliferative responses compared with cells from Ag-fed wild-type mice. CCL2−/− and CCR2−/− mice also produced high amounts of Th1 cytokines such as IL-2 and IFN-γ and very low amounts of IL-4 and IL-10. The ability of APCs from the gut of CCL2−/− and CCR2−/− OVA-fed mice to stimulate an indicator T cell line was evaluated. APCs from the Peyer’s patch of OVA-fed knockout animals could induce a T cell response measured by an increase in proliferation and generation of IL-12 and IFN-γ with a concomitant reduction of TGF-β compared with wild-type controls that did not induce a Th1 response. These data indicate that CCL2 and signaling through its receptor CCR2 is critical for the induction of oral tolerance by regulating Ag presentation leading to a disruption in the balance of inflammatory and regulatory cytokines.

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The Nomenclature of Chemokines

Cited by 43 publications

References 2 publications

Effects of Phosphatidylinositol-3-Kinase Inhibitors on Degranulation and Gene Induction in Allergically Triggered Mouse Mast Cells

Effects of Phosphatidylinositol-3-Kinase Inhibitors on Degranulation and Gene Induction in Allergically Triggered Mouse Mast Cells

Identification of novel chemoattractant peptides for human leukocytes

CC Chemokine Ligand 2 and Its Receptor Regulate Mucosal Production of IL-12 and TGF-β in High Dose Oral Tolerance

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