In vivo expression of IL-4, IL-5, IL-13 and IFN-γ mRNAs in peripheral blood mononuclear cells and effect of cyclosporin A in a patient with Kimura's disease

Katagiri, Kazumoto; Itami, Satoshi; Hatano, Yutaka; Yamaguchi, Tomiko; Takayasu, Susumu

doi:10.1111/j.1365-2133.1997.tb01562.x

Cited by 100 publications

(59 citation statements)

References 24 publications

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“…However, there is a possibility that mast cells secrete these cytokines in the lesions of Kimura’s disease by this slow degranulation mechanism. It has been reported that Kimura’s disease was completely cured and IL-4 and IL-5 expression decreased to a minimum level by surgical resection or radiotherapy [20]. These findings suggest the possibility that the skin lesion itself provides some factors that increase IL-4 and IL-5 levels in Kimura’s disease patients.…”

Section: Discussionsupporting

confidence: 47%

The Ultrastructural Patterns of Mast Cell Degranulation in Kimura’s Disease

Aoki

Kawana²

1999

Dermatology

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Background: Although Kimura’s disease has been considered an atopic disease because of the association of peripheral blood eosinophilia and elevated serum IgE, the mechanisms of these phenomena are still unknown. Objective: It is now established that mast cells are a source of cytokines that are involved in eosinophil recruitment or IgE production. In order to understand the role of mast cells in Kimura’s disease, we conducted ultrastructural studies. Method: The 45 mast cells obtained from 2 patients with Kimura’s disease were classified into two subgroups: S type, with a predominance of scroll or crystal subelements in their granules, and P type, predominantly possessing a particulate or filamentous substructure. Results: We observed numerous P type mast cells with focal losses of granule contents in the absence of granule extrusion in Kimura’s disease. Conclusion: These results indicate the possibility that slow release of mediators or cytokines from mast cells by piecemeal degranulation may contribute to the pathomechanism of Kimura’s disease.

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Section: Discussionsupporting

confidence: 47%

The Ultrastructural Patterns of Mast Cell Degranulation in Kimura’s Disease

Aoki

Kawana²

1999

Dermatology

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“…The mainstay of therapy has been oral corticosteroids, even though steroid withdrawal can result in recurrence. Recently, 3 cases of successful treatment of Kimura’s disease with cyclosporine have been described [10, 11, 12]. In our case, the treatment with cyclosporine rapidly improved the subcutaneous nodules accompanied by the improvement of peripheral blood eosinophilia.…”

Section: Discussionmentioning

confidence: 56%

Lichen amyloidosus Associated with Kimura’s Disease: Successful Treatment with Cyclosporine

Teraki¹,

Katsuta²,

Shiohara³

2002

Dermatology

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We describe here a case of a 33-year-old man who had lichen amyloidosus associated with Kimura’s disease. In this case, treatment with cyclosporine dramatically improved the lesions of both Kimura’s disease and lichen amyloidosus. Although Kimura’s disease and lichen amyloidosus are both rare distinct entities, to our knowledge, 11 cases of association of Kimura’s disease and lichen amyloidosus have been described previously.

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“…Several studies reported that the serum levels of Th2-type cytokines such as IL-4, IL-5, and IL-13 were elevated [10, 11, 12]. In another study, activated lymphocytes released cytokines such as GM-CSF and TNF-α, and these released cytokines caused eosinophil activation [24].…”

Section: Discussionmentioning

confidence: 99%

“…Most previous studies reported that lymphocytes and mast cells were important in the pathogenesis of ALHE [10, 11, 12, 22, 23]although ALHE is known as an eosinophilic inflammatory disorder. Several studies reported that the serum levels of Th2-type cytokines such as IL-4, IL-5, and IL-13 were elevated [10, 11, 12].…”

Section: Discussionmentioning

confidence: 99%

“…We have previously reported that helper T lymphocytes from ALHE patients produced an eosinophil chemoattractant which was induced by a monocyte-derived factor [9]. However, the precise mechanism of such eosinophilia is still unclear, although several studies have suggested that Th2-type cytokines, such as IL-4, IL-5, and Il-13, are involved in the eosinophilia [10, 11, 12]. Galectin-9 may play a role in tissue eosinophilia of Hodgkin’s disease (HD).…”

Section: Introductionmentioning

confidence: 99%

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Association of Galectin-9 with Eosinophil Apoptosis

Saita

Goto

Yamamoto

et al. 2002

Int Arch Allergy Immunol

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Background: There is no information whether galectin-9 (a novel eosinophil chemoattractant) was associated with pathogenesis of eosinophilic disorders. Methods: We assessed the expression of galectin-9 with imunostaining and in situ hybridization both in the lesion of angiolymphoid hyperplasia with eosinophilia, and peripheral blood eosinophils of eosinophilic patients (E-Eos) in comparison with those of normal volunteers (N-Eos). Regulation of expression of galectin-9 on eosinophils and the effect of galectin-9 on apoptosis of eosinophil were also evaluated. Results: Many eosinophils infiltrating the site were positive for galectin-9. Surface and intracellular immunoreactive galectin-9 was more evident in E-Eos than N-Eos. When eosinophils were cultured with IL-5 in vitro, the surface galectin-9 expression of E-Eos was significantly downregulated, although that of N-Eos was not affected. Treatment of eosinophils with dexamethasone or anti-Fas antibody significantly upregulated the surface galectin-9 expression of E-Eos. In contrast, dexamethasone partially downregulated the surface galectin-9 of N-Eos, although anti-Fas antibody failed to affect on the surface galectin-9 expression. We also found that recombinant galectin-9 significantly suppressed apoptosis of E-Eos (p = 0.0431), whereas it apparently enhanced apoptosis of N-Eos (p = 0.0173). Furthermore, dexamethasone-induced apoptosis of N-Eos was significantly suppressed by galectin-9 (p = 0.0431), whereas galectin-9 failed to induce significant change in dexamethasone-induced apoptosis of E-Eos. In contrast, apoptosis induced by anti-Fas antibody in both N-Eos (p = 0.0431) and E-Eos (p = 0.0431) was enhanced by galectin-9. Conclusions: These findings suggested that galectin-9 was produced by eosinophils, and galectin-9 showed heterogeneous effects and kinetics to eosinophils, and this factor might be one of crucial factors in eosinophilic inflammation.

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In vivo expression of IL-4, IL-5, IL-13 and IFN-γ mRNAs in peripheral blood mononuclear cells and effect of cyclosporin A in a patient with Kimura's disease

Cited by 100 publications

References 24 publications

The Ultrastructural Patterns of Mast Cell Degranulation in Kimura’s Disease

The Ultrastructural Patterns of Mast Cell Degranulation in Kimura’s Disease

Lichen amyloidosus Associated with Kimura’s Disease: Successful Treatment with Cyclosporine

Association of Galectin-9 with Eosinophil Apoptosis

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