This new edition covers recent advances in understanding immunological and inflammatory responses in the nervous system, research driven by the potential to use knowledge of the molecules and mechanisms involved to intervene in, and arrest, neurodegenerative disease processes.Immune and Inflammatory Responses in the Nervous System covers developmental aspects of immune/inflammatory responses in the CNS, basic aspects of glial function, as well as inflammatory mediators, their mechanisms of action, clinical importance and sites of infection. There is also coverage of themajor diseases of the CNS, including stroke, brain injury, multiple sclerosis and Alzheimer's disease. Throughout, the focus is on the underlying basic neuroscience, clinical relevance and the potential for therapeutic interventions.This will be an invaluable aid to understanding and improving the diagnosis of neuroimmune diseases and determining therapeutic measures.The contributors are all leading experts in the field and the content will be of interest to neuroscientists, neurologists, neuropathologists, neurosurgeons and immunologists.

Aging is one of the major risk factors for the onset and progression of various neurodegenerative diseases. Neuroinflammation is a common feature of virtually every central nervous system disease, and is acknowledged as a likely mediator of cognitive impairments. Systemic inflammation levels are augmented with advanced age and neurodegeneration. The influence of age on neuroinflammatory responses including glial activation, increased production of proinflammatory cytokines, and aberrant neuronal signaling could magnify the deterioration of the central nervous system microenvironment in disease, and may contribute to enhanced cognitive impairment. This eBook is a collection of highly informative original research articles, providing comprehensive aspect of neuroinflammation and possible therapeutic interventions in rescuing cognitive impairments.

This PIR volume presents a comprehensive collection of reviews that focus on the role of the blood-brain barrier (BBB) during steady-state and inflamed conditions. Within the central nervous system (CNS) the constantly changing bloodstream is strictly separated from the CNS parenchyma by the BBB. However, viruses, bacteria, parasites and auto-aggressive immune cells can penetrate the barrier and significantly contribute to CNS inflammation. The BBB can actively contribute to neuroinflammation by presentation of chemokines, expression of cell adhesion molecules and alterations of barrier properties. As such, understanding the role of the BBB under healthy and pathological conditions is essential to the development of new drugs to efficiently combat inflammatory diseases of the CNS.

The Molecular Immunology of Neurological Diseases provides a comprehensive review of current updates in molecular immunogenetics of different neurological diseases. Readers will learn about the role of immune cells and their modulation strategies to help in the development of therapeutic approaches for both acute and chronic neurodegenerative disorders. There is no other book available on the topic. It has long been thought that the brain is an immune-privilege organ with very limited immune response. However recent studies have made clear that both systemic 'brain' and peripheral 'blood' immune cell responses play key roles in determining brain pathology in neurodegenerative disorders. This book summarizes the role of immune cell activation in the central nervous system microenvironment in acute and chronic neurodegenerative disorders. In addition, it discusses the key role of immune cells and their modulation strategies for the development of current therapeutic approaches. Discusses the molecular immunogenetics of different neurological diseases Covers strategies for the development of therapeutic approaches Encompasses both acute and chronic neurogenerative disorders Describes the molecular pathogenesis of viral genes in various diseases Features chapters on migraine, muscular dystrophy and cancer

Offers answers to challenges in clinical immunology. This book contains immunology knowledge and includes a companion web site to give you two ways to find the answers you need.

Many molecules and mechanisms traditionally associated with the peripheral immune system have been found to be active within the central nervous system. The investigation of immune activation is a rapidly expanding field of research, particularly since it is directly related to acute neuronal damage and in degenerative disorders of the nervous system such as Alzheimer's disease and multiple sclerosis. This volume brings together a team of internationally recognized experts who address topics such as neuronal transplantation, leukocyte migration, the role of inflammation and immune responses in neurological diseases and brain injury, and the potential benefits of treatment with modulators of cytokine action. It will be of interest to all researchers and clinicians involved in the understanding, diagnosis and treatment of neuroimmune diseases.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) mediated by autoreactive T cells specific for myelin proteins. A recent development in MS treatment is the discovery that B cell depletion with Rituximab reduced the numbers of lesions and new relapses in MS patients. The role of B cells has been studied in the animal model of MS, experimental autoimmune encephalomyelitis (EAE), but results from these studies have been variable and contradictory, and the contribution of B cells to CNS autoimmune disease is still unclear. We examined the role of B cells in C3H mice and found that both C3HeB/Fej and C3H.SW [omega]MT mice had a reduced incidence of EAE, suggesting an important role for B cells in the initiation of disease. B cells were the predominant MHC class II+ cells in the healthy CNS and were able to secrete cytokines, indicating that they could be influencing T cell responses before inflammation is initiated. Myelin-specific T cells were able to migrate to the CNS in the absence of B cells, but were unable to initiate immune responses. The ability of the early infiltrating T cells to secrete cytokines and initiate the recruitment of additional T cells to the CNS from the periphery before onset of EAE was defective in B cell deficient mice. Recruitment of T cells from the periphery constituted the majority of the increase in T cell number in the CNS of wildtype mice prior to onset. In vitro, B cells preferentially reactivated effector Th1 cells and not Th17 cells in the absence of IL-1[beta]. Induction of EAE with Th1- or Th17-skewed cells led to reduced numbers of IFN-[gamma]- and IL-17-producing cells in the brains of B cell deficient mice after onset of EAE. However, there was a greater effect on the numbers of IFN-[gamma]-producing cells, and in B cell deficient recipients of Th1-skewed cells, the localization of inflammation changed to permit inflammation in the brain. These studies indicate that B cells are important for T cell responses in the initiation of CNS autoimmunity, and can influence the localization of inflammation in EAE.