Редактирование: CD200 (раздел)

==Publications==

{{medline-entry
|title=Age exacerbates surgery-induced cognitive impairment and neuroinflammation in Sprague-Dawley rats: the role of IL-4.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28414034
|abstract=Age is the most prominent risk factor for the development of postoperative cognitive dysfunction. This study investigated the potential role of anti-inflammatory interleukin (IL)-4 in age-related differences of surgery-induced cognitive deficits and neuroinflammatory responses. Both adult and aged Sprague-Dawley male rats were subjected to partial hepatectomy or partial hepatectomy with a cisterna magna infusion of IL-4. On postoperative days 1, 3, and 7, the rats were subjected to a reversed Morris water maze test. Hippocampal IL-1β, IL-6, IL-4, and IL-4 receptor (IL-4R) were measured at each time point. Brain derived neurotrophic factor ([[BDNF]]), synaptophysin, Ionized calcium-binding adapter molecule 1 (Iba-1), microglial M2 phenotype marker Arg1, and [[CD200]] were also examined in the hippocampus. Age induced an exacerbated cognitive impairment and an amplified neuroinflammatory response triggered by surgical stress on postoperative days 1 and 3. A corresponding decline in the anti-inflammatory cytokine IL-4 and [[BDNF]] were also found in the aged rats at the same time point. Treatment with IL-4 downregulated the expression of proinflammatory cytokines (e.g., IL-1β and IL-6), increased the levels of [[BDNF]] and synaptophysin in the brain and improved the behavioral performance. An increased Arg1 expression and a high level of [[CD200]] were also observed after a cisterna magna infusion of IL-4. An age-related decrease in IL-4 expression exacerbated surgery-induced cognitive deficits and exaggerated the neuroinflammatory responses. Treatment with IL-4 potentially attenuated these effects by enhancing [[BDNF]] and synaptophysin expression, inhibiting microglia activation and decreasing the associated production of proinflammatory cytokines.
|mesh-terms=* Aging
* Animals
* Cognitive Dysfunction
* Disease Models, Animal
* Hippocampus
* Inflammation
* Interleukin-4
* Microglia
* Rats, Sprague-Dawley
|keywords=* Aging
* Cytokines
* Hippocampus
* Neuroinflammation
* Postoperative cognitive dysfunction (POCD)
|full-text-url=https://sci-hub.do/10.1016/j.brainres.2017.04.004
}}
{{medline-entry
|title=Prior stressor exposure delays the recovery of surgery-induced cognitive impairment and prolongs neuroinflammation in aged rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27487302
|abstract=Increasing evidence indicates that stress potentiates pro-inflammatory response to a subsequent peripheral immune challenge. The present study investigated if prior exposure to inescapable tailshock (IS) delayed the recovery of surgery-induced spatial learning and memory impairment and prolonged hippocampus interleukin (IL)-1β and IL-6 expression. A total of 192 aged rats were trained with Morris water-maze (MWM) for 6 consecutive days. A single session of inescapable tailshock was performed on day 6 after training. Then, the rats subjected to partial hepatectomy. Hippocampal-dependent spatial learning and memory were assessed on postoperative days 1, 3 and 7. The cytokines IL-1β and IL-6 and ionized calcium binding adaptor protein (Iba)-1 were measured at each time point. Cluster of differentiation 200 ([[CD200]]) was also measured to explore potential mechanisms of glial cell activation. Exposure of IS alone failed to affect the