Dendritic cells in brain diseases

Ludewig, Peter; Gallizioli, Mattia; Urra, Xabier; Behr, Sarah; Brait, Vanessa H; Gelderblom, Mathias; Magnus, Tim; Planas, Anna M.

doi:10.1016/j.bbadis.2015.11.003

Cited by 58 publications

(41 citation statements)

References 239 publications

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“…This leads to a privileged immune status of the brain maintained by certain structural and functional features: (1) the BBB and the blood–cerebrospinal fluid barrier (BCSFB) are well-structured barrier systems that tightly control the free penetration of immune cells into the brain parenchyma. (2) Antigen presentation within the brain and at the regional lymph nodes is restricted due to (i) the absence of constitutive expression of major histocompatibility I molecules on neurons of the adult brain (1); (ii) the low number of professional antigen-presenting cells (APCs)—mainly dendritic cells (DCs)—and resident T cells in the brain parenchyma (2); and (iii) the lack of lymphatic vessels in the brain parenchyma, which would drain CNS-related antigens and APCs directly to the regional lymph nodes (3). …”

Section: The Immune Status Of the Healthy Brainmentioning

confidence: 99%

Ionizing Radiation-Induced Immune and Inflammatory Reactions in the Brain

2017

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Radiation-induced late brain injury consisting of vascular abnormalities, demyelination, white matter necrosis, and cognitive impairment has been described in patients subjected to cranial radiotherapy for brain tumors. Accumulating evidence suggests that various degrees of cognitive deficit can develop after much lower doses of ionizing radiation, as well. The pathophysiological mechanisms underlying these alterations are not elucidated so far. A permanent deficit in neurogenesis, chronic microvascular alterations, and blood–brain barrier dysfunctionality are considered among the main causative factors. Chronic neuroinflammation and altered immune reactions in the brain, which are inherent complications of brain irradiation, have also been directly implicated in the development of cognitive decline after radiation. This review aims to give a comprehensive overview on radiation-induced immune alterations and inflammatory reactions in the brain and summarizes how these processes can influence cognitive performance. The available data on the risk of low-dose radiation exposure in the development of cognitive impairment and the underlying mechanisms are also discussed.

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Section: The Immune Status Of the Healthy Brainmentioning

confidence: 99%

Ionizing Radiation-Induced Immune and Inflammatory Reactions in the Brain

2017

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“…Further study is needed to clarify fully the identity and function of these DC-like brain cells. Following stroke, microglia, infiltrated macrophagesmonocytes, and DCs express MHC class II, and costimulatory molecules, thus they can act as APCs in the ischemic brain parenchyma [2,8,10]. However, antigen processing differs between macrophages and DCs, as the latter regulate lysosomal acidification better than the former in order to preserve peptides for T-cell recognition [48].…”

Section: Innate Versus Adaptive Immunity In Strokementioning

confidence: 99%

“…Acute brain damage generates a genuine inflammatory reaction triggered by necrotic neuronal cells that leak their content to the extracellular space and trigger strong innate immune responses involving resident microglia and infiltrating leukocytes [4,5]. Notably, antigen-presenting cells (APC) accumulate in the brain parenchyma during the days that follow experimental stroke [6][7][8][9][10]. These cells express major histocompatibility complex (MHC) class II and co-stimulatory molecules, as well as markers of conventional dendritic cells (DCs).…”

Section: Introductionmentioning

confidence: 99%

Antigen Presentation After Stroke

et al. 2016

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“…A recent fluorescence-activated cell sorting (FACS)-based investigation unraveled a time-dependent inflammatory infiltration with a sharp increase in cells belonging to the innate immune system (macrophages and neutrophils) on day 1 and a maximum of lymphocyte infiltration around day 3 after transient middle cerebral artery occlusion (tMCAO) [11] . Dendritic cells (DC) are professional antigen-presenting cells that sense foreign molecules and present them to T cells, leading to an immune response or tolerance induction [12] . DC are bone marrow derived and can be classified as classical DC (cDC), plasmacytoid DC (pDC), inflammatory DC (infDC), Tip-DC, and other subtypes [12] .…”

Section: Introductionmentioning

confidence: 99%

“…Dendritic cells (DC) are professional antigen-presenting cells that sense foreign molecules and present them to T cells, leading to an immune response or tolerance induction [12] . DC are bone marrow derived and can be classified as classical DC (cDC), plasmacytoid DC (pDC), inflammatory DC (infDC), Tip-DC, and other subtypes [12] . A common marker of cDC is the cluster of differentiation (CD)11c, but CD11c expression is not exclusive to cDC, and pDC do not express CD11c [13] .…”

Section: Introductionmentioning

confidence: 99%

Depletion of CD11c<sup>+</sup> Cells Does Not Influence Outcomes in Mice Subjected to Transient Middle Cerebral Artery Occlusion

Kraft

Scholtyschik²,

Schuhmann³

et al. 2017

Neuroimmunomodulation

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Objective: While it has been shown that different T-cell subsets have a detrimental role in the acute phase of ischemic stroke, data on the impact of dendritic cells (DC) are missing. Classic DC can be characterized by the cluster of differentiation (CD)11c surface antigen. Methods: In this study, we depleted CD11c⁺ cells by using a CD11c-diphtheria toxin (DTX) receptor mouse strain that allows selective depletion of CD11c⁺ cells by DTX injection. For stroke induction, we used the model of transient middle cerebral artery occlusion (tMCAO) and analyzed stroke volume and functional outcome on days 1 and 3 as well as expression of prototypical pro- and anti-inflammatory cytokines on day 1 after tMCAO. Three different protocols for CD11c⁺ cell depletion, tMCAO duration, and readout time point were applied. Results: Injection of DTX (5 or 100 ng/g) reliably depleted CD11c⁺ cells without influencing the fractions of other immune cell subsets. CD11c⁺ cell depletion had no impact on stroke volume, but mice with a longer DTX pretreatment performed worse than those with vehicle treatment. CD11c⁺ cell depletion led to a decrease in cortical interleukin (IL)-1β and IL-6 messenger ribonucleic acid levels. Conclusions: We show, for the first time, that CD11c⁺ cell depletion does not influence stroke volume in a mouse model of focal cerebral ischemia. Nevertheless, given the unspecificity of the CD11c surface antigen for DC, mouse models that allow a more selective depletion of DC are needed to investigate the role of DC in stroke pathophysiology.

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Dendritic cells in brain diseases

Cited by 58 publications

References 239 publications

Ionizing Radiation-Induced Immune and Inflammatory Reactions in the Brain

Ionizing Radiation-Induced Immune and Inflammatory Reactions in the Brain

Antigen Presentation After Stroke

Depletion of CD11c<sup>+</sup> Cells Does Not Influence Outcomes in Mice Subjected to Transient Middle Cerebral Artery Occlusion

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