Cited by 154Neuroinflammation and Neurodegeneration MechanismsParkinson's Disease Mechanisms and TreatmentsNuclear Receptors and Signaling

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CD200-CD200R dysfunction exacerbates microglial activation and dopaminergic neurodegeneration in a rat model of Parkinson's disease

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Zhang, Shi, Wang, Xi-Jin, Tian, Li-Peng, Pan, Jing, Lu, Guo-Qiang, Zhang, Ying-Jie, Ding, Jian-Qing, Chen, Sheng-Di·2011·Journal of Neuroinflammation

DOI 10.1186/1742-2094-8-154PMC PMC3226566

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Abstract

BACKGROUND: Increasing evidence suggests that microglial activation may participate in the aetiology and pathogenesis of Parkinson's disease (PD). CD200-CD200R signalling has been shown to be critical for restraining microglial activation. We have previously shown that expression of CD200R in monocyte-derived macrophages, induced by various stimuli, is impaired in PD patients, implying an intrinsic abnormality of CD200-CD200R signalling in PD brain. Thus, further in vivo evidence is needed to elucidate the role of malfunction of CD200-CD200R signalling in the pathogenesis of PD. METHODS: 6-hydroxydopamine (6-OHDA)-lesioned rats were used as an animal model of PD. CD200R-blocking antibody (BAb) was injected into striatum to block the engagement of CD200 and CD200R. The animals were divided into three groups, which were treated with 6-OHDA/Veh (PBS), 6-OHDA/CAb (isotype control antibody) or 6-OHDA/BAb, respectively. Rotational tests and immunohistochemistry were employed to evaluate motor deficits and dopaminergic neurodegeneration in animals from each group. HPLC analysis was used to measure monoamine levels in striatum. Morphological analysis and quantification of CD11b- (or MHC II-) immunoreactive cells were performed to investigate microglial activation and possible neuroinflammation in the substantia nigra (SN). Finally, ELISA was employed to assay protein levels of proinflammatory cytokines. RESULTS: Compared with 6-OHDA/CAb or 6-OHDA/Veh groups, rats treated with 6-OHDA/BAb showed a significant increase in counts of contralateral rotation and a significant decrease in TH-immunoreactive (TH-ir) neurons in SN. A marked decrease in monoamine levels was also detected in 6-OHDA/BAb-treated rats, in comparison to 6-OHDA/Veh-treated ones. Furthermore, remarkably increased activation of microglia as well as up-regulation of proinflammatory cytokines was found concomitant with dopaminergic neurodegeneration in 6-OHDA/BAb-treated rats. CONCLUSIONS: This study shows that deficits in the CD200-CD200R system exacerbate microglial activation and dopaminergic neurodegeneration in a 6-OHDA-induced rat model of PD. Our results suggest that dysfunction of CD200-CD200R signalling may be involved in the aetiopathogenesis of PD.

