Exploring the mechanisms of neural cell dystrophy and demyelination in Multiple Sclerosis with a special emphasis on the CD40-CD40L pathway between microglia/macrophage and T cells

Biswas, Debshruti (2023) Exploring the mechanisms of neural cell dystrophy and demyelination in Multiple Sclerosis with a special emphasis on the CD40-CD40L pathway between microglia/macrophage and T cells. Masters thesis, Indian Institute of Science Education and Research Kolkata.

Text (MS dissertation of Debshruti Biswas (18MS141)) Thesis_18MS141.pdf - Submitted Version Restricted to Repository staff only Download (12MB)

Abstract

Multiple Sclerosis (MS) is a chronic illness that affects the central nervous system, characterized by inflammation, autoimmune reactions, and neurodegeneration. It is caused by the immune system's malfunction, which allows immune cells to invade the CNS and cause damage to nerve fibres and myelin coating. While the exact reasons behind the development and progression of MS are not fully understood, factors such as genetics, environmental triggers, autoimmunity, and infectious agents are believed to be involved. The disease involves CD4+ and CD8+ T cells that attack myelin antigens in the CNS. Certain viruses, including Epstein-Barr virus (EBV), Human herpes Virus-6, Varicella-Zoster virus, Cytomegalovirus, and endogenous viruses, have been implicated in the development of MS, but their exact role is not yet fully understood. To better understand the disease's progression, animal models such as experimental autoimmune encephalitis (EAE), Theiler's murine encephalomyelitis virus-induced demyelinating disease, and Mouse Hepatitis Virus (MHV) induced demyelination and inflammation in mice are useful experimental models for research. These models of MS disease pivots the process of understanding the underlying immune mechanism and the roles of different immune players in progression and exacerbation of this debilitating disease. Microglia/macrophage interaction with T cells plays a pivotal role in the development of characteristic features of MS disease like lesions, neural cell dystrophy and demyelination. Cellular crosstalks are responsible for the interaction of Antigen presenting cells with T cell. CD40R-CD40L dyad is one such crucial crosstalk that helps in better understanding of the role of microglia/macrophage and T cell interaction mediated disease progression in a virus induced neuroinflammatory demyelination model of MS.

Actions (login required)

View Item