Signaling through the β2 integrin prolongs eosinophil survival

Chihara, Junichi; Kakazu, Tomokazu; Higashimoto, Ikkou; Saito, Norihiro; Honda, Kazuo; Sannohe, Satoshi; Kayaba, Hiroyuki; Urayama, Osamu

doi:10.1067/mai.2000.106884

Cited by 23 publications

(19 citation statements)

References 24 publications

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“…In this regard, fibronectin-a component of the ECM-and adhering molecules such as intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 can prolong eosinophil survival via interaction with their receptor, integrins. [30][31][32][33][34] In primary systemic vasculitis, including CSS, increased levels of the fibronectin-containing complex have been reportedly observed in the serum. 35 Thus, the interaction between the eosinophil surface molecules and the components in the tissue microenvironment appears to play a pivotal role in eosinophil survival.…”

Section: Discussionmentioning

confidence: 99%

Discoidin domain receptor 1 contributes to eosinophil survival in an NF-κB–dependent manner in Churg-Strauss syndrome

Matsuyama

Mitsuyama

Ono

et al. 2006

Blood

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Churg-Strauss syndrome (CSS) is a systemic disease that shows marked eosinophilia along with eosinophil infiltration in the tissue. Prolonged eosinophil survival plays an important role in the pathogenesis of CSS; however, its detailed molecular mechanism remains unclear. Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase, and its ligand is collagen. DDR1 was expressed in human leukocytes and fibroblasts, and it plays an important role in leukocyte cytokine production and fibroblast survival in an NF-κB–dependent manner. In this study, we examined in vitro and in vivo eosinophil DDR1 expression and its function in CSS patients. The expression level of DDR1 was significantly higher in the eosinophils of CSS patients, and the predominant isoform was DDR1b. Immunohistochemical findings revealed that the tissue-infiltrating eosinophils expressed endogenous DDR1. In CSS patients, DDR1 activation inhibited Fas agonistic antibody–induced apoptosis and up-regulated Fas agonistic antibody–induced cytokine production of eosinophils in an NF-κB–dependent manner. Suppression of DDR1 expression in the eosinophils by using RNA interference and addition of the DDR1-blocking protein abolished these effects. We propose that DDR1 contributes to the eosinophil survival in the tissue microenvironment of CSS and that it might be involved in the development of CSS.

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Section: Discussionmentioning

confidence: 99%

Discoidin domain receptor 1 contributes to eosinophil survival in an NF-κB–dependent manner in Churg-Strauss syndrome

Matsuyama

Mitsuyama

Ono

et al. 2006

Blood

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“…contributed equally to this study. [4,5] . Moreover, we and others have previously reported that RANTES and eotaxin induce eosinophil activation without changes in the expression of ␤ 2 integrins on purifi ed eosinophils [3,6,7] .…”

Section: Introductionmentioning

confidence: 99%

RANTES and Eotaxin Enhance CD11b and CD18 Expression on Eosinophils from Allergic Patients with Eosinophilia in the Application of Whole Blood Flow Cytometry Analysis

Chiba

Kamada

Saito

et al. 2005

Int Arch Allergy Immunol

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Background: C-C chemokines and adhesion molecules expressed on eosinophils play an important role in the pathology of allergic inflammatory disease. C-C chemokines such as eotaxin or RANTES are involved in β₂ integrin expression on purified eosinophils; so far we have no data on unpurified eosinophils in the peripheral blood. We measured β₁ and β₂ integrin activation after stimulation with eotaxin or RANTES in vitro using whole-blood flow-cytometric analysis. Methods: Heparinized whole blood obtained from allergic patients with eosinophilia or normal subjects was diluted with the same volume of RPMI 1640, and then cells were incubated in the presence or absence of PMA/ionomycin or chemokines for 45 min at 37°C. After hemolyzation with lysing solution, expression of CD11b, CD11a, CD18 and CD49d on eosinophils was measured using flow cytometry. Results: The expression of CD11b, CD11a and CD18 in allergic patients was significantly higher than that in normal subjects. CD11b and CD18 expression showed a significant increase after stimulation with C-C chemokines, which was remarkable in allergic patients. Conclusion: Eosinophils in the blood of allergic patients exhibited a higher expression of β₂ integrins and were more sensitive to RANTES and eotaxin than those of normal subjects.

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“…Furthermore, it has previously been demonstrated that it takes more than 24 h after an allergen-induced degranulation until the content of the mast cell granules is fully restored [35]. A recent study by Macfarlane et al [44]has shown that, compared to diluent sites, the number of tryptase+ cells in skin biopsies obtained from allergen-challenged sites is significantly reduced 6–48 h after intradermal allergen challenge.…”

Section: Discussionmentioning

confidence: 99%

A Hypoallergenic Derivative of the Major Allergen of the Dust Mite <i>Lepidoglyphus destructor</i>, Lep d 2.6Cys, Induces Less IgE Reactivity and Cellular Response in the Skin than Recombinant Lep d 2

Kronqvist

Johansson²,

Whitley

et al. 2001

Int Arch Allergy Immunol

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Background: The major allergen of the dust mite Lepidoglyphus destructor, Lep d 2, has been produced as a recombinant allergen (rLep d 2) with IgE reactivity both in vivo and in vitro. A modified form of rLep d 2 (rLep d 2.6Cys) obtained by site-directed mutagenesis has been shown to have a reduced IgE reactivity in vitro. In this study we have compared the ability of rLep d 2 and rLep d 2.6Cys to elicit positive skin prick tests and cellular responses among L. destructor-sensitized subjects. Methods: Seventeen subjects were skin prick-tested with rLep d 2, rLep d 2.6Cys, histamine and negative controls and 17–20 h later skin biopsy specimens were taken from the skin prick-tested sites. The biopsy specimens were stained immunohistochemically for EG2+, CD3+, CD1a+, mast cell tryptase+, and IgE+ cells. Dermal cell infiltrates were judged in hematoxylin and eosin staining. Total IgE and allergen-specific IgE were determined by CAP-RAST. Results: Compared to rLep d 2, rLep d 2.6Cys induced significantly smaller and fewer skin prick test reactions (p < 0.001) and dermal cell infiltrates (p < 0.05). Further, rLep d 2.6Cys induced fewer EG2+ cells (p < 0.001) but more tryptase+ cells (p < 0.05) than rLep d 2. A positive RAST to rLep d 2 was obtained for 88.2% of the subjects, while only 35.2% displayed a positive RAST to rLep d 2.6Cys. Conclusion: This study demonstrates that rLep d 2.6Cys is less able to evoke IgE-mediated reactions and cellular responses, as measured both in skin and in serum, than rLep d 2. In the future this hypoallergenic derivative may be a promising candidate molecule for immunotherapy of L. destructor-allergic patients.

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Signaling through the β2 integrin prolongs eosinophil survival

Cited by 23 publications

References 24 publications

Discoidin domain receptor 1 contributes to eosinophil survival in an NF-κB–dependent manner in Churg-Strauss syndrome

Discoidin domain receptor 1 contributes to eosinophil survival in an NF-κB–dependent manner in Churg-Strauss syndrome

RANTES and Eotaxin Enhance CD11b and CD18 Expression on Eosinophils from Allergic Patients with Eosinophilia in the Application of Whole Blood Flow Cytometry Analysis

A Hypoallergenic Derivative of the Major Allergen of the Dust Mite <i>Lepidoglyphus destructor</i>, Lep d 2.6Cys, Induces Less IgE Reactivity and Cellular Response in the Skin than Recombinant Lep d 2

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