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Figure 1 BAb exacerbates 6-OHDA-induced behavioural deficits. Contralateral rotation measurements following administration of apomorphine in each experimental group are shown in bar graph at 7 days and 21 days post-6-OHDA injection. Data are presented as mean ±S.E.M (n = 5 rats/group). (#)Statistical differences from 6-OHDA/Veh- or 6-OHDA/CAb-treated animals are P < 0.001.CC BY · PubMed Central

Figure 2 Neurodegeneration is exacerbated in the SN of hemi-parkinsonian rats. Animals (5 rats per groups) were sacrificed at 21-day post 6-OHDA injection to characterize and quantify loss of dopaminergic neurons in whole SN. (B-G) Representative sections (~24 sections per rat) of SN were immunostained with antibodies against tyrosine hydroxylase (TH). (B,E) SN of 6-OHDA/Veh group, (C,F) SN of 6-OHDA/CAb group, (D,G) SN of 6-OHDA/BAb group. The bottom photos (E-G) are higher magnifications of the cells in black rectangles of ipsilateral SN in the upper photos (B-D). Scale bar: 1 mm (B-D); scale bar: 50 μm (E-G). Arrows: neurons; arrowheads: fibers. (A) Stereological cell counts of total TH-ir neurons on the ipsilateral side of the SN are shown as a percentage of the cells on the contralateral side (n = 5/group, # P < 0.0001). All the results were obtained in a two-blinded procedure. No significant difference was found between the group treated with 6-OHDA/Veh and the group treated with 6-OHDA/CAb (P = 0.5108). Data are presented as mean ± S.E.M.CC BY · PubMed Central

Figure 3 Effects of BAb on microglial morphology and cell number in SN. Representative sections of SN in different groups were immunostained with antibodies against CD11b (a microglia marker) (D-I) and MHC II (a marker for activated microglia) (J-O) 21 days after 6-OHDA-injection. G-I and M-O are higher magnifications of the fields outlined by rectangles in D-F and J-L respectively. Scale bar: 500 μm in D-F and J-L; scale bar: 50 μm in G-I and M-O. Representative microglia in different stages (stage1-4) of CD11b immunostaining are shown in yellow circles (stage1: P1; stage2: P2; stage3: P3; stage4: P4), and a representative of stage 4 MHC II-ir microglia is shown in panel Q. Scale bar:10 μm in P1-P4 and Q. Microglia cell numbers and morphology were stereologically analyzed in each group. (A) Data represents average increase of CD11b-ir microglia cell number in ipsilateral SN as compared to contralateral SN (n = 5) ± S.E.M. #:P < 0.001. (B) Stereological quantification of each stage of CD11b-ir microglia is depicted as the average percentage distribution per group. # p < 0.001 compared to every other group. (C) Stereological quantification of stage 4 MHC II-ir cells throughout the SN from different experimental groups is shown in bar graph; n = 5, value = mean ± S.E.M. #: P < 0.001 significant difference compared to every other group.CC BY · PubMed Central

Figure 4 BAb regulates pro-inflammatory factor production in SN. Concentrations of TNF-α and IL-6 in SN were assayed using ELISA at 21 days post-6-OHDA injection. Values are shown as mean ± S.E.M. The concentrations of cytokines in the 6-OHDA/BAb co-treated group were significantly higher than those in the other groups. There was no significant difference between the 6-OHDA/CAb- and the 6-OHDA/Veh-treated groups. Data are representative of three individual experiments. # P < 0.001, significant difference compared to every other group.CC BY · PubMed Central

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PROTEIN MEASUREMENT WITH THE FOLIN PHENOL REAGENT
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Unbiased stereological estimation of the total number of neurons in the subdivisions of the rat hippocampus using the optical fractionator
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Background
Microglial Activation in Metal Neurotoxicity: Impact in Neurodegenerative Diseases
Martínez-Hernández, M. I., Acosta‐Saavedra, L. C., Hernández‐Kelly, L. C., Loaeza‐Loaeza, J., & Ortega, A. (2023) · BioMed Research International · doi:10.1155/2023/7389508 · Cited by 63
“The interaction CD200/CD200R maintains microglia in a quiescent state; therefore, CD200/CD200R signaling disruption can cause microglial over reactivity [47].”
Background
Current perspectives on microglia-neuron communication in the central nervous system: Direct and indirect modes of interaction
Hu, Y., & Tao, W. (2024) · Journal of Advanced Research · doi:10.1016/j.jare.2024.01.006 · Cited by 64
CD200R1 and CD200 expression are regulated by PPAR‐γ in activated glial cells
Dentesano, G., Serratosa, J., Tusell, J. M., Ramon-Cañellas, P., Valente, T., Saura, J., & Solà, C. (2014) · Glia · doi:10.1002/glia.22656 · Cited by 62
“, 2012) and the inhibition of CD200R1 function potentiates it (Lyons et al., 2007; Wang et al., 2011; Zhang et al., 2011), suggesting that CD200-CD200R1 interaction is involved in the suppression of the pro-inflammatory phenotype in microglia.”