latency to platform and increase hippocampal cytokine levels at each time point. However, IS alone significantly increased the expression levels of Iba-1. A prolonged latency and additional significant increase in hippocampal levels of IL-1β and IL-6 were observed when partial hepatectomy was performed in aged rats exposed to IS 24h later. The combination of IS and surgical trauma dramatically upregulated the levels of Iba-1 and significantly decreased the expression of [[CD200]]. IS alone failed to induce cognitive deficits and increase pro-inflammatory cytokines expression. However, IS delayed the recovery of surgery-induced spatial learning and memory impairment and prolonged pro-inflammatory response to the subsequent surgery challenge.
|mesh-terms=* Animals
* Antigens, CD
* Calcium-Binding Proteins
* Cognitive Dysfunction
* Electroshock
* Encephalitis
* Glial Fibrillary Acidic Protein
* Glucocorticoids
* Hippocampus
* Interleukin-1beta
* Interleukin-6
* Male
* Microfilament Proteins
* Postoperative Complications
* Rats
* Rats, Sprague-Dawley
* Recovery of Function
* Spatial Learning
* Stress, Psychological
|keywords=* Aging
* Hippocampus
* Inescapable tailshock (IS)
* Neuroinflammation
* Postoperative cognitive dysfunction (POCD)
* Prior stress
|full-text-url=https://sci-hub.do/10.1016/j.brainres.2016.07.045
}}
{{medline-entry
|title=Brain innate immunity in the regulation of neuroinflammation: therapeutic strategies by modulating [[CD200]]-[[CD200]]R interaction involve the cannabinoid system.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24588829
|abstract=The central nervous system (CNS) innate immune response includes an arsenal of molecules and receptors expressed by professional phagocytes, glial cells and neurons that is involved in host defence and clearance of toxic and dangerous cell debris. However, any uncontrolled innate immune responses within the CNS are widely recognized as playing a major role in the development of autoimmune disorders and neurodegeneration, with multiple sclerosis (MS) Alzheimer's disease (AD) being primary examples. Hence, it is important to identify the key regulatory mechanisms involved in the control of CNS innate immunity and which could be harnessed to explore novel therapeutic avenues. Neuroimmune regulatory proteins (NIReg) such as CD95L, [[CD200]], [[CD47]], sialic acid, complement regulatory proteins (CD55, [[CD46]], fH, C3a), [[HMGB1]], may control the adverse immune responses in health and diseases. In the absence of these regulators, when neurons die by apoptosis, become infected or damaged, microglia and infiltrating immune cells are free to cause injury as well as an adverse inflammatory response in acute and chronic settings. We will herein provide new emphasis on the role of the pair [[CD200]]-[[CD200]]R in MS and its experimental models: experimental autoimmune encephalomyelitis (EAE) and Theiler's virus induced demyelinating disease (TMEV-IDD). The interest of the cannabinoid system as inhibitor of inflammation prompt us to introduce our findings about the role of endocannabinoids (eCBs) in promoting [[CD200]]-[[CD200]] receptor ([[CD200]]R) interaction and the benefits caused in TMEV-IDD. Finally, we also review the current data on [[CD200]]-[[CD200]]R interaction in AD, as well as, in the aging brain.
|mesh-terms=* Aging
* Alzheimer Disease
* Antigens, CD
* Antigens, Surface
* Brain
* Encephalitis
* Endocannabinoids
* Humans
* Immunity, Innate
* Multiple Sclerosis
* Orexin Receptors
* Receptors, Cell Surface

