Publications by authors named "Natosha N Gatson"

Article Synopsis
  • During pregnancy, relapses of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) are significantly reduced, potentially due to changes in immune response.
  • Serum exosomes, which increase during pregnancy, suppress T cell activation and help oligodendrocyte precursor cells (OPC) mature and migrate to lesions in the central nervous system.
  • Both pregnancy-derived and non-pregnancy-derived exosomes can lessen the severity of established EAE, suggesting that exosomes play a key role in immune modulation during pregnancy.
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More than four decades ago, Dr. Judah Folkman hypothesized that angiogenesis was a critical process in tumor growth. Since that time, there have been significant advances in understanding tumor biology and groundbreaking research in cancer therapy that have validated his hypothesis.

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Extracellular vesicles (microvesicles), such as exosomes and shed microvesicles, contain a variety of molecules including proteins, lipids, and nucleic acids. Microvesicles appear mostly to originate from multivesicular bodies or to bud from the plasma membrane. Here, we review the convergence of microvesicle biogenesis and aspects of viral assembly and release pathways.

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Multiple sclerosis (MS) is a demyelinating disease of the CNS involving T cell targeting of myelin antigens. During pregnancy, women with MS experience decreased relapses followed by a post partum disease flare. Using murine experimental autoimmune encephalomyelitis, we recapitulate pregnancy findings in both relapsing and progressive models.

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Article Synopsis
  • * Research using an animal model (EAE) indicates that pregnancy reduces the likelihood and severity of MS-like symptoms when immunization occurs during this time, whereas symptoms worsen if immunization happens postpartum.
  • * The study found that pregnant mice had lower levels of inflammatory cytokines like TNF-alpha and IL-17 compared to non-pregnant mice, suggesting that pregnancy creates a protective immune environment rather than simply suppressing the immune response.
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