New tools to trace populations of inflammatory cells in the CNS

Flügel, Alexander; Bradl, Monika

doi:10.1002/glia.1102

Cited by 18 publications

(8 citation statements)

References 104 publications

(129 reference statements)

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“…In this condition NGF, which is mainly produced by astrocytes and stored in the extracellular matrix, can inhibit the inflammatory infiltrates by preventing perivascular macrophages and mast cells from crossing the BBB. This interaction protects CNS integrity and aids recovery after inflammation (Words, 2001). Also, levels of NGF increase in the cerebrospinal fluid (Laudiero et al, 1992) and optic nerves (Micera et al, 1999) of patients affected by MS.…”

Section: Discussionmentioning

confidence: 99%

Involvement of AMPK, IKβα-NFκB and eNOS in the sildenafil anti-inflammatory mechanism in a demyelination model

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Involvement of AMPK, IKβα-NFκB and eNOS in the sildenafil anti-inflammatory mechanism in a demyelination model

et al. 2015

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“…Once autoreactive T cells traffic to the CNS, they undergo a second round of reactivation by local APCs such as macrophages and microglia. It is this intricate interaction between cells of the immune system, which communicate via a complex network of cytokines, chemokines and adhesion molecules that shapes the nature and severity of the disease [51], [52]. During this inflammatory process, microglia/macrophages play an important role in clearance of myelin debris, eventually promoting the resolution of inflammation [53].…”

Section: Discussionmentioning

confidence: 99%

Nogo-Receptor 1 Deficiency Has No Influence on Immune Cell Repertoire or Function during Experimental Autoimmune Encephalomyelitis

et al. 2013

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The potential role of Nogo-66 Receptor 1 (NgR1) on immune cell phenotypes and their activation during neuroinflammatory diseases such as multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), is unclear. To further understand the function of this receptor on haematopoietically-derived cells, phenotypic and functional analyses were performed using NgR1-deficient (ngr1-/-) animals. Flow cytometry-based phenotypic analyses performed on blood, spleen, thymus, lymph nodes, bone marrow and central nervous-system (CNS)-infiltrating blood cells revealed no immunological defects in naïve ngr1-/- animals versus wild-type littermate (WTLM) controls. EAE was induced by either recombinant myelin oligodendrocyte glycoprotein (rMOG), a model in which B cells are considered to contribute pathogenically, or by MOG35–55 peptide, a B cell-independent model. We have demonstrated that in ngr1-/- mice injected with MOG35–55, a significant reduction in the severity of EAE correlated with reduced axonal damage present in the spinal cord when compared to their WTLM controls. However, despite a reduction in axonal damage observed in the CNS of ngr1-/- mice at the chronic stage of disease, no clinical differences could be attributed to a specific genotype when rMOG was used as the encephalitogen. Following MOG35–55-induction of EAE, we could not derive any major changes to the immune cell populations analyzed between ngr1-/- and WTLM mice. Collectively, these data demonstrate that NgR1 has little if any effects on the repertoire of immune cells, their activation and trafficking to the CNS.

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“…Attaining this information requires experimental tools to distinguish the peptide/MHC-restricted T cells from the bystanders of an irrelevant specificity. Fortunately, with the latest methodological advances, 17,[113][114][115][116][117] the particular localization and function of antigen-specific T cells can now be investigated in a variety of in vivo systems that rely on identifiable or traceable populations of T cells. It is important to note that these recent advances will undoubtedly refine our understanding of T-cell biology in physiological microenvironments and facilitate the identification of novel therapeutic targets.…”

Section: Discussionmentioning

confidence: 99%

The Role of Bystander T Cells in CNS Pathology and Pathogen Clearance

McGavern

2005

Crit Rev Immunol

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It is generally accepted that both self- and pathogen-specific T lymphocytes have the potential to mediate immunopathogenesis and contribute to a variety of human ailments. Despite this unfortunate tendency to induce tissue injury, these cells are guided by interactions with peptide-loaded major histocompatibility complexes (MHC) and adhere appropriately to a vital evolutionary constraint imposed by the host: specificity. More recently, a series of studies have demonstrated that bystander T cells of an irrelevant specificity can bypass peptide/MHC restriction and become active participants in immunopathology. This review critically evaluates the role of bystander T cells in immunopathogenesis and pathogen clearance in the periphery as well as the central nervous system and attempts to establish the likelihood of their participation in human disease.

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New tools to trace populations of inflammatory cells in the CNS

Cited by 18 publications

References 104 publications

Involvement of AMPK, IKβα-NFκB and eNOS in the sildenafil anti-inflammatory mechanism in a demyelination model

Involvement of AMPK, IKβα-NFκB and eNOS in the sildenafil anti-inflammatory mechanism in a demyelination model

Nogo-Receptor 1 Deficiency Has No Influence on Immune Cell Repertoire or Function during Experimental Autoimmune Encephalomyelitis

The Role of Bystander T Cells in CNS Pathology and Pathogen Clearance

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