Inflammatory Disorders of the Nervous System: Pathogenesis, by Alireza Minagar (Editor), J. Steven Alezander (Editor)

By Alireza Minagar (Editor), J. Steven Alezander (Editor)

A state of the art overview of the elemental organic ideas underlying the extra universal inflammatory issues of the frightened method. The authors offer huge updates at the newest findings in regards to the mechanisms of irritation and introduce such new suggestions and methodologies as "endothelial and leukocyte microparticles" and "gene microarray expertise" to assist clarify vital hyperlinks among the principal worried approach (CNS) and common inflammatory tactics. one of the illnesses tested from an inflammatory point of view are a number of sclerosis, acute disseminated encephalomyelitis, optic neuritis, transverse myelitis, CNS vasculitis, neuropsychiatric systemic lupus erythematosis, Alzheimer's ailment, and Parkinson's illness. The function of the immune procedure in neuroinflammation is usually explored in such issues as neurosarcoidois, HIV-Associated dementia, and HTLV-associated neurological issues.

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Additional info for Inflammatory Disorders of the Nervous System: Pathogenesis, Immunology, and Clinical Management (Current Clinical Neurology)

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Recently several studies have demonstrated that not all forms of CNS inflammation are detrimental to CNS function. For example, less CNS regeneration is observed after mechanical trauma and more severe dysfunction results after cytokine-induced injury in mice deficient in T cells or APCs (23,99,100). In vitro, antigen stimulation causes human lymphocytes to produce neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) (101). BDNF-positive cells morphologically resembling lymphoctyes have also been found within human MS lesions, indicating the potential for local antigen presentation within the CNS to promote growth factor production at the site of damage (101).

Conversely, anti-CNS immune responses could be initiated outside the CNS by viruses or other pathogens expressing an antigen target similar in molecular structure to an endogenous CNS antigen (a molecular mimic) (20,21). If a sufficiently strong anti-CNS immune response was initiated outside the CNS, the activated immune cells were presumed to breach the BBB, encounter their CNS antigen targets, and launch destructive CNS autoimmunity. In this paradigm, the CNS is a passive victim of the immune system; thus, the damage to CNS myelin and neurons observed in the histopathology of MS was previously viewed as the inevitable and sequential result of failing to prevent macrophages and T cells from infiltrating the CNS and becoming aware of CNS antigens.

Because of the difficulty of separately measuring the relative abilities of microglia and macrophages to present antigen in vivo, most of the studies we have described examined these functions in vitro. To specifically examine the antigen-presenting function of microglia in vivo, some groups have selectively depleted the peripheral macrophage populations by treating animals with mannosylated liposome-encapsulated dichloromethyline diphophonate (Cl2MDP) (94,95). Without a peripheral myeloid population, an effective immune response cannot be generated after peripheral immunization of myelin proteins in adjuvant (the active immunization form of EAE).

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