Helminths, as complex pathogens, possess a large number of different epitopes, some of which may be similar to the epitopes of the host. Besides being the cause for the activation of self-reactive immune cells, molecular mimicry may also be the cause for the expansion of regulatory T cells, crucial for the host tolerance of self-antigens. Amelioration of experimental autoimmune encephalomyelitis (EAE), animal model of multiple sclerosis (MS), caused by Trichinella spiralis infection or application of its muscle larvae excretory-secretory products (ES L1), was achieved through activation of Th2 and regulatory responses. The present study aimed to reveal whether the cause of observed immunomodulation could be the existence of shared epitopes between ES L1 antigens and auto-antigens. Serum samples from 92 MS patients were tested in Western blot for the reactivity toward components of ES L1. Immunoglobulins from the sera of MS patients recognized several ES L1 components, but 45, 49 and 58 kDa proteins dominated others by the frequency of interaction. According to the logistic regression analysis, these interactions were statistically significantly associated with MS, regardless of the disease phenotype or severity. Selected molecules might share homology with self-antigens and as such are worthy of further investigation in terms of potential immunomodulatory capacity and involvement in the parasite's provoked amelioration of EAE.
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http://dx.doi.org/10.1016/j.imbio.2020.151954 | DOI Listing |
Int J Surg
January 2025
Department of Orthopedics, Civil Aviation General Hospital, Beijing, China.
Background: Dural arteriovenous fistulas (DAVFs) pose a significant health threat owing to their high misdiagnosis rate. Case reports suggest that DAVFs or related acute events may follow medication use; however, drug-related risk factors remain unclear. In clinical practice, the concomitant use of multiple drugs for therapy is known as "polypharmacy situations," further increasing the risk of drug-induced DAVF.
View Article and Find Full Text PDFCureus
December 2024
Basic Sciences, Hawler Medical University, Erbil, IRQ.
Background Multiple sclerosis is a chronic, progressive, disabling disease associated with a high rate of infection, evidence of chronic inflammation, and a high mortality rate. Abnormalities of serum cytokines and changes in the activity of inflammatory cells were associated with relapsing-remitting multiple sclerosis (MS-RR). This study aims to introduce new inflammatory ratios derived from hematological and lipid indices as discriminators of T-helper (Th)-1/Th-2 activity in RR-MS.
View Article and Find Full Text PDFDemyelination, or the loss of myelin in the central nervous system (CNS) is a hallmark of multiple sclerosis (MS) and occurs in various forms of CNS injury and neurodegenerative diseases. The regeneration of myelin, or remyelination, occurs spontaneously following demyelination. The lysophosphatidylcholine (LPC)-induced focal demyelination model enables investigations into the mechanisms of remyelination, providing insight into the molecular basis underlying an evolving remyelinating microenvironment over a tractable time course.
View Article and Find Full Text PDFOligodendroglial lineage cells (OLCs) are critical for neuronal support functions, including myelination and remyelination. Emerging evidence reveals their active roles in neuroinflammation, particularly in conditions like Multiple Sclerosis (MS). This study explores the inflammatory translatome of OLCs during the early onset of experimental autoimmune encephalomyelitis (EAE), an established MS model.
View Article and Find Full Text PDFEpstein-Barr Virus (EBV) infects over 95% of the world's population and is the most common cause of infectious mononucleosis (IM). Epidemiologic studies have linked EBV with certain cancers or autoimmune conditions, including multiple sclerosis (MS). Recent studies suggest that molecular mimicry between EBV proteins, particularly EBV nuclear antigen 1 (EBNA-1), and self-proteins is a plausible mechanism through which EBV infection may contribute to the development of autoimmune disorders.
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