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157566
}}
{{medline-entry
|title=Understanding the neurobiology of [[CD200]] and the [[CD200]] receptor: a therapeutic target for controlling inflammation in human brains?
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24198718
|abstract=[[CD200]] and its receptor, [[CD200]] receptor ([[CD200]]R), have uniaue roles in controlling damaging inflammatory processes. At present, the only identified function for [[CD200]] is as a ligand for [[CD200]]R. These proteins interact resulting in the activation of anti-inflammatory signaling by [[CD200]]R-expressing cells. When this interaction becomes deficient with aging or disease, chronic inflammation occurs, Experimental animal studies have demonstrated the consequences of disrupting [[CD200]]-[[CD200]]R interactions in the brain, but there have been few studies in human brains. Deficiency in neuronal [[CD200]] may explain the chronic inflammation in human neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and multiple sclerosis; however, deficits in the microglial expression of [[CD200]]R may also be of functional significance. The purpose of this review is to assess the data regarding the role of [[CD200]]-[[CD200]]R interactions in relation to the brain in order to determine if this could be a therapeutic target for human brain diseases with inflammatory components, and what additional studies are needed.

|keywords=* aging
* alternative activation
* anti-inflammatory signaling
* cell surface protein
* endogenous inflammatory regulator
* inflammation
* neurodegenerative disease
* neuropathology
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815586
}}
{{medline-entry
|title=The immune inhibitory complex [[CD200]]/[[CD200]]R is developmentally regulated in the mouse brain.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22323214
|abstract=The [[CD200]]/[[CD200]]R inhibitory immune ligand-receptor system regulates microglial activation/quiescence in adult brain. Here, we investigated [[CD200]]/[[CD200]]R at different stages of postnatal development, when microglial maturation takes place. We characterized the spatiotemporal, cellular, and quantitative expression pattern of [[CD200]] and [[CD200]]R in the developing and adult C57/BL6 mice brain by immunofluorescent labeling and Western blotting. [[CD200]] expression increased from postnatal day 1 (P1) to P5-P7, when maximum levels were found, and decreased to adulthood. [[CD200]] was located surrounding neuronal bodies, and very prominently in cortical layer I, where [[CD200]]( ) structures included glial fibrillary acidic protein (GFAP)( ) astrocytes until P7. In the hippocampus, [[CD200]] was mainly observed in the hippocampal fissure, where GFAP( ) /[[CD200]]( ) astrocytes were also found until P7. [[CD200]]( ) endothelium was seen in the hippocampal fissure and cortical blood vessels, notably from P14, showing maximum vascular [[CD200]] in adults. [[CD200]]R( ) cells were a population of ameboid/pseudopodic Iba1( ) microglia/macrophages observed at all ages, but significantly decreasing with increasing age. [[CD200]]R( ) /Iba1( ) macrophages were prominent in the pial meninges and ventricle lining, mainly at P1-P5. [[CD200]]R( ) /Iba1( ) perivascular macrophages were observed in cortical and hippocampal fissure blood vessels, showing maximum density at P7, but being prominent until adulthood. [[CD200]]R( ) /Iba1( ) ameboid microglia in the cingulum at P1-P5 were the only [[CD200]]R( ) cells in the nervous tissue. In conclusion, the main sites of [[CD200]]/[[CD200]]R interaction seem to include the molecular layer and pial surface in neonates and blood vessels from P7 until adulthood, highlighting the possible role of the [[CD200]]/[[CD200]]R system in microglial development and renewal.
|mesh-terms=* Aging
* Animals
* Animals, Newborn
* Antibody Specificity
* Antigen-Antibody Reactions
* Antigens, CD
* Brain Chemistry
* Female
* Hippocampus
* Macrophages
* Male
* Membrane Glycoproteins
* Mice
* Mice, Inbred C57BL
* Microglia
* Neocortex
* Neural Inhibition
* Neurogenesis

|full-text-url=https://sci-hub.do/10.1002/cne.23062
}}
{{medline-entry
|title=[[CD200]] fusion protein decreases microglial activation in the hippocampus of aged rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22041297
|abstract=The glycoprotein, [[CD200]], is primarily expressed on neurons and its cognate receptor [[CD200]]R is expressed principally on cells of the myeloid lineage, including microglia. The interaction of [[CD200]] with its receptor plays a significant role in maintaining microglia in a quiescent state and therefore a decrease in [[CD200]] expression in brain is associated with evidence of microglial activation. Conversely, activation of [[CD200]]R, for example using a [[CD200]] fusion protein ([[CD200]]Fc), should result in a decrease in microglial activation. Here we assessed the effect of delivery of [[CD200]]Fc intrahippocampally on microglial activation and on long-term potentiation (LTP) in perforant path-granule cell synapses in young and aged rats. We hypothesized that the age-related changes in microglial activation would be attenuated by [[CD200]]Fc resulting in an improved ability of aged rats to sustain LTP. The data indicate that expression of markers of microglial activation including major histocompatibility complex Class II (MHCII) and [[CD40]] mRNA, as well as MHCII immunoreactivity, were increased in hippocampus of aged, compared with young, rats and that these changes were associated with a deficit in LTP; these changes were attenuated in hippocampal tissue prepared from aged rats which received [[CD200]]Fc. Microglial activation and a deficit in LTP have also been reported in lipopolysaccharide (LPS)-treated rats and, here, we report that these changes were also attenuated in [[CD200]]Fc-treated animals. Thus the negative impact of microglial activation on the ability of aged and LPS-treated rats to sustain LTP is ameliorated when [[CD200]]R is activated by [[CD200]]Fc.
|mesh-terms=* Actins
* Aging
* Animals
* Antigens, CD
* Blotting, Western
* Chemokines
* Cytokines
* Excitatory Postsynaptic Potentials
* Genes, MHC Class II
* Hippocampus
* Inflammation
* Lipopolysaccharides
* Long-Term Potentiation
* Macrophage Activation
* Male
* Membrane Proteins
* Microglia
* Microinjections
* Neuronal Plasticity
* Rats
* Rats, Wistar
* Real-Time Polymerase Chain Reaction
* Recombinant Fusion Proteins
* Synaptophysin

