To describe the prevalence of human papillomavirus (HPV) and its genotype distribution among females in the suburb of Shanghai. A total of 33 562 participants were enrolled in this study from January to December 2016. HPV GenoArray test kit was used to perform HPV genotyping and was also used in DNA amplification and HybriBio's proprietary flow-through hybridization technique. The overall prevalence of HPV was 18.98% and the top ten genotypes of HPV infection were HPV 16 (3
Background
Increased human endogenous retroviruses E clone 4–1 (HERV-E clone 4–1) mRNA expression is observed in systemic lupus erythematosus (SLE) patients and associates with the disease activity. In this study, we want to further investigate the mechanism of HERV-E clone 4–1 mRNA upregulation and its roles in SLE progression.
Methods
CD4
+
T cells were isolated from venous blood of SLE patients or healthy controls and qRT-PCR was used to detect HERV-E clone 4–1 mRNA expression. We then investigated the regulation of Nuclear factor of activated T cells 1 (NFAT1) and Estrogen receptor-α (ER-α) on HERV-E clone 4–1 transcription and the functions of HERV-E clone 4–1 3′ long terminal repeat (LTR) on DNA hypomethylation and IL-17 release.
Results
We found HERV-E clone 4–1 mRNA expression was upregulated in CD4
+
T cells from SLE patients and positively correlated with SLE disease activity. This is associated with the activation of Ca
2+
/calcineurin (CaN)/NFAT1 and E2/ER-α signaling pathway and DNA hypomethylation of HERV-E clone 4–1 5’LTR. HERV-E clone 4–1 also takes part in disease pathogenesis of SLE through miR-302d/Methyl-CpG binding domain protein 2 (MBD2)/DNA hypomethylation and IL-17 signaling via its 3’LTR.
Conclusions
HERV-E clone 4–1 mRNA upregulation is due to the abnormal inflammation/immune/methylation status of SLE and it could act as a potential biomarker for diagnosis of SLE. HERV-E clone 4–1 also takes part in disease pathogenesis of SLE via its 3’LTR and the signaling pathways it involved in may be potential therapeutic targets of SLE.
Electronic supplementary material
The online version of this article (10.1186/s12964-019-0416-5) contains supplementary material, which is available to authorized users.
Vitiligo is an acquired disfiguring dermatosis characterized by patchy depigmentation due to the selective loss of functioning melanocytes. The incidence rate of vitiligo is approximately 0.5%-1.0% of the world's population. 1 At present, the aetiology of vitiligo remains unclear. Multiple studies demonstrated that massive oxidative stress may lead to vitiligo. Oxidation pathway is regarded as the important steps in the development of vitiligo. 2 In human skin, each melanocyte forms an epidermal melanin unit with 36 keratinocytes, which play an important role in maintaining melanocyte homeostasis. 3 Various growth factors produced by keratinocytes affect melanocyte proliferation and differentiation, such as endothelin-1, stem cell factor and basic fibroblast growth factor. 4-6 Additionally, keratinocyte-derived soluble factors regulate the melanogenesis of neighbouring melanocytes. 7 Moreover, various hormonal and peptide factors produced
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