Cytoskeletal changes in neuro-glial cells, in response to neuropsychiatric Systemic Lupus Erythematosus patient serum

Biswal, Sanskruti (2021) Cytoskeletal changes in neuro-glial cells, in response to neuropsychiatric Systemic Lupus Erythematosus patient serum. Masters thesis, Indian Institute of Science Education and Research Kolkata.

Text (MS Dissertation of Sanskruti Biswal (16MS017)) 16MS017_Thesis_file.pdf - Submitted Version Restricted to Repository staff only Download (2MB)

Abstract

Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease displaying multi-organ effects facilitated by humoral and cell-mediated immunity against self-antigens. Genetic susceptibility along with environmental triggers are thought to be the important factors for SLE disease onset. Mechanism of this disease includes hyperactivation of B and T lymphocytes that leads to excessive production of autoantibodies, cytokines, deposition of immune complexes in the tissues, thus causing an overall systemic proinflammatory state. Previous studies in both experimental animal models and human subjects have shown neuronal and psychiatric symptoms in SLE and is termed neuropsychiatric SLE or NPSLE. CNS (Central Nervous System) pathology has been attributed to the loss of Blood-Brain-Barrier along with a production of autoantibodies against an individual’s own proteins in the brain. Our study aims to develop an in-vitro cell culture model to elucidate the mechanism of neuronal dysfunction in SLE. This will help understand the disease pathogenesis in SLE as well as NPSLE condition. One of the most significant challenges of SLE is that diagnostic markers are rare and inconclusive, specifically in NPSLE, wherein CNS manifestations are varied. Excessive production of autoantibodies and chemokines are observed in NPSLE patients, while the causative agent(s) for neuronal cell necrosis has not been ascertained. Studying the effect of blood serum of SLE and NPSLE patients on an in-vitro model can help uncover what factors are responsible for this.

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