Background
The prenatal challenge with lipopolysaccharide and polyinosinic:polycytidylic acid disrupts CX3CL1-CX3CR1 and CD200-CD200R signalling in the brains of male rat offspring: a link to schizophrenia-like behaviours
Chamera, K., Kotarska, K., Szuster-Głuszczak, M., Trojan, E., Skórkowska, A., Pomierny, B., Krzyżanowska, W., Bryniarska, N., & Basta‐Kaim, A. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01923-0 · Cited by 57
“In prenatally LPStreated offspring, we also demonstrated dysfunction of the CD200-CD200R interaction and IL-1β upregulation, which, in turn, both potentiate dopaminergic-induced neurodegeneration [100] and contribute to cognitive impairment [101].”
Background
Regulation of N6-methyladenosine (m6A) RNA methylation in microglia-mediated inflammation and ischemic stroke
Zhang, F., Ran, Y., Tahir, M., Li, Z., Wang, J., & Chen, X. (2022) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2022.955222 · Cited by 57
“Within hours of initiating ischemia, microglia respond to the changing environment (Zhang et al., 2011).”
Background
CD200R1 agonist attenuates glial activation, inflammatory reactions, and hypersensitivity immediately after its intrathecal application in a rat neuropathic pain model
Hernangómez, M., Klusáková, I., Joukal, M., Hradilová‐Svíženská, I., Guaza, C., & Dubový, P. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0508-8 · Cited by 54
“In contrast to neurodegenerative diseases [19, 25, 64], sciatic nerve injury probably activated endogenous regulatory mechanisms including upregulation of CD200/ CD200R.”
Background
Understanding the Neurobiology of Cd200 and the Cd200 Receptor: A Therapeutic Target For Controlling Inflammation In Human Brains?
Walker, D. G., & Lue, L. (2013) · Future Neurology · doi:10.2217/fnl.13.14 · Cited by 52
“Blocking of CD200R resulted in significantly more severe PD-like movement dys function and a significantly greater loss of tyro sine hydroxylase-positive dopaminergic neurons in SN [51].”
Background
Role of microglia in methamphetamine-induced neurotoxicity.
Xu, E., Liu, J., Liu, H., Wang, X., & Xiong, H. (2017) · Europe PMC (PubMed Central) · Cited by 52
Self-citation
Disease progression-dependent expression of CD200R1 and CX3CR1 in mouse models of Parkinson's disease
Wang, L., Liu, Y., Yan, S., Du, T., Fu, X., Gong, X., Zhou, X., Zhang, T., & Wang, X. (2020) · Aging and disease · doi:10.14336/ad.2019.0615 · Cited by 49
“found that a CD200R1blocking antibody injected into the striatum exacerbates microglial activation and dopaminergic neurodegeneration in a rat model of 6-OHDA-induced PD [11].”
BackgroundSelf-citation
Dok2 mediates the CD200Fc attenuation of Aβ-induced changes in glia
Lyons, A., Downer, E. J., Costello, D. A., Murphy, N., & Lynch, M. A. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-107 · Cited by 50
“-20 0 20 40 60 80 140 200 Control A [1-40] CD200+A [1-40]”
BackgroundInfluential
Dysregulated CD200-CD200R signaling in early diabetes modulates microglia-mediated retinopathy
Pfeifer, C. W., Walsh, J. T., Santeford, A. C., Lin, J. B., Beatty, W. L., Terao, R., Liu, Y. A., Hase, K., Ruzycki, P. A., & Apte, R. S. (2023) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2308214120 · Cited by 48
“Interestingly, decreased expression of CD200 in CNS neurons, or blocking of CD200R binding, correlates with increases in myeloid cell CD200R expression and neurodegeneration (57, 79, 80).”
Background
Interplay between human microglia and neural stem/progenitor cells in an allogeneic co‐culture model
Liu, J., Hjorth, E., Zhu, M., Calzarossa, C., Samuelsson, E., Schultzberg, M., & Åkesson, E. (2013) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.12123 · Cited by 48
Sweepers in the CNS: Microglial Migration and Phagocytosis in the Alzheimer Disease Pathogenesis
Noda, M., & Suzumura, A. (2012) · International Journal of Alzheimer s Disease · doi:10.1155/2012/891087 · Cited by 52
“Blocking of CD200R increases neurodegeneration in mouse model of Parkinson’s disease [88].”
