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Single cell RNA sequencing of SCLE reveals cell heterogeneiy in skin lesions

ABSTRACT: SCLE is a clinical subtype of cutaneous lupus erythematosus with psoriatic-like or annular papules with scaly erythematosus, the pathological mechanism of SCLE has been poorly understood. To investigate the immune pathogenesis of SCLE, we performed single-cell RNA sequencing of SCLE skin lesions and integrated with single cell RNA sequencing data of healthy skin. Our results firstly demonstrated that immune cells such as T, B, macrophage/DC and NK cells increased in the skin lesions of SCLE patients. Secondly, through sub-clustering analysis, GO enrichment analysis and cell communication analysis, we revealed that stromal cells such as keratinocytes and fibroblasts in skin lesions of SCLE enhanced chemotactic function for recruiting immune cells. Importantly, we found widespread high expression of interferon-related genes across almost all cell subtypes in SCLE lesions. Additionally, we revealed a general augmentation in lymphocyte subtypes and an increase in inflammatory myeloid cells such as M1 macrophages and pDC in SCLE lesions. In addition to secreting autoreactive antibodies, B cell subsets were verified to assist local immune responses in SCLE lesions. In conclusion, our investigation provides a comprehensive description of skin lesions in SCLE and suggests a range of potential therapeutic targets.

ORGANISM(S): Homo sapiens

PROVIDER: GSE210939 | GEO | 2023/02/21

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 of SCLE reveals cell heterogeneiy in skin lesions

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