1. How are B cells involved in the immune pathways that target this demyelination in multiple sclerosis? The whole things about b cells involved with multiple sclerosis About b-cell therapy with...

1) How are B cells involved in the immune pathways that target this demyelination in multiple sclerosis? The whole things about b cells involved with multiple sclerosis. About b-cell therapy with multiple sclerosis (especially for relapsing multiple sclerosis)- the cu
ent treatment available and what it does, the faults associated with it.
Multiple sclerosis is a T-cell mediated disease, which results in the demyelination of the nerve sheath layer. It causes active disruption of the nerve axon terminals and synapsis, which severely affects the central nervous system (CNS). They impair the motor, sensory, and coordination function in the body of the affected humans leads to various neurological disorders. Multiple sclerosis is often the outcome of lethal genetic variations, oncogenic viral infection, and damaging environmental exposures.
During multiple sclerosis, the progressive activating T-cells in the body become autoreactive and attack the neuronal axon myelin sheath. It subsequently damages the neurons and causes severe inflammation with demyelination. However, sometimes it can even lead to neuronal death. Since multiple sclerosis occurs due to the demyelination of axons, the other possible causative is the dysfunctional mode of Schwann cells which are the chief producer of myelin sheath over the axons (Comi et al., 2021).
As T-cell is a subtype of lymphocytes, the other subtype can contribute its role in the cause of multiple sclerosis in B-cells. Previously, only T-cells were held responsible for the progression of multiple sclerosis. Genes such as DR-15 and DQ6 located in the proximity of major histocompatibility complex (MHC) get altered due to random genetic variations or infections like the Epstein-Ba
virus, which results in the formation of autoreactive T-cells. But some studies relate the higher proliferation of B-cells in response to the oncogenic viruses especially, the Epstein-Ba
virus (Disanto et al., 2012). The Epstein-Ba
virus is one of the notorious and infectious viruses that cause severe polyclonal lymphoma in humans along with multiple sclerosis. Therefore, leaving B-cells out of the pathway for understanding the progression of the mentioned disease can miss their potential usage in the therapeutic drug design (Disanto et al., 2012; Wekerle, 2017).
B-cells are one of the antigenic presenting cells (APC) and an abundant producer of antibodies against the revolving antigens present in the body. Since B-cells are APC’s they can activate T-helper cells to signal T-cytotoxic cells for activation. Also, upon exposure to the activated T-helper cells, they can clonally expand and produce several different antibodies against the exposed antigens. The observed presence of B-cell activity in the progression of multiple sclerosis from polyclonal bands of IgG bands in the cere
ospinal fluid (CSF) indicates their active role as B-cells can convert to polyclonal expanding plasma cells after exposure to several antigens. Thus, different studies were conducted to understand the structure of antigens that activated the clonally expanding plasma cells in the infection site to check targeted anti-myelin antibodies.
According to Jelcic et al. (2018), the progression of multiple sclerosis initiates with the production of autoreactive T-cytotoxic cells. It results in the formation of inflammation and CNS lesions. The inflammation triggers the immune response, which helps the cytokines...