Flamenbaum H S, Safai B, Siegal F P, Pahwa S
J Am Acad Dermatol. 1982 May;6(5):918-20. doi: 10.1016/s0190-9622(82)70081-7.
The exact pathogenic mechanism involved in lichen planus (LP) remains obscure. Two patients who have severe immunodeficiency diseases and who developed LP during the course of their illness are reported here. Both patients had hypogammaglobulinemia and disturbed immune function prior to the development of LP. Although such an association could be coincidental, the development of LP may be related to the underlying immune disturbances. Association of LP with several other disorders of the immune system has been previously observed. Other evidence for the possible involvement of an immunopathogenic mechanism in LP includes (1) deposition of immunoglobulin within the colloid bodies and at the dermoepidermal junction, (2) predominantly T cell dermal infiltrate in LP lesions, and (3) existence of clinical and histologic similarities between graft-versus-host disease and LP.
扁平苔藓(LP)的确切致病机制仍不清楚。本文报告了两名患有严重免疫缺陷疾病且在病程中发生扁平苔藓的患者。两名患者在发生扁平苔藓之前均有低丙种球蛋白血症和免疫功能紊乱。尽管这种关联可能是巧合,但扁平苔藓的发生可能与潜在的免疫紊乱有关。此前已观察到扁平苔藓与其他几种免疫系统疾病有关。支持免疫致病机制可能参与扁平苔藓发病的其他证据包括:(1)免疫球蛋白在胶样小体和真皮表皮交界处沉积;(2)扁平苔藓皮损中主要为T细胞真皮浸润;(3)移植物抗宿主病与扁平苔藓之间存在临床和组织学相似性。