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Single cell RNA sequencing reveals cellular heterogeneity of DLE and SLE

ABSTRACT: Lupus, a server and complex autoimmune disease, is clinically divided into cutaneous lupus erythematosus (CLE) which featured in skin damage, and systemic lupus erythematosus (SLE) which characterized in systemic multi-organ damage. The distinction of these two types of lupus is widely unknown. Here, we collected 23 skin biopsies of healthy control(HC), DLE (discoid lupus erythematosus, a main type of CLE) and SLE, separated epidermis and dermis and performed single cell RNA sequencing through microfluidics based 10x genomics system. Our results demonstrated larger numbers of immune cells infiltrated in skin lesions of DLE than SLE, which may help to distinguish them. Then, non-immune cells such as keratinocytes and fibroblasts were showed functions like immune cells. Moreover, ISGs(interferon stimulated genes), HSP70 coding genes were found to be overexpressed in multi expanded subclusters. Some biological progresses such as autophagy and neutrophil activation were enriched in expanded subclusters.

ORGANISM(S): Homo sapiens

PROVIDER: GSE179633 | GEO | 2022/10/17

REPOSITORIES: GEO

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Project description:Cutaneous lupus erythematosus (CLE) is an autoimmune disease that localizes to the skin and is known to contain elevated glycosaminoglycans (GAGs) on Hale’s stain of skin biopsy specimens. Recently, different GAG species have been shown to have distinct effects on the recruitment and activation of immune cells and stimulation of cytokine production (Taylor and Gallo, FASEB, 2006; 20: 9-22). Thus, we speculate that the elevated GAGs observed in CLE play a role in the local inflammatory process that produces skin lesions in these patients. In order to further investigate a molecular basis for the elevated expression of these GAGs in CLE skin lesions, we would like to determine the gene expression profiles of GAG synthesis, degradation, and modifier genes in lesional and non-lesional skin samples from CLE patients and compare to those from healthy controls. A microarray approach will give us a broader understanding of the genetic regulation of the expression of various GAG species in CLE skin. We will then be able to target future quantitative gene expression experiments by real-time RT-PCR to the genes that are shown to be involved in CLE. In order to accomplish our goal, we would like to examine the GAG gene expression profiles of DLE, TLE, and SCLE subtypes due to the differences in CS and HA staining that we found among these subtypes. Since HA and CS are elevated in DLE and HA in TLE, but not in SCLE, the SCLE samples will also serve as an internal control. We would like to examine both lesional and non-lesional skin biopsies to determine if CLE skin prior to developing a lesion is different at the genetic level from healthy control skin and how it changes once a lesion does develop. We will separate the dermis from the epidermis of the skin biopsies and extract RNA just from the dermis to enrich for dermal fibroblast RNA. We aim to submit four patient biopsies per subtype as well as four samples from healthy control skin for comparison. This number is necessary in order to account for the biologic variability among different patients. We would submit more samples per subtype but are limited by availability of patients in clinic. Thus, we will have a total of 28 samples to submit for microarray. This study design will allow us to analyze the GAG gene expression profiles among different CLE subtypes and enable us to identify which GAc

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Single cell RNA sequencing reveals cellular heterogeneity of DLE and SLE

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