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Analysis of salivary glands of patients with primary Sjögren's syndrome has yielded conflicting results with respect to T helper (Th)1/Th2 polarization. This balance might parallel the progress of the local lesions. B-cells are now taking center stage in this disease. They can also be primed to differentiate into two cytokine-production pathways, dubbed B effector (Be) 1 and Be2 cells. This is discussed in the light of our recent finding that Be1 accompany Th1, while Be2 accompany in the tissue lesions.
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http://dx.doi.org/10.1016/j.autrev.2007.01.010 | DOI Listing |
Genet Med
September 2025
Division of Genetics and Epidemiology, The Institute of Cancer Research, London, UK; The Royal Marsden NHS Foundation Trust, Fulham Road, London, UK. Electronic address:
Purpose: Hereditary Leiomyomatosis and Renal Cell Cancer (HLRCC) is a rare cancer susceptibility syndrome exclusively attributable to pathogenic variants in FH (HGNC:3700). This paper quantitatively weights the phenotypic context (PP4/PS4) of such very rare variants in FH.
Methods: We collated clinical diagnostic testing data on germline FH variants from 387 individuals with HLRCC and 1,780 individuals with renal cancer, and compared the frequency of 'very rare' variants in each phenotypic cohort against 562,295 population controls.
ESC Heart Fail
September 2025
Department of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Heart failure (HF) is a multifactorial and pathophysiological complex syndrome, involving not only neurohormonal activation but also oxidative stress, chronic low-grade inflammation, and metabolic derangements. Central to the cellular defence against oxidative damage is nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor that orchestrates antioxidant and cytoprotective responses. Preclinical in vitro and in vivo studies reveal that Nrf2 signalling is consistently impaired in HF, contributing to the progression of myocardial dysfunction.
View Article and Find Full Text PDFCurr Opin Neurol
October 2025
Neuromuscular Diseases Unit, Department of Neurology, IR SANT PAU, Hospital de la Santa Creu i Sant Pau, CIBERER, Barcelona, Spain.
Purpose Of Review: Autoimmune nodopathies (AN) are a recognized distinct group of immune-mediated peripheral neuropathies with unique immunopathological features and therapeutic implications. This review synthesizes recent advances in their pathogenesis, diagnosis, and management, which have refined their clinical classification and informed targeted treatment strategies.
Recent Findings: AN are characterized by autoantibodies targeting surface proteins in the nodal-paranodal area (anti-contactin-1, anti-contactin-associated protein 1, anti-neurofascin-155, anti-pan-neurofascin), predominantly of IgG4 subclass.
Macrophage Migration Inhibitory Factor (MIF) is a pleiotropic cytokine that acts as a central regulator of inflammation and immune responses across diverse organ systems. Functioning upstream in immune activation cascades, MIF influences macrophage polarization, T and B cell differentiation, and cytokine expression through CD74, CXCR2/4/7, and downstream signaling via NF-κB, ERK1/2, and PI3K/AKT pathways. This review provides a comprehensive analysis of MIF's mechanistic functions under both physiological and pathological conditions, highlighting its dual role as a protective mediator during acute stress and as a pro-inflammatory amplifier in chronic disease.
View Article and Find Full Text PDFMov Disord Clin Pract
September 2025
Department of Neurology, National Taiwan University Hospital Hsin-Chu Branch, Hsinchu, Taiwan.