NF-κB Links Keratinocytes and Lymphocytes in the Pathogenesis of Psoriasis
NF-κB Links Keratinocytes and Lymphocytes in the Pathogenesis of Psoriasis
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DOI:
10.2174/187221309787158399
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发表时间:
2009-01-01
影响因子:
4.2
通讯作者:
Tsuruta, Daisuke
中科院分区:
文献类型:
--
作者:
Tsuruta, Daisuke
Psoriasis is a common, chronic and relapsing autoimmune skin disease. Clinical characteristics of this disease are sharply-demarcated erythematous plaques covered with silver scales. Histologically, it is characterized by increased epidermal thickness, elongated papillae, and a moderate inflammatory infiltrate composed of lymphocytes, macrophages and neutrophils. The histological hallmark of psoriasis is Munro's microabscess, which is an accumulation of polymorphonuclear leukocytes in the keratinous layer. The mechanism of this disease is still an enigma, but genetic susceptibility, abnormal function of keratinocytes, or immunological disturbance, especially in T cells, are postulated. Over the past decades, there have been arguments about "keratinocyte-dependent" pathology as opposed to "immunocyte-dependent" pathology. Thus far, there have been some rodent models for psoriasis. Among them, the recent article from Rebholz et al. is quite intriguing because they explain the crosstalk between keratinocytes and lymphocytes: now evidence has been presented that while the aberrant NF-kappa B activation in either keratinocytes or lymphocytes could not reproduce psoriasis-like histology, such activation in both reproduced all of the aforementioned "hallmarks" of psoriasis pathology. Therefore, NF-kappa B may well act as a link between the T cell-mediated and keratinocyte-mediated arguments concerning the pathogenesis of psoriasis. This article also discusses some recent patent related to the field.