|full-text-url=https://sci-hub.do/10.1016/j.bbi.2011.10.004
}}
{{medline-entry
|title=Age-related changes in the hippocampus (loss of synaptophysin and glial-synaptic interaction) are modified by systemic treatment with an NCAM-derived peptide, FGL.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/21986303
|abstract=Altered synaptic morphology, progressive loss of synapses and glial (astrocyte and microglial) cell activation are considered as characteristic hallmarks of aging. Recent evidence suggests that there is a concomitant age-related decrease in expression of the presynaptic protein, synaptophysin, and the neuronal glycoprotein [[CD200]], which, by interacting with its receptor, plays a role in maintaining microglia in a quiescent state. These age-related changes may be indicative of reduced neuroglial support of synapses. FG Loop (FGL) peptide synthesized from the second fibronectin type III module of neural cell adhesion molecule (NCAM), has previously been shown to attenuate age-related glial cell activation, and to 'restore' cognitive function in aged rats. The mechanisms by which FGL exerts these neuroprotective effects remain unclear, but could involve regulation of [[CD200]], modifying glial-synaptic interactions (affecting neuroglial 'support' at synapses), or impacting directly on synaptic function. Light and electron microscopic (EM) analyses were undertaken to investigate whether systemic treatment with FGL (i) alters [[CD200]], synaptophysin (presynaptic) and [[PSD]]-95 (postsynaptic) immunohistochemical expression levels, (ii) affects synaptic number, or (iii) exerts any effects on glial-synaptic interactions within young (4 month-old) and aged (22 month-old) rat hippocampus. Treatment with FGL attenuated the age-related loss of synaptophysin immunoreactivity (-ir) within [[CA3]] and hilus (with no major effect on [[PSD]]-95-ir), and of [[CD200]]-ir specifically in the [[CA3]] region. Ultrastructural morphometric analyses showed that FGL treatment (i) prevented age-related loss in astrocyte-synaptic contacts, (ii) reduced microglia-synaptic contacts in the [[CA3]] stratum radiatum, but (iii) had no effect on the mean number of synapses in this region. These data suggest that FGL mediates its neuroprotective effects by regulating glial-synaptic interaction.
|mesh-terms=* Aging
* Animals
* Antigens, CD
* CA3 Region, Hippocampal
* Disks Large Homolog 4 Protein
* Glial Fibrillary Acidic Protein
* Hippocampus
* Image Processing, Computer-Assisted
* Immunohistochemistry
* Injections, Intraperitoneal
* Intracellular Signaling Peptides and Proteins
* Male
* Membrane Proteins
* Microscopy, Electron
* Neural Cell Adhesion Molecules
* Neuroglia
* Rats
* Rats, Wistar
* Synapses
* Synaptophysin

|full-text-url=https://sci-hub.do/10.1016/j.bbi.2011.09.013
}}
{{medline-entry
|title=Impaired [[CD200]]-[[CD200]]R-mediated microglia silencing enhances midbrain dopaminergic neurodegeneration: roles of aging, superoxide, NADPH oxidase, and p38 MAPK.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/21295135
|abstract=[[CD200]]-[[CD200]]R signaling holds microglia in a quiescent state. Parkinson disease (PD) neurodegeneration may be associated with impairment of [[CD200]]-[[CD200]]R-mediated microglia silencing in the substantia nigra (SN). In this study, an anti-[[CD200]]R blocking antibody (ACDR) selectively and significantly enhanced the susceptibility of dopaminergic neurons to neurotoxicity induced by rotenone (Rot) and iron (Ir) in mesencephalic neuron/glia cultures. Microglia were shown to mediate dopaminergic neurotoxicity induced by ACDR/Rot (combination of ACDR and Rot) and ACDR/Ir (combination of ACDR and Ir). ACDR significantly enhanced the microglial activation induced by Rot and Ir in neuron/glia cultures. NADPH oxidase-mediated superoxide generation was a key contributor to dopaminergic neurotoxicity induced by ACDR/Rot and ACDR/Ir. p38 MAPK contributed to NADPH oxidase activation induced by ACDR/Rot and ACDR/Ir. Interestingly, there were a decrease in [[CD200]] expression (mRNA and protein) and an enhancement of microglial response (MHCII mRNA and ICAM-1 protein) in the rat SN with aging. ICAM-1 expression was significantly inversely correlated with [[CD200]] expression. These results strongly indicate the participation of SN [[CD200]]-[[CD200]]R dysfunction in the etiopathogenesis of PD and provide a new insight into the molecular mechanisms underlying the involvement of aging in PD and help to elucidate the mechanisms of the combined involvement of immune/inflammatory factors, environmental substances, and aging in PD.
|mesh-terms=* Aging
* Animals
* Antibodies, Blocking
* Antigens, CD
* Cell Culture Techniques
* Cells, Cultured
* Dopamine
* Gene Expression
* Intercellular Adhesion Molecule-1
* Iron
* Mesencephalon
* Microglia
* NADPH Oxidases
* Neurons
* Parkinson Disease
* Polymerase Chain Reaction
* Rats
* Rats, Sprague-Dawley
* Receptors, Immunologic
* Rotenone
* Superoxides
* p38 Mitogen-Activated Protein Kinases

