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| PubMed | |
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Article by LI Feng |
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Article by JIN Hong-zhong |
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����ŧ�岡�ķ��������漰����ϸ������֢���ӡ������̼���,�����γ�ϸ��ͨ��CCL20/CCR6ϵͳ��C5a�ֱ�����T�ܰ�ϸ����������ϸ����T�ܰ�ϸ��ͨ��������/����øBϵͳ��Fas/FasLϵͳ�ٽ���Ƥ��ˮ���γ�,���CXCL8����������ϸ�����ٽ������γ�ϸ����ʿ�ԭ��ͬʱ,�����������ϸ�����Ա���˰�ϸ��DR��ԭ,�̼�Tϸ��,�Ŵ���֢������,�ֲ���ȫ��Ƥ������ϸ������øˮƽ����Ҳ�ٽ�ŧ����γɡ�
Pathogenesis of sterile pustulosis
Department of Dermatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China
Department of Dermatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China
The pathogenesis of sterile pustulosis involves various cells and inflammatory mediators. Upon outside stimulation, keratinocytes induce the accumulation of T lymphocytes and neutrophils respectively by CCL20/CCR6 system and peptide C 5a . T lymphocytes not only facilitate the formation of intraepidermal vesicles by the perforin/granzyme B and Fas/Fasl system, but also produce CXCL8 to enhance the recruitment of neutrophils and antigen presentation of keratinocytes. Meanwhile, activated neutrophils could express human leukocyte antigen (HLA)-DR and excite T lymphocytes to amplify the inflammation. Besides, the decrease of local or systemic levels of skin-derived antileukoproteinase also contributes to the formation of pustules.
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