Being one of the most common dermatological inflammatory disorders, psoriasis is a frequent subject of research. It is considered to be a T cell-dependent immune disease whose pathogenesis is influenced by cytokines, such as IL-10, IL-17A, IL-17RA, IL-23A and IL-23R. The present study examines whether the expression of selected genes is correlated with the clinical course of psoriasis, assessed by the PASI, BSA and DLQI scales. Skin biopsies and blood from 60 patients with psoriasis and 24 healthy controls were obtained for RNA isolation. These were subjected to RT-PCR for IL-10, IL-17A, IL-17RA, IL-23A and IL-23R genes. The results were presented as an RQ value. IL-17A and IL-23R expression levels were higher in psoriatic skin compared to controls, while IL-10 expression was lower. A positive correlation was also found between RQ for IL-23A and PASI index. Psoriatic skin is characterised by elevated expression of IL-17A and IL-23R and decreased expression of IL-10. This indicates that the selected cytokines may be one of the factors involved in the pathogenesis and pathomechanism of psoriasis, but more studies need to be made before we can elucidate the exact reason for the unbalance in cytokine expression levels.

Vitiligo is a persistent autoimmune disease characterized by progressive depigmentation of the skin caused by the selective destruction of melanocytes. Although its etiopathogenesis remains unclear, multiple factors are involved in the development of this disease, from genetic and metabolic factors to cellular oxidative stress, melanocyte adhesion defects, and innate and adaptive immunity. This review presents a comprehensive summary of the existing knowledge on the role of different cellular mechanisms, including cytokines and chemokines interactions, in the pathogenesis of vitiligo. Although there is no definitive cure for vitiligo, notable progress has been made, and several treatments have shown favorable results. A thorough understanding of the basis of the disease uncovers promising drug targets for future research, providing clinical researchers with valuable insights for developing improved treatment options.

Psoriasis is a common immune-mediated inflammatory dermatosis affecting 2–3% of the northern European population. Although its aetiology is not completely elucidated, it is widely accepted that activated immune cells and keratinocytes stimulate keratinocyte hyperproliferation by production of...

Objectives: As a chronic, recurrent, immunologically mediated systemic disease and a common cause of dermatological problems, psoriasis is often a subject of scientific research. Skin changes located on the hands can cause difficulties and limitations in the performance of professional activities, especially manual ones. The main role in pathogenesis is played by immunological factors - improper functioning of the components of the immune system, among others, T lymphocytes and cytokines like interleukin-12 (IL-12), interleukin-22 (IL-22) and interferon gamma (IFN-gamma). Material and Methods: The obtained tissue and blood were destined for RNA isolation. The RNA was then subjected to a reverse transcription reaction. The relative gene expression level was evaluated by the real-time polymerase chain reaction for IL-12B, IL-22 and IFN-gamma genes, and presented as the relative quantification (RQ) value, relative to the reference gene GAPDH. In addition, a correlation analysis of the expression level of selected genes with the clinical course of the disease, as assessed by the Psoriasis Area and Severity Index (PASI), the Body Surface Area (BSA) and the Dermatology Life Quality Index (DLQI) scores was performed. Results: Statistical analysis confirmed a significant increase in RQ values for IL-12B, IL-22 and IFN-gamma in the group of psoriatic patients vs. the control group. A positive correlation was also found between BSA and PASI and RQ for the IL-12B gene. Conclusions: Increased expression levels of IL-12B, IL-22 and IFN-gamma genes in psoriatic skin confirm that selected cytokines play an important role in the initiation and sustenance of psoriasis.

Senear–Usher syndrome, or pemphigus erythematosus (PE), is a rare autoimmune disorder characterized by the coexistence of features from both lupus erythematosus (LE) and pemphigus foliaceus (PF). We describe a 41-year-old patient initially diagnosed with cutaneous and then systemic lupus erythematosus (SLE), who after a few years developed new skin lesions: erythematous and erosive eruptions partially covered by crusts located on the trunk and flaccid blisters on the extremities. Direct immunofluorescence of perilesional skin revealed deposits of IgG in the intercellular space of the epidermis and granular deposits of C3 at the dermo–epidermal junction. Additional testing, revealing autoantibodies against the intercellular space of the epidermis, and direct immunofluorescence (DIF) examination allowed a diagnosis of pemphigus vulgaris coexisting with lupus. Further, DIF study revealed granular deposits of immunoglobulin G (IgG) in the intercellular spaces of the epidermis and granular deposits of the C3 along the basement membrane. Clinical appearance led to suspicion of Senear–Usher syndrome. in this patient. This case report explores the diagnostic challenges posed by the patient’s overlapping symptoms and immunological findings, suggesting an infrequent manifestation of Senear–Usher syndrome or a combination of SLE and pemphigus vulgaris. The case highlights the complexity of chronic inflammatory skin diseases and the need for tailored treatment approaches in such cases. Despite temporary improvement, the patient experienced relapses. We performed a descriptive literature review of the case reports of PE published in the last 24 years and prepared a summary of the characteristics, emphasizing the importance of proper recognition, clinical features, and treatment of this uncommon syndrome.

Dermatomyositis (DM) is a rare, autoimmune inflammatory myopathy characterized by a heterogeneous clinical course and complex etiopathogenesis. Although classically defined by the coexistence of muscle inflammation and distinctive skin lesions, DM frequently presents as a systemic disease, and, in some patients, cutaneous manifestations may precede muscle involvement or represent the sole clinical feature. The spectrum of skin lesions in DM is broad and includes pathognomonic, characteristic, rare, or atypical manifestations, ranging from classic Gottron’s sign and heliotrope rash to uncommon subtypes such as vesiculobullous dermatomyositis, Wong-type dermatomyositis, or flagellate dermatitis. Particular cutaneous phenotypes often correlate with distinct clinical subtypes, autoantibody profiles, systemic involvement, and prognosis. The diversity of dermatological presentations and their resemblance to other dermatoses may delay accurate diagnosis, especially in amyopathic and hypomyopathic forms of the disease. The aim of this review is to comprehensively discuss the wide spectrum of cutaneous manifestations of dermatomyositis, emphasize less recognized and rare dermatological clinical presentations, and highlight their diagnostic and prognostic significance. However, histopathological examination may support the diagnostic process in challenging cases. Early identification of characteristic skin lesions remains crucial for prompt diagnosis, appropriate screening for systemic complications and malignancy, and optimal management. Close interdisciplinary cooperation among dermatologists, rheumatologists, and other specialists is essential to ensure accurate diagnosis and improve outcomes in patients with dermatomyositis.