|full-text-url=https://sci-hub.do/10.1016/j.freeradbiomed.2011.01.032
}}
{{medline-entry
|title=Postoperative cognitive deficits and neuroinflammation in the hippocampus triggered by surgical trauma are exacerbated in aged rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/20691747
|abstract=Postoperative cognitive dysfunction (POCD) is characterized by the progressive deterioration of intellectual/cognitive function following surgery. It has been suggested that the senile brain, which characteristically expresses higher levels of central proinflammatory cytokines, interleukin (IL)-6, IL-1β, and tumor necrosis factor ([[TNF]])-α, is more susceptible to additional insult following surgery. The authors of this study investigated the expression of central cytokines IL-1β, IL-6 and [[TNF]]-α and hippocampal glial cell activation in aged and adult rats following partial hepatectomy. Cognitive function was assessed in a reversal-learning version of the Morris water maze (MWM) before and after surgery. Hippocampal pro-inflammatory cytokines IL-1β, IL-6 and [[TNF]]-α and glial cell activation markers glial fibrillary acidic protein (GFAP) and S100β were measured at each time point; [[CD200]] and [[CD200]]R were also measured to explore potential mechanisms of glial cell activation. Surgical trauma resulted in impairments in distance and latency only on postoperative day 1 (p<0.001, respectively) in adult rats. Aged rats exhibited impairments on day 1 (p<0.001) that persisted until postoperative day 3 (p=0.002 and p=0.001, respectively). All significant impairments paralleled upregulated cytokine IL-1β and IL-6 expression. Immunohistochemistry assay further showed more hippocampal glial cell activation in aged rats compared to that in adults. Overall, these findings suggest that surgical trauma, rather than anesthesia, resulted in cognitive function impairment potentiated by aging. Hippocampal pro-inflammatory cytokines and glial cell activation might mediate trauma-induced POCD.
|mesh-terms=* Aging
* Animals
* Cognition Disorders
* Disease Progression
* Hepatectomy
* Hippocampus
* Inflammation
* Maze Learning
* Neurons
* Postoperative Complications
* Random Allocation
* Rats
* Rats, Sprague-Dawley

|full-text-url=https://sci-hub.do/10.1016/j.pnpbp.2010.07.027
}}
{{medline-entry
|title=Hedgehog signaling maintains hair follicle stem cell phenotype in young and aged human skin.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/20050020
|abstract=Skin hair follicles (HF) contain bulge stem cells (SC) that regenerate HFs during hair cycles, and repair skin epithelia following injury. As natural aging is associated with decreased skin repair capacity in humans, we have investigated the impact of age on human scalp HF bulge cell number and function. Here, we isolated human bulge cells, characterized as [[CD200]] /[[KRT15]] /[[KRT19]]  cells of the HF, by dissection-combined [[CD200]] selection in young and aged human skin. Targeted transcriptional profiling indicates that [[KRT15]], [[KRT19]], Dkk3, Dkk4, Tcf3, [[S100A4]], Gas1, [[EGFR]] and CTGF/CCN2 are also preferentially expressed by human bulge cells, compared to differentiated HF keratinocytes (KC). Our results demonstrate that aging does not alter expression or localization of these HF SC markers. In addition, we could not detect significant differences in HF density or bulge cell number between young and aged human scalp skin. Interestingly, hedgehog (Hh) signaling is activated in human bulge cells in vivo, and down-regulated in differentiated HF KCs, both in young and aged skin. In addition, activation of Hh signaling by lentivirus-mediated overexpression of transcription factor Gli1 induces transcription of HF SC markers [[KRT15]], [[KRT19]], and Gas1, in cultured KCs. Together with previously reported knock-out mouse results, these data suggest a role for Hh signaling in maintaining bulge cell phenotype in young and aged human skin.
|mesh-terms=* Adult
* Aged
* Aging
* Antigens, CD
* Cell Cycle Proteins
* Cell Separation
* GPI-Linked Proteins
* Hair Follicle
* Hedgehog Proteins
* Humans
* Keratin-15
* Keratinocytes
* Membrane Proteins
* Stem Cells

