It is believed that autoimmune T cell responses against antigens generated from the central nervous system are what cause multiple sclerosis. Multiple sclerosis individuals' clinical outcomes, symptoms, and pathology vary widely, indicating that different pathogenic pathways may be responsible for the disease in various persons. When self-reactive T cells are specific for CNS antigens are activated in the periphery, whether by a molecular mimic of the self-antigen or by the presentation of the self-antigen in the CNS-draining lymph nodes, autoimmune illness of the CNS results. Activated T cells can pass across the blood-cerebrospinal fluid (CSF) or blood-brain barrier, in contrast to naive T cells. It is thought that activated T cells first pass through the blood-CSF barrier and reach the subarachnoid space. There, they are reactivated, allowing T cells to next enter the perivascular space by activating the vascular endothelium.

The peripheral T cells that promote CNS autoimmunity in animal models are typically myelin-specific CD4+ T cells that avoided central tolerance because of their poor avidity for their cognate antigen. TH17 cells, which secrete interleukin-17 (IL-17), and CD4+ T helper 1 (TH1) cells, which secrete interferon (IFN), can both cause CNS autoimmune illness. It is unclear how these T cell subsets interact with one another and with other CNS cells, but this interaction is likely to be crucial in determining how the inflammatory response develops in various CNS regions. Numerous cell types can present antigen to CD4+ T cells during inflammation, and the relative contribution and activation level of these various antigen-presenting cells greatly affects the effector function and long-term survival of T cells in the CNS.

In the CNS of people with multiple sclerosis, CD8+ T cells show stronger signs of antigen-driven growth, and myelin-specific CD8+ T cells are more harmful in experimental autoimmune disease. However, numerous other forms of regulatory CD8+ T cells have been found that, in addition to CD4+ regulatory T cells may be significant in the pathogenesis of multiple sclerosis.

Depletion of B cells is a promising therapeutic approach for individuals with multiple sclerosis, despite the fact that T cells are thought to be the main effector cells in the pathology of multiple sclerosis. It is not yet known whether the therapeutic benefit of this treatment results from a reduction in B cells' capacity to make antibodies or from their ability to present antigens. In illnesses of the central nervous system (CNS), such as multiple sclerosis, autoreactive T cell responses play a critical role. According to recent research, two different CD4+ T cell lineages that are characterised by the production of either interferon or interleukin-17 can mediate CNS autoimmunity. The pathophysiology and clinical course of disease are influenced by the activity of these CD4+ T cell subsets within the CNS. Myelin-specific CD8+ T cells can also induce CNS autoimmunity, according to new animal studies.

Clinical Pathology & Laboratory Medicine Peer- reviewed which will be dedicated to advancing diagnosis of diseases based on the laboratory analysis of bodily fluids, such as blood, urine, and tissue homogenates or extracts using the tools of biochemistry, microbiology, haematology and molecular pathology.

Authors can submit their manuscripts as an email attachment to clincalpatho@scholarlypub.org.

Best Wishes,
Journal Co-ordinator
Clinical Pathology & Laboratory Medicine