Background Vitiligo is an acquired disorder of pigmentation with an elusive pathogenesis, though various theories have been proposed. The presence of peri-lesional autoreactive CD8+ T cell infiltrate suggests the involvement of abnormal immune responses and autoimmunity in vitiligo. Recent studies have identified the IFN-γ-CXCL9/CXCL-10 axis as a key component of the autoimmune response that perpetuates disease activity in vitiligo. Objectives The primary objective was to estimate serum CXCL9 and CXCL10 levels in vitiligo patients compared to age- and sex-matched controls. Additionally, the study aimed to find correlations between CXCL9 and CXCL10 levels and disease severity and stability. Secondary objectives included comparing levels in segmental/nonsegmental vitiligo and stable/progressive vitiligo and assessing the impact of age and gender. Methods A hospital-based cross-sectional study included 60 vitiligo patients and 30 age- and sex-matched controls. Serum levels of CXCL9 and CXCL10 were assessed using Enzyme-linked immunosorbent assay (ELISA). Cases were clinically evaluated for the type of vitiligo (segmental or non-segmental), disease severity (VASI score), and disease stability (VIDA score). Statistical analysis included t-tests, chi-square tests, and correlation coefficients. P value less than 0.5 was taken as significant. Results Serum CXCL9 and CXCL10, both, were significantly raised in vitiligo patients as compared to controls (p-value = 0.001* & 0.001* respectively) and correlated positively with both VASI score (p-value = 0.001* & 0.001* respectively) and with VIDA score (p-value = 0.032* & 0.001* respectively). Serum CXCL10 showed significant elevation in progressive vitiligo, and CXCL9 exhibited a non-significant trend. No significant difference was observed between segmental and non-segmental vitiligo. Both chemokines positively correlated with disease severity and stability, while age and gender did not significantly impact chemokine levels. Limitations Small sample size of control population. The voluntary sampling technique led to an unequal number of patients in progressive and stable vitiligo groups, as well as in segmental and non-segmental groups. The current study did not include blister fluid analysis and the effect of therapy on the chemokine levels. Conclusion The expression of chemokines CXCL9 and CXCL10 is markedly increased and correlates positively with disease severity and instability, underscoring their mechanistic role in vitiligo pathogenesis. The values were also higher in the progressive group than in the stable group, inferring their conceivable potential as serum biomarkers. *represents statistically significant results.
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http://dx.doi.org/10.25259/IJDVL_793_2023 | DOI Listing |
Int Immunopharmacol
January 2025
Department of Immunology, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, China. Electronic address:
Objective: Aberrant 6-phosphofructo-2kinase/fructose-2,6-bisphoshatase 3 (PFKFB3) expression is tightly correlated with multiple steps of tumorigenesis; however, the pathological significance of PFKFB3 in macrophages in patients with rheumatoid arthritis (RA) remains obscure. In this study, we examined whether PFKFB3 modulates macrophage activation and promotes RA development.
Method: Peripheral blood mononuclear cells (PBMCs) from patients with RA, THP-1 cells, and bone marrow-derived macrophages from conditional PFKFB3-knockout mice were used to investigate the mechanism underlying PFKFB3-induced macrophage regulation of RA.
Ann Clin Transl Neurol
January 2025
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA.
Defining the CSF cytokine/chemokine and injury biomarker signature of glial fibrillary acidic protein (GFAP) autoimmunity can inform immunopathogenesis. CSF GFAP-IgG-positive samples (N = 98) were tested for 17 cytokines/chemokines, neurofilament light chain (NfL), and GFAP (ELLA, Bio-Techne). Controls included non-inflammatory (N = 42), AQP4-IgG-positive (N = 83), CNS infections (N = 13), and neurosarcoidosis (N = 32).
View Article and Find Full Text PDFJID Innov
March 2025
Department of Dermatology, University Hospital of Zurich, University of Zurich, Schlieren, Switzerland.
In cutaneous melanoma, epigenetic dysregulation is implicated in drug resistance and tumor immune escape. However, the epigenetic mechanisms that influence immune escape remain poorly understood. To elucidate how epigenetic dysregulation alters the expression of surface proteins that may be involved in drug targeting and immune escape, we performed a 3-dimensional surfaceome screen in primary melanoma cultures and identified the DNA-methyltransferase inhibitor decitabine as significantly upregulating the costimulatory molecule ICAM-1.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Key Laboratory of Tropical Disease Control (Sun Yat-Sen University), Ministry of Education, Guangzhou, Guangdong, 510080, China.
Angiostrongylus cantonensis (AC) is the leading cause of eosinophilic meningoencephalitis worldwide. The neuroimmune interactions between peripheral and central immune systems in angiostrongyliasis remain unclear. In this study, significant infiltration of eosinophils, myeloid cells, macrophages, neutrophils, and Ly6C monocytes is observed in the brains of AC-infected mice, with macrophages being the most abundant.
View Article and Find Full Text PDFImmunohorizons
January 2025
Section of Infectious Diseases and Epidemiology, Department of Pediatrics, University of Colorado, Aurora, CO, United States.
Respiratory syncytial virus (RSV) is a major contributor to morbidity and mortality in infants. We developed an in vitro model of human respiratory infection to study cellular immune responses to RSV in infants, children, and adults. The model includes human lung epithelial A549 cells or human fetal lung fibroblasts infected with a clinical strain of RSV at a multiplicity of infection of 0.
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