Psoriasis is a skin disease characterized by hyperproliferation of keratinocytes and chronic inflammation. Mesenchymal stem/stromal cells (MSCs) exhibit an immunoregulatory function that can be altered in the skin of these patients. However, to date, the presence and functional capacity of MSCs in the dermis and epidermis of patients with psoriasis have not been fully established. In the present study, we evaluated the presence of MSCs in the skin of patients by obtaining adherent cells from the dermis and epidermis of lesional and nonlesional areas and characterizing them in a comparative manner with corresponding cells obtained from the dermis (HD-MSCs) and epidermis (HE-MSCs) of healthy donors. We determined whether the adherent cells had immunophenotypic profiles and differentiation potentials that were characteristic of MSCs. In addition, we analyzed their immunosuppression function by evaluating their capacity to decrease T cell proliferation. Our results indicate the presence of MSCs in the dermis and epidermis of healthy donors and patients with psoriasis; adherent cells from all skin sources exhibited MSC characteristics, such as expression of CD73, CD90, and CD105 markers and a lack of hematopoietic and endothelial marker expression. However, the cell populations obtained showed differences in differentiation potential toward adipogenic, osteogenic, and chondrogenic lineages. In addition, we observed a low MSC obtention frequency in nonlesional epidermal samples (NLE-MSCs), which also showed alterations in morphology and proliferation rate. Interestingly, MSCs from both the nonlesional dermis (NLD-MSCs) and lesional dermis (LD-MSCs) showed higher HLA class I antigen (HLA-I) expression than HD-MSCs. Moreover, NLD-MSCs showed a low T cell proliferation suppression capacity. In summary, this study demonstrates the presence of MSCs in the epidermis and dermis of patients with psoriasis and suggests that such cells may favor the inflammatory process and thus psoriatic lesion development through high HLA-I expression and low immunosuppression capacity.

Psoriasis is an inflammatory autoimmune disease characterized by cutaneous lesions in plaques. It has been proposed that the immune response has a key role in the disease progression. Particularly, the Th17 cells through IL-17 can contribute to maintain the inflammatory process. The pathogenic Th17 phenotype has been described in human diseases and associated with high severity in inflammatory experimental models. However, it is not clear if the pathogenic phenotype could be present in the skin and peripheral blood as well as its possible association to severity in psoriasis. In the lesional skin, we found high infiltration of Th17 cells and the pathogenic phenotype, finding a correlation between the frequency of Th17 cells and the Psoriasis Area and Severity Index (PASI) score. In peripheral blood, we observed a pool of Th17 lymphocytes with potential to acquire pathogenic features. Interestingly, the percentage of pathogenic Th17 cells (CD4⁺ RORγt⁺ IFN-γ⁺) correlates with disease severity. Moreover, we distinguished three groups of patients based on their IL-17/IFN-γ production by Th17 lymphocytes, which seems to be related with a dynamic or stable potential to express these cytokines. Remarkably, we evaluated the cytokine production by Th17 cells as an immunological marker for the adequate selection of biologic therapy. We found that patients analyzed by this immunological approach and treated with antibodies against IL-17 and TNFα showed great improvement depicted by reduction in PASI and Dermatology Life Quality Index (DLQI) score as well as the percentage of Body Surface Area (BSA). Altogether, our results highlight the importance of the assessment of the pathogenic phenotype in Th17 cells as an immune personalized analysis with the potential to support the therapy choice in the clinical practice.

Psoriasis is a chronic inflammatory disease distinguished by an excessive proliferation and abnormal differentiation of keratinocytes. Immune cells, such as T lymphocytes and neutrophils, and inflammatory cytokines, such as Tumor Necrosis Factor-α (TNF-α) and interleukin 17 (IL-17), are essential for maintaining psoriatic lesions. Additionally, a hypoxic milieu present in the skin promotes the expression of transcriptional factor hypoxia-inducible factor-1 alpha (HIF-1α). This protein regulates the expression of angiogenic and glycolytic factors, such as vascular endothelial grown factor and lactate dehydrogenase (LDH), both relevant in chronic inflammation. The von Hippel–Lindau protein (pVHL) is a negative regulator of HIF-1α. Previously, we found that pVHL was almost absent in the lesions of psoriasis patients; therefore, we investigated the impact of rescue pVHL expression in lesional skin. We used the imiquimod-induced psoriasis-like mouse model as an adenoviral vector that allowed us to express pVHL in the skin. Our data show that, in lesional skin, pVHL expression was reduced, whereas HIF-1α was increased. Remarkably, the retrieval of pVHL prevented psoriatic lesions, diminishing erythema, scale, and epidermal and vascular thickness. Furthermore, pVHL expression was capable of reducing HIF-1α, LDH, TNF-α and immune cell infiltration (mainly IL-17⁺ neutrophils). In conclusion, our results demonstrate that pVHL has a protective role to play in the pathophysiology of psoriasis.

One of the main goals in the treatment of patients with type 2 diabetes (T2D) is the prevention of its complications. Most existing studies have evaluated a limited and isolated number of inflammatory molecules and metabolic factors, and only rarely have clinical and lifestyle variables been jointly considered. The objective of this study is to describe the protocol design for a comprehensive assessment of patients with T2D, considering glycemic control and the development of complications. A cross-sectional, observational, and multicenter study was conducted in three primary care units located in the states of Coahuila, Jalisco, and Veracruz. Glycemic dysregulation will be assessed by measuring glycated hemoglobin, while diabetic nephropathy will be identified through alterations in the glomerular filtration rate. Additionally, clinical and biochemical parameters, lifestyle habits, physical condition, type of treatment, treatment adherence, and nutritional aspects will be evaluated. Furthermore, transcriptomic analysis using RNA-Seq will be performed to identify the genes that best stratify and distinguish patients with glycemic dysregulation, metabolic alterations, and diabetic nephropathy through principal component analysis and ROC curves based on relative RNA expression. To determine clinical factors associated with the link between molecular profiles and glycemic dysregulation, multiple logistic regression models will be developed to identify a pathological molecular signature characteristic of the disease.

Objectives: Despite the availability of effective vaccines, achieving the seroprevalence thresholds recommended by the World Health Organization (WHO) for eliminating measles, rubella, and mumps remains a public health challenge. Methods: A retrospective, cross-sectional serological survey was conducted, including 9,587 serum samples collected from 31 of the 32 federal entities of Mexico between September and December 2024. IgG antibody levels against measles, rubella, and mumps were quantified using chemiluminescent immunoassays. Seroprevalence was analyzed by age, sex, and geographic region. Results: The overall seroprevalence was 78.3% for measles, 88.6% for rubella, and 81.5% for mumps (p<0.05). Age-stratified analysis revealed significant gaps in immunity against measles and mumps, particularly in the 10–39-year-old group, in which seroprevalence dropped below 70%. In contrast, more consistent protection against rubella was observed across all age groups, although younger children showed lower antibody titers. Regional analysis indicated that only older adults reached the protective threshold against measles in all states. Conclusions: This study demonstrates that current levels of seroprevalence in Mexico do not correspond to the vaccination coverage recommended by the WHO and highlights the urgent need to strengthen vaccination strategies, conduct catch-up campaigns, and carry out continuous seroepidemiological surveillance to maintain elimination goals.