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Immunologically Mediated Diseases and Allergic Reactions
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Kim A. Campbell, Caroline C. Whitacre
The vast majority of the autoimmune diseases listed in Table 10.1 are thought to be due to humoral immunity and autoantibody formation; however, there are autoimmune diseases in which cell-mediated immunity is the primary mediator. For example, multiple sclerosis is due to a cellular immune response to myelin in the central nervous system. Lesions in the brain and spinal cord of MS patients have been shown to contain lymphocytes and macrophages, which mediate demy-elination of the myelin sheath. As a result of these lesions, MS patients, who are generally adults between the age of twenty and forty years, suffer vision and motor abnormalities.
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Oligodendrocytes generate myelin within the CNS (see Figure 9.3). Schwann cells, also a type of glial cell, generate myelin in the PNS. Schwann cells wrap around axons, forming a myelin sheath. The outer layer includes the Schwann cell’s cytoplasm and nucleus and is called the neurolemma. The neurolemma is thought to promote axon regeneration in the PNS. When a myelinated axon is examined microscopically, there appear to be gaps in the myelin called nodes of Ranvier. One Schwann cell myelinates the segment of axon between two nodes of Ranvier; myelinated nerves will therefore have several Schwann cells (see Figures 9.3 and 9.4).
Transforming Growth Factor-β: A Cytokine Paradigm
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Michelle R. Frazier-Jessen, Nancy McCartney-Francis, Sharon M. Wahl
On the basis of the findings in animal models, trials of oral tolerization to bovine myelin have been carried out in individuals with early relapsing-remitting MS [63]. Fewer myelin-treated patients had major exacerbations of disease than placebo-treated patients. Although the overall change in disability scores was not greater with myelin than with placebo, gender and MHC phenotype also affected treatment outcome. No toxicities were associated with treatment, and, in fact, several patients in the placebo group subsequently treated with myelin experienced disease stabilization in open-label treatment [63]. T cell lines generated from these myelin-treated MS patients had a marked increase in the relative frequency of MBP-specific TGF-β1 secretion as compared to those of nontreated MS patients. These antigen-specific TGF-β1-secreting Th3 cells are believed to localize to the target organ and then suppress inflammation in the local microenvironment. Oral tolerization with self-antigens may provide a therapeutic approach for the treatment of cell-mediated autoimmune disease which does not necessarily depend upon knowledge of the antigen specificity of the original T cell clone triggering the autoimmune cascade [64].
Honokiol exerts protective effects on neural myelin sheaths after compressed spinal cord injury by inhibiting oligodendrocyte apoptosis through regulation of ER-mitochondrial interactions
Published in The Journal of Spinal Cord Medicine, 2022
Yong Tan, Haijun Yu, Shanquan Sun, Shengwei Gan, Rui Gong, Ke-jie Mou, Jun Xue, Shiye Xu, Jiangfeng Wu, Lan Ma
Due to the complex pathophysiology, high incidence, and severe disability, compressed spinal cord injury (CSCI) has become one of the most common serious spinal disorders worldwide.1 There are many mechanical injuries, such as spinal trauma, epidural hematoma, and intramedullary tumors which may cause CSCI.1 They can result in a series of biochemical changes, such as microcirculatory disturbance and electrolyte imbalance, that ultimately lead to secondary damage including apoptosis and demyelination.2 Once the myelin sheath is lost, axonal dysfunction and degeneration will occur, and nerve impulse conduction is blocked, which affects patients’ motor and sensory functions.3,4 Thus, the key to effective treatment of CSCI is how to avoid or reduce demyelination, and facilitate functional recovery.
Remyelination therapies for multiple sclerosis: optimizing translation from animal models into clinical trials
Published in Expert Opinion on Investigational Drugs, 2021
Rujapope Sutiwisesak, Terry C. Burns, Moses Rodriguez, Arthur E. Warrington
The pathology of MS is characterized by areas of progressive demyelination or ‘plaques’ at multiple sites within the CNS [6]. Although demyelination is the main pathology, MS lesions occur in both white and gray matter. A healthy myelin sheath, formed by oligodendrocytes in the CNS, enables efficient nerve impulse transmission by utilizing saltatory conduction and maintaining axonal health [7]. Damage to myelin sheaths results in axonal conduction block in the early stages of disease. Axonal damage is usually acute and reversible but axonal loss and dysfunction are the causes of permanent neurological deficits. Progressive neurodegeneration can result from untreated or chronic disease progression. As such, a central goal of MS treatments is axonal preservation, which could be achievable by preventing ongoing damage to myelin sheaths and promoting remyelination.
Exome sequencing of a Pakistani family with spastic paraplegia identified an 18 bp deletion in the cytochrome B5 domain of FA2H
Published in Neurological Research, 2021
Safdar Abbas, Beatrice Brugger, Muhammad Zubair, Sana Gul, Jasmin Blatterer, Julian Wenninger, Khurram Rehman, Benjamin Tatrai, Muzammil Ahmad Khan, Christian Windpassinger
Myelination is the process in which myelin proteins and lipids are conjugated by myelinating glial cells. The enzyme that catalyzes 2-hydroxylation of myelin galactolipids, galactosyl-ceramide is encoded by FA2H. Sphingolipids involved in several cellular processes and modification in the hydrophobic ceramide moiety leads to structural diversity. Cellular studies have revealed that mutations in this gene result in defective enzymes that cannot catalyze the synthesis of fatty acids of myelin galactolipids. Myelin is a lipid-enriched component of neuronal cell membranes, which is produced by the oligodendrocytes and Schwann cells. It is predominantly rich in glycosphingolipids, termed as galactocerebrosides. Most of these sphingolipids contain α-hydroxylated fatty acids that may enhance the stability of the myelin sheath [27]. Myelin sheaths provide protection for the axons of nervous system and are responsible for the conduction of proper nerve transmission. Damage to myelin sheaths may lead to defects in the neuronal communication system and several other related disorders like multiple sclerosis and leukodystrophies [25, 28].