Background
Microglia under psychosocial stressors along the aging trajectory: Consequences on neuronal circuits, behavior, and brain diseases
Tian, L., Hui, C. W., Bisht, K., Tan, Y., Sharma, K. P., Chen, S., Zhang, X., & Tremblay, M. (2017) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2017.01.007 · Cited by 52
Self-citation
CD200-CD200R imbalance correlates with microglia and pro-inflammatory activation in rat spinal cords exposed to amniotic fluid in retinoic acid-induced spina bifida
Oria, M., Figueira, R. L., Scorletti, F., Sbragia, L., Owens, K. J., Li, Z., Pathak, B., Corona, M. U., Marotta, M., Encinas, J. L., et al. (2018) · Scientific Reports · doi:10.1038/s41598-018-28829-5 · Cited by 46
Immune-mediated processes in neurodegeneration: where do we stand?
Fakhoury, M. (2016) · Journal of Neurology · doi:10.1007/s00415-016-8052-0 · Cited by 43
“described in several inflammatory neurodegenerative diseases [54, 62], and dysfunction of this interaction was shown to exacerbate the course of neurodegeneration [63].”
Background
Analysis of the Impact of CD200 on Phagocytosis
Lyons, A., Minogue, A. M., Jones, R. S., Fitzpatrick, O. M., Noonan, J., Campbell, V. A., & Lynch, M. A. (2016) · Molecular Neurobiology · doi:10.1007/s12035-016-0223-6 · Cited by 45
“This finding has led to the proposal that the decreased interaction between CD200R and CD200 in AD is a factor in driving the observed neuroinflammation [8], and similar changes have been described in animal models of Parkinson’s disease [9] and multiple sclerosis [4].”
Result
Age-related differences in neuroinflammatory responses associated with a distinct profile of regulatory markers on neonatal microglia
Christensen, L. B., Woods, T. A., Carmody, A., Caughey, B. W., & Peterson, K. E. (2014) · Journal of Neuroinflammation · doi:10.1186/1742-2094-11-70 · Cited by 42
“Deficiency in CD200R has been linked to increased inflammation in models of experimental autoimmune encephalitis (EAE) and Parkinson’s disease [43,44], while CD172a negatively regulates CD11b-mediated adhesion, migration and phagocytosis [35,45].”
Background
Neuronal influence behind the central nervous system regulation of the immune cells
Chavarría, A., & Cárdenas, G. (2013) · Frontiers in Integrative Neuroscience · doi:10.3389/fnint.2013.00064 · Cited by 40
“Also, defects in CD200-CD200R pathway play a critical role in neurodegenerative disease development such as multiple sclerosis (MS), Parkinson’s and Alzheimer’s diseases (Koning et al., 2007; Walker et al., 2009; Zhang et al., 2011).”
