AB009. Characterization of helper T cell subpopulations in early, mid-, and late-stage discoid lupus erythematosus (DLE)

AB009. 盘状红斑狼疮(DLE)早期、中期和晚期辅助性T细胞亚群的特征分析

阅读:1

Abstract

Discoid lupus erythematosus (DLE) is characterized by early erythematous papules and plaques that progress to hyperpigmented and hypopigmented plaques with central scarring. The immunopathology of early and late stage DLE is not well characterized. In a previous study comparing multiple immune cell populations in different DLE stages, we found higher CD8(+) T cells and lower CD20(+) B cells in early DLE skin versus later DLE skin. To follow up on these findings, we compared helper T (Th) cell subpopulations in early (inflammatory), mid (inflammatory with scarring) and late-stage (scaring) DLE skin. We hypothesized a shift from Th1 response (pro-inflammatory) in early DLE skin to Th2 (pro-fibrotic) response in late DLE skin. We performed double immunohistochemistry to compare Th1 (CD4(+)T-bet(+)) and Th2 (CD4(+)GATA3(+)) cells in formalin-fixed, paraffin-embedded skin biopsies of early (N=4), mid (N=4), and late stage DLE (N=3). Single positive and double-positive cells were manually counted in representative high-powered field areas of the epidermal-dermal junction (interface), perifollicular and perivascular areas. There were non-significantly higher percentages of Th2 cells within the perivascular (P=0.11) and interface (P=0.14) areas in late DLE skin compared with early and mid DLE skin. Early DLE skin also showed higher percentages of Th1 cells than Th2 cells in the perifollicular (P=0.13) and perivascular areas (P=0.13) but did not reach statistical significance. Larger samples are being collected to verify our findings. Elucidating immunologic differences in various stages of DLE will be important to finding therapies that reduce the chronic skin sequelae of scarring and dyspigmentation in DLE.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。