|full-text-url=https://sci-hub.do/10.1111/j.1474-9726.2009.00526.x
}}
{{medline-entry
|title=A novel phospholipid-based drug formulation, VP025, modulates age- and LPS-induced microglial activity in the rat.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19609089
|abstract=A common change that occurs with age in the central nervous system is an increase in microglial-associated inflammation. This is usually coupled with an increase in the concentration of the inflammatory cytokine interleukin-1beta (IL-1beta) in the hippocampus and an inhibition in long-term potentiation. To assess the effects of a novel preparation of phospholipid nanoparticles incorporating phosphatidylglycerol, VP025, on inflammatory changes in hippocampus of aged and lipopolysaccharide (LPS)-treated rats. We report that a possible initial target cell of the putative anti-inflammatory actions of VP025 may be macrophages, as VP025 is engulfed by, and has the capacity to alter the activity of, these cells. VP025 reversed the increase in IFN-gamma concentration in supernatant taken from peritoneal macrophages harvested from LPS-treated rats. In addition, markers of microglial activity, major histocompatibility complex class II (MHC II) mRNA expression, [[CD40]] expression and IL-1beta concentration were increased, and [[CD200]] expression was reduced, in the hippocampus of these rats. VP025 reversed changes in [[CD40]], IL-1beta and [[CD200]] in aged rats, and also restored long-term potentiation in aged and LPS-treated rats. We conclude that VP025 has the ability to modulate the activity of macrophage, microglia and neurons in response to stressors such as ageing and LPS treatment.
|mesh-terms=* Adult
* Aging
* Animals
* Anti-Inflammatory Agents
* Encephalitis
* Gliosis
* Hippocampus
* Humans
* Immunomodulation
* Interferon-gamma
* Interleukin-1beta
* Long-Term Potentiation
* Macrophages
* Male
* Memory Disorders
* Microglia
* Nanoparticles
* Perforant Pathway
* Phagocytosis
* Phosphatidylglycerols
* Phospholipids
* Rats
* Rats, Wistar
* Tumor Cells, Cultured
* Tumor Necrosis Factor-alpha

|full-text-url=https://sci-hub.do/10.1159/000228915
}}
{{medline-entry
|title=mRNA up-regulation of MHC II and pivotal pro-inflammatory genes in normal brain aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/15890435
|abstract=In normal brain aging, CNS resident macrophages exhibit increased expression of major histocompatibility complex (MHC) II expression. However, the transcriptional basis for this observation has not been clarified nor have age-related alterations in pivotal pro-inflammatory genes been characterized. Age-related mRNA alterations in MHC II, MHC II accessory molecules and several pro-inflammatory mediators were measured in older (24 months) and younger (3 months) male F344xBN F1 rats. Real time RT-PCR was utilized to measure steady state mRNA levels in hippocampus. Older as compared to younger animals exhibited increased mRNA levels of MHC II, [[CD86]], [[CIITA]] and IFN-gamma. Furthermore, IL-10 and [[CD200]] mRNA, molecules that down-regulate macrophage activation, was decreased in older animals. The present results indicate that normal brain aging is characterized by a shift towards a pro-inflammatory microenvironment in the CNS.
|mesh-terms=* Aging
* Animals
* Antigens, CD
* Brain
* DNA Primers
* DNA, Complementary
* Gene Expression Regulation, Developmental
* Genes, MHC Class II
* Inflammation
* Male
* Neurons
* RNA, Messenger
* Rats
* Rats, Inbred F344
* Receptors, Immunologic
* Reverse Transcriptase Polymerase Chain Reaction
* Up-Regulation

|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2005.03.013
}}