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B cells represent a relatively minor cell population within both the healthy and diseased central nervous system (CNS), yet they can have profound effects. This is emphasized in multiple sclerosis, in which B cell-depleting therapies are arguably the most efficacious treatment for the condition. In this Review, we discuss how B cells enter and persist in the CNS and how, in many neurological conditions, B cells concentrate within CNS barriers but are rarely found in the parenchyma. We highlight how B cells can contribute to CNS pathology through antibody secretion, antigen presentation and secretion of neurotoxic molecules, using examples from CNS tumours, CNS infections and autoimmune conditions such as neuromyelitis optica and, in particular, multiple sclerosis. Overall, understanding common and divergent principles of B cell accumulation and their effects within the CNS could offer new insights into treating these devastating neurological conditions., (© 2021. Springer Nature Limited.)

The article focuses on research on immune responses, regulatory T cells and T-cell signaling. Papers discussed which were published in other periodicals include "Dendritic Cell Stimulation By Mycobacterial Hsp70 is Mediated Through CCR5," by R. A. Floto et al and "Alterations in CD46-Mediated Tr1 Regulatory T Cells in Patients With Multiple Sclerosis," by A. L. Astier et al.

The article presents research highlights from the field of autoimmunity based on the original research paper "Contactin-2/TAG-1-directed autoimmunity is identified in multiple sclerosis patients and mediates gray matter pathology in animals," by T. Derfuss et al. that appeared in the April 28, 2009 issue of "Proceedings of the National Academy of Sciences USA." The article discusses a protein known as Contactin 2 that may help mediate grey matter pathology in multiple sclerosis patients.

The article discusses the possible role of osteopontin in multiple sclerosis relapse. Daily injection of osteopontin in mice with autoimmune encephalomyelitis with milder relapses triggered increased relapse leading to a fatal disease. On the basis of these observations a model was proposed where the presence of osteopontin in the brain promotes disease progression by protecting the death of T cells.

Presents the results of a study on the use of cannabis-based treatments for multiple sclerosis. Effect of cannabinoid compounds on patients; Comparison of the effectiveness of cannabis treatments with placebo; Significance of cannabinoids to cell death.

Discusses research being done on the identification of a new form of tolerance in which CD8+T cells interact with their major histocompatibility complex class-I-restricted epitope on dendritic cells. Reference to a study by A. Perchellet, I. Stromnes, J. M. Pang and J. Goverman in a 2004 issue of "Nature Immunology"; Experimentation on a mouse model of the autoimmune disease multiple sclerosis; Discussion on the inhibitory effect of 8.8 T cells.

Large-scale analyses of messenger RNA transcripts and autoantibody responses, taken from the actual sites of disease, provide us with an unprecedented view of the complexity of autoimmunity. Despite an appreciation of the large number of pathways and pathological processes that are involved in these diseases, a few practical targets and several new strategies have emerged from these studies. This review focuses on multiple sclerosis and on the approaches that are being used to identify new targets that might be manipulated to control this disease. [ABSTRACT FROM AUTHOR]

The article discusses a study by Y. Liu and colleagues which describes a regulatory T cell population that depends its development and functions on forkhead box A1 (FOXA1) transcription factor. It says that also examined whether FOXA1 regulatory T cells might mediate the clinical responsiveness of patients with multiple sclerosis to interferon-β (IFN β) therapy. It states that the results suggest a beneficial effect of IFNβ on central nervous system (CNS) inflammation.

The article offers information on a study conducted by researchers which reveals that nanoparticles with myelin protein induces T cell tolerance in multiple sclerosis. They attached a peptide from myelin proteolipid protein (PLP) to polystyrene nanoparticles and examined their ability to prevent and treat autoimmune encephalomyelitis (EAE). It highlights that the nanoparticles prevented initiation of the disease when given during early symptoms.

The article presents the study by Inoue M. and colleagues on the efficacy of interferon-ß in treating experimental autoimmune encephalomyelitis (EAE). Researchers did the research on mice with EAC and found that interferon-ß is effective in treating individuals with multiple sclerosis. Moreover, they also discovered that it is not effective to some patients due to the inflammasome involvement of their illnesses.

The article reports that multiple sclerosis develop in genetically predisposed individuals after an environmental trigger activates myelin-specific T cells in the central nervous system (CNS). It states that peptidoglycan activates antigenpresenting cells in the CNS to provide this trigger. It states that pro-inflammatory signalling cascade downstream of the nucleotidebinding oligomerization domain proteins is mediated by receptor-interacting protein 2.

The article discusses how interferon-beta inhibits autoimmune inflammation in the central nervous system (CNS) as it reduces disease in many patients with multiple sclerosis. Researchers revealed that the effect of type I interferon-beta on myeloid cells is crucial to the protective effect of this cytokine in the animal model of experimental autoimmune encephalomyelitis (EAE). The study also provides hints as to how interferon-beta therapy might work in patients with multiple sclerosis.

The article discusses research being done on dysregulated T cell expression of TIM3 in multiple sclerosis. It references a study by K. Koguchi et al., published in a 2006 issue of "The Journal of Experimental Medicine." Details of how the study was conducted are given. The association between the destruction of myelin sheaths and a T-cell-mediated inflammatory process is examined. The authors then asked if there was a mechanistic link between reciprocally dysregulated TIM3 expression and interferon-y.

Discusses research being done on the loss of functional suppression by CD4 CD25 regulatory T cells in patients with multiple sclerosis (MS). Reference to a study made by V. Viglietta et al., which was published in the 2004 issue of the "Journal of Experimental Medicine"; Comparison of CD4+ CD25hi TReg cells isolated from untreated patients with relapsing/remitting MS and healthy control individuals; Significance of the study.

Discusses the findings of several studies on health-related issues. Influence of dectin-1 on inflammatory response; Immunoregulation of multiple sclerosis; Development of T lymphocytes from embryonic stem cell progenitors.

Discusses research being done on the gene expression in multiple sclerosis microarrays. Reference to a study conducted by C. Lock published in the 'Nature Medicine.'