Background
Beneficial impact of intracerebroventricular fractalkine administration on behavioral and biochemical changes induced by prenatal stress in adult rats: Possible role of NLRP3 inflammasome pathway
Ślusarczyk, J., Trojan, E., Wydra, K., Głombik, K., Chamera, K., Kucharczyk, M. W., Budziszewska, B., Kubera, M., Lasoń, W., Filip, M., et al. (2016) · Biochemical Pharmacology · doi:10.1016/j.bcp.2016.05.008 · Cited by 41
Increased Expression of CD200 on Circulating CD11b+ Monocytes in Patients with Neovascular Age-related Macular Degeneration
Singh, A., Falk, M. K., Hviid, T. V. F., & Sørensen, T. L. (2013) · Ophthalmology · doi:10.1016/j.ophtha.2012.11.002 · Cited by 40
T cells, α-synuclein and Parkinson disease
Garretti, F., Monahan, C., Sette, A., Agalliu, D., & Sulzer, D. (2022) · Handbook of clinical neurology · doi:10.1016/b978-0-12-819410-2.00023-0 · Cited by 39
Reduced Dendritic Cells Expressing CD200R1 in Children with Inflammatory Bowel Disease: Correlation with Th17 and Regulatory T Cells
Elshal, M. F., Aldahlawi, A., Saadah, O. I., & McCoy, J. P. (2015) · International Journal of Molecular Sciences · doi:10.3390/ijms161226143 · Cited by 36
“Consistent with this premise, dysfunction in CD200/CD200R1 signaling has been reported in numerous autoimmune diseases, including Parkinson’s disease [23], Alzheimer’s disease [24], rheumatoid arthritis [25], uveoretinitis [26], lupus [27], autoimmune and inflammatory skin disorders [28] and spontaneous fetal loss [29…”
Background
The Role of Microglia and Astrocytes in the Pathomechanism of Neuroinflammation in Parkinson’s Disease—Focus on Alpha-Synuclein
Harackiewicz, O., & Grembecka, B. (2024) · Journal of Integrative Neuroscience · doi:10.31083/j.jin2311203 · Cited by 39
“[127] on a rat model of PD induced by 6-hydroxydopamine (6-OHDA) administration.”
Innate Immune Signaling and Role of Glial Cells in Herpes Simplex Virus- and Rabies Virus-Induced Encephalitis
Feige, L., Zaeck, L. M., Sehl‐Ewert, J., Finke, S., & Bourhy, H. (2021) · Viruses · doi:10.3390/v13122364 · Cited by 37
Changes in CD200 and intercellular adhesion molecule-1 (ICAM-1) levels in brains of Lewy body disorder cases are associated with amounts of Alzheimer's pathology not α-synuclein pathology
Walker, D. G., Lue, L.-F., Tang, T. M., Adler, C. H., Caviness, J. N., Sabbagh, M. N., Serrano, G. E., Sue, L. I., & Beach, T. G. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.03.007 · Cited by 33
“, 2011, 2014), while blocking CD200 and CD200R interactions can result in significantly increased tissue inflammation (Meuth et al., 2008; Wang et al., 2011; Zhang et al., 2011).”
Background
CD200 in dentate gyrus improves depressive-like behaviors of mice through enhancing hippocampal neurogenesis via alleviation of microglia hyperactivation
Chen, X., Cui, Q., Hu, X.-H., Ye, J., Liu, Z.-C., Mei, Y.-X., Wang, F., Hu, Z., & Chen, J. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02836-4 · Cited by 33
The CD200R1 microglial inhibitory receptor as a therapeutic target in the MPTP model of Parkinson’s disease
Rabaneda‐Lombarte, N., Serratosa, J., Bové, J., Vila, M., Saura, J., & Solà, C. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02132-z · Cited by 33
“By contrast, when CD200R1 is blocked, an exacerbation of microglial activation and dopaminergic neurodegeneration in 6-OHDA-treated rats has been described [87], as well as increased dopaminergic neuron death in the LPS model of PD [83] and a worse outcome in experimental autoimmune encephalomyelitis [55].”
Background
Maternal Immune Activation Sensitizes Male Offspring Rats to Lipopolysaccharide-Induced Microglial Deficits Involving the Dysfunction of CD200–CD200R and CX3CL1–CX3CR1 Systems
Chamera, K., Szuster-Głuszczak, M., Trojan, E., & Basta-Kaim, A. (2020) · Cells · doi:10.3390/cells9071676 · Cited by 31
“Disturbances in the CD200–CD200R communication stimulate microglia and alter their phenotype to the activated state, which in turn may result in an exacerbated inflammatory response and neurodegeneration [33].”
Background
CD200 dysfunction in neuron contributes to synaptic deficits and cognitive impairment
Feng, D., Huang, A., Yan, W., & Chen, D. (2019) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2019.06.134 · Cited by 34
Neurogenesis promoted by the CD200/CD200R signaling pathway following treadmill exercise enhances post-stroke functional recovery in rats
Sun, H., Li, A., Hou, T., Tao, X., Chen, M., Wu, C., Chen, S., Zhu, L., & Liao, H. (2019) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2019.09.005 · Cited by 32
Self-citation
Potential targets of microglia in the treatment of neurodegenerative diseases: Mechanism and therapeutic implications
Zhao, W., Liu, Z., Wu, J., Liu, A., & Yan, J. (2025) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-24-01343 · Cited by 37
“One blocking antibody against CD200R resulted in increases in microglial activation and the expression of pro-inflammatory factors in a 6-hydroxydopamine-induced PD mouse model (Zhang et al., 2011).”
Newly Formed Endothelial Cells Regulate Myeloid Cell Activity Following Spinal Cord Injury via Expression of CD200 Ligand
Cohen, M., Ben-Yehuda, H., Porat, Z., Rapôso, C., Gordon, S., & Schwartz, M. (2016) · Journal of Neuroscience · doi:10.1523/jneurosci.2199-16.2016 · Cited by 31
“…signaling leads to tissue damage derived from microglia-induced inflammation, and is associated with increased susceptibility to autoimmune and neurodegenerative diseases (Hoek et al., 2000; Broderick et al., 2002; Frank et al., 2006; Koning et al., 2007; Walker et al., 2009; Zhang et al., 2011).”
BackgroundInfluential
Evaluation of the immediate effects of a single transcranial direct current stimulation session on astrocyte activation, inflammatory response, and pain threshold in naïve rats
Callai, E. M. M., Zin, L. E. F., Catarina, L. S., Ponzoni, D., Gonçalves, C. A., Vizuete, A. F. K., Cougo, M. C. R., Boff, J., Puricelli, E., Fernandes, E. K., et al. (2022) · Behavioural Brain Research · doi:10.1016/j.bbr.2022.113880 · Cited by 30
Sneaky Entry of IFNγ Through Arsenic-Induced Leaky Blood–Brain Barrier Reduces CD200 Expression by Microglial pro-Inflammatory Cytokine
Singh, V., Kushwaha, S., Gera, R., Ansari, J. A., Mishra, J., Dewangan, J., Patnaik, S., & Ghosh, D. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1155-0 · Cited by 30
Tackling the physiological barriers for successful mesenchymal stem cell transplantation into the central nervous system
Vocht, N. D., Praet, J., Reekmans, K., Blon, D. L., Hoornaert, C., Daans, J., Berneman, Z. N., der Linden, A. V., & Ponsaerts, P. (2013) · Stem Cell Research & Therapy · doi:10.1186/scrt312 · Cited by 29
“Alternatively, increased numbers of activated microglia as well as an upregulation of the production of pro-inflammatory cytokines was observed upon blocking of CD200-CD200R signalling with a CD200R blocking antibody [88].”
Background
CD200+ and CD200− macrophages accumulated in ischemic lesions of rat brain: The two populations cannot be classified as either M1 or M2 macrophages
Matsumoto, S., Tanaka, J., Yano, H., Takahashi, H., Sugimoto, K., Ohue, S., Inoue, A., Aono, H., Kusakawa, A., Watanabe, H., et al. (2015) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2015.03.013 · Cited by 28
Spatio-temporal dynamics of microglia phenotype in human and murine cSVD: impact of acute and chronic hypertensive states
Morton, L., Arndt, P., Garza, A. P., Henneicke, S., Mattern, H., Gonzalez, M., Dityatev, A. E., Yilmazer‐Hanke, D., Schreiber, S., & Dunay, I. R. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01672-0 · Cited by 28
“…coupled with its significant reduction in hypertensive brains, implies inefficient regulation of pro-inflammatory conditions that ultimately lead to deficient feedback loops in the induction of inflammatory mechanisms that can contribute to vascular inflammation and neurodegeneration [10, 73–75].”
Background
“Sentinel or accomplice”: gut microbiota and microglia crosstalk in disorders of gut–brain interaction
Zheng, H., Zhang, C., Zhang, J., & Duan, L. (2023) · Protein & Cell · doi:10.1093/procel/pwad020 · Cited by 29
CD200-CD200R signaling and diseases: a potential therapeutic target?
Ngwa, C., & Liu, F. (2019) · PubMed Central · Cited by 27
Neural inflammation and the microglial response in diabetic retinopathy
Abcouwer, S. F. (2011) · Journal of ocular biology, diseases, and informatics · doi:10.1007/s12177-012-9086-x · Cited by 27
“A lack of these ligands on neurons or a lack of the corresponding receptors on microglia greatly impacts microglial function and activation [26, 27].”
Background
CD4 T cells react to local increase of α-synuclein in a pathology-associated variant-dependent manner and modify brain microglia in absence of brain pathology
Olesen, M. N., Christiansen, J. R., Petersen, S. V., Jensen, P. H., Pasławski, W., Romero‐Ramos, M., & Sánchez-Guajardo, V. (2018) · Heliyon · doi:10.1016/j.heliyon.2018.e00513 · Cited by 28
“In animal models of PD, binding to CD200 on neurons prevents microglia activation and dopaminergic neurodegeneration (Zhang et al., 2011).”
Background
Role of Polyinosinic:Polycytidylic Acid-Induced Maternal Immune Activation and Subsequent Immune Challenge in the Behaviour and Microglial Cell Trajectory in Adult Offspring: A Study of the Neurodevelopmental Model of Schizophrenia
Chamera, K., Trojan, E., Kotarska, K., Szuster-Głuszczak, M., Bryniarska, N., Tylek, K., & Basta‐Kaim, A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22041558 · Cited by 25
“For instance, IL-1β up-regulation potentiates neurodegeneration induced by dopaminergic signalling [49], whereas excessive secretion of TNF-α contributes to cognitive impairment [128].”
Background
Anti-inflammation conferred by stimulation of CD200R1 via Dok1 pathway in rat microglia after germinal matrix hemorrhage
Feng, Z., Ye, L., Klebe, D., Ding, Y., Guo, Z.-N., Flores, J. J., Yin, C., Tang, J., & Zhang, J. H. (2019) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x17725211 · Cited by 23
“CD200–CD200R1 signaling has been shown to suppress microglia activation in Alzheimer’s disease and Parkinson’s disease.(19,23) Lack of CD200 also results in rapid onset of experimental autoimmune encephalomyelitis.”
Background
Maresin1 Decreased Microglial Chemotaxis and Ameliorated Inflammation Induced by Amyloid-β 42 in Neuron-Microglia Co-Culture Models
Yin, P., Wang, S., Wei, Y., Wang, X., Zhang, J., Yin, X., Feng, J., & Zhu, M. (2020) · Journal of Alzheimer’s Disease · doi:10.3233/jad-190682 · Cited by 24
“Blocking CD200R result in neurodegeneration in Parkinson’s disease mouse models [34].”
Self-citation
Immunomodulator CD200 Promotes Neurotrophic Activity by Interacting with and Activating the Fibroblast Growth Factor Receptor
Pankratova, S., Björnsdóttir, H., Christensen, C., Zhang, L., Li, S., Dmytriyeva, O., Bock, E., & Berezin, V. (2014) · Molecular Neurobiology · doi:10.1007/s12035-014-9037-6 · Cited by 23
“Additionally, blocking CD200R with antibody injected into the striatum has been shown to aggravate microglial activation and the degeneration of dopaminergic neurons in a rat model of Parkinson’s disease [16].”
Patients with a fast progression profile in geographic atrophy have increased CD200 expression on circulating monocytes
Nielsen, M. K., Subhi, Y., Molbech, C. R., Falk, M. K., Singh, A., Nissen, M. H., & Sørensen, T. L. (2018) · Clinical and Experimental Ophthalmology · doi:10.1111/ceo.13362 · Cited by 22
CD200-CD200R Interaction: An Important Regulator After Stroke
Zhao, X., Li, J., & Sun, H. (2019) · Frontