European journal of dermatology : EJD · 2014
A possible mechanism in the recruitment of eosinophils and Th2 cells through CD163(+) M2 macrophages in the lesional skin of eosinophilic cellulitis.
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Fujimura Taku, Kambayashi Yumi, Furudate Sadanori, Kakizaki Aya, Aiba Setsuya
Аннотация
BACKGROUND: M2 macrophages play a critical role in the recruitment of T helper 2 (Th2) regulatory T cells (Treg).
OBJECTIVES: To study the role of M2 macrophages and Treg cells in eosinophilic celulitis.
MATERIAL AND METHODS: We employed immunohistochemical staining for CD163( )and CD206 (macrophages) as well as FoxP3 (Treg), in lesional skin of four cases of eosinophilic cellulitis.
RESULTS: CD163(+) CD206(+) M2 macrophages, which were previously reported to produce CCL17 to induce Th2 cells and Treg cells, were predominantly infiltrating the subcutaneous tissues and interstitial area of the dermis. M2 macrophages derived from PBMC showed significantly increased expression of CCL11, CCL17, CCL24 and CCL26 mRNA and production of CCL17 and CCL24, when stimulated by IL-4 or IL- 13. In addition, CCL17-producing cells and CCL24-producing cells were prominent in the lesional skin of EC.
CONCLUSION: Our study sheds light on one of the possible immunological mechanisms of eosinophilic cellulitis.
OBJECTIVES: To study the role of M2 macrophages and Treg cells in eosinophilic celulitis.
MATERIAL AND METHODS: We employed immunohistochemical staining for CD163( )and CD206 (macrophages) as well as FoxP3 (Treg), in lesional skin of four cases of eosinophilic cellulitis.
RESULTS: CD163(+) CD206(+) M2 macrophages, which were previously reported to produce CCL17 to induce Th2 cells and Treg cells, were predominantly infiltrating the subcutaneous tissues and interstitial area of the dermis. M2 macrophages derived from PBMC showed significantly increased expression of CCL11, CCL17, CCL24 and CCL26 mRNA and production of CCL17 and CCL24, when stimulated by IL-4 or IL- 13. In addition, CCL17-producing cells and CCL24-producing cells were prominent in the lesional skin of EC.
CONCLUSION: Our study sheds light on one of the possible immunological mechanisms of eosinophilic cellulitis.