Keloid is a common fibrotic disease, which is difficult to treat. It often causes itching and pain, which greatly disturbs patients in their work and daily life and causing difficulties in social interaction. Its pathogenesis is not clear, but may be related to several aspects: genetic susceptibility, environmental, immunological and endocrine factors, trauma and tension. The central point of its pathogenesis is the excessive proliferation of fibroblasts, with excessive synthesis and secretion of extracellular matrix such as collagen. However, the cause of fibroblast excessive proliferation and differentiation is not clear. Immune abnormalities may play an important role, with cytokines, chemokines, growth factors, and other important immune molecules acting on fibroblasts. This paper presents a detailed and comprehensive literature review on this subject.

Although traditionally used for the diagnosis of skin tumors, in the past few years dermoscopy as a clinical diagnostic aid for inflammatory and infectious skin manifestations has also received more and more attention. The clinical variability of cutaneous sarcoidosis (CS) often makes its correct diagnosis challenging. Dermoscopy can be used as an auxiliary examination method. Our aim was to evaluate the role of dermoscopy in the diagnosis and differential diagnosis of CS. This was a retrospective analysis of 39 CS clinical and dermoscopic images collected in the Department of Dermatology, Huashan Hospital Affiliated with Fudan University from August 2013 to February 2021. Retrospective dermoscopic evaluation revealed small grouped, translucent orange globular structures in all 39 cases. Variable diameter linear vessels were found in 38 cases. A central scar-like area was seen in 26 cases. Bright white streaks were seen in 30 cases. The follicular plugs were seen in 15 cases. First, the number of cutaneous sarcoidosis cases the authors collected is small. Second, due to the lack of a control group, the sensitivity and specificity of the proposed criteria were not calculated. Finally, since our study mainly includes suspicious lesions that were biopsied for diagnostic purposes, there may be a selection bias. Lesions showing on dermoscopy grouped translucent orange ovoid structures associated with linear vessels should raise the suspicion of CS. Central scar-like areas and bright white streaks are also helpful in the diagnosis of CS.

Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by immune dysregulation, microvascular damage, and multi-organ fibrosis. Recent breakthroughs in single-cell and spatial multi-omics technologies have profoundly revealed the high heterogeneity of the SSc immune microenvironment, including extensive aberrant activation of innate immunity (e.g., dendritic cells, macrophages, neutrophils) and adaptive immunity (T cells, B cells), and their interaction with fibroblasts and endothelial cells through an “immune-stromal-vascular” network that collectively drives the fibrotic process. These findings have advanced disease subtyping based on molecular features (e.g., inflammatory, fibrotic) and the development of precision therapeutic strategies. Emerging therapies targeting the IL-6 receptor (tocilizumab), B cells (rituximab, belimumab, CAR-T), the JAK-STAT pathway (tofacitinib, baricitinib), and T-cell co-stimulation (abatacept) have shown potential to improve disease progression in clinical studies. However, heterogeneity in treatment response, difficulty in reversing fibrosis, and the lack of biomarkers remain current challenges. Future efforts require integrating multi-omics and artificial intelligence technologies to build dynamic predictive models, promoting multi-target combination and individualized therapies, ultimately aiming for early intervention and long-term remission in SSc.

To evaluate the effect of T-helper 17 (Th17) cells and Th9 cells on the activation of dermal vascular smooth muscle cells (DVSMCs) in systemic scleroderma (SSc) and regulation of tanshinone IIA. The expression of interleukin 17 receptor (IL-17R) and interleukin 9 receptor (IL-9R) in the skin of SSc patients was assessed by immunofluorescence. The expression of IL-9 and IL-9R mRNA in peripheral blood mononuclear cells (PBMCs) of SSc patients were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The proportion of Th9 cells in PBMCs of SSc patients was sorted by flow cytometry. The effect of IL-9 on the differentiation of Th17 and IL-17 on that of Th9 was detected by flow cytometry. The proportion of Th9 and Th17 cells in SSc patients was detected by flow cytometry. The level of collagen I, III, α-SMA, IL-9R, IL-17R, JNK, P38, and ERK were analyzed using western blot (WB). Th9 cells were highly expressed in SSc. IL-9 stimulated the differentiation of immature T cells into Th17 cells. IL-17 induced the differentiation of immature T cells into Th9 cells. Tanshinone IIA inhibited the differentiation of immature T lymphocytes into Th17 and Th9. WB showed that the combined action of IL-17 and IL-9 upregulated the inflammation and proliferation of DVSMCs. Anti-IL17, anti-IL9, and tanshinone IIA inhibited the functional activation of DVSMCs. For Th17, Th9 and vascular smooth muscle cells, the study on the signal pathway of their interaction is not thorough enough. More detailed studies are needed to explore the mechanism of cell-cell interaction. The current results suggested that Th17 and Th9 cells induced the activation of DVSMCs in SSc through crosstalk in vitro, and tanshinone IIA inhibited the process.

B cells play a central role in the pathogenesis of systemic sclerosis (SSc). Most B-cell studies have focused on their pathological role as antibody producers. However, in addition to immunoglobulin secretion, these cells have a wide range of functions in the immune response, including antigen presentation to T cells and cytokine production. Importantly, not all B-cell subsets promote the immune response. Regulatory B cells (Bregs) attenuate inflammation and contribute to the maintenance of immune tolerance. However, effector B cells (Beffs) positively modulate the immune response through the production of various cytokines. In SSc, Bregs are insufficient and/or dysfunctional. B-cell-targeting biologics have been trialled with promising results in the treatment of SSc. These therapies can affect Bregs or Beffs, which can potentially limit their long-term efficacy. Future strategies might involve the modulation of effector B cells in combination with the stimulation of regulatory subsets. Additionally, the monitoring of individual B-cell subsets in patients may lead to the discovery of novel biomarkers that could help predict disease relapse or progression. The purpose of this review is to summarize the relevant literatures and explain how Bregs and Beffs jointly participate in the pathogenesis of SSc.

Keloids and bullous pemphigoid (BP) are two clinically and pathophysiologically distinct dermatologic disorders – the former involves abnormal scar formation due to excess collagen deposition, while the latter is an autoimmune blistering disease. We report a case of a 67-year-old man with a 19-year history of abdominal keloids and the subsequent appearance of vesicular skin lesions. Histopathologic examination revealed both keloidal fibrosis and subepidermal blister formation. Serum testing demonstrated elevated anti-BP180 antibody levels. Initial treatment with topical and systemic agents, including neomycin, glycyrrhizin, spironolactone, and minocycline, resulted in limited improvement. Subsequently, dupilumab – a monoclonal antibody against the interleukin (IL)-4 receptor α – was introduced. After two months of dupilumab therapy, the vesicular lesions resolved, keloids stabilized, serum anti-BP180 antibody levels normalized, and the Dermatology Life Quality Index (DLQI) score decreased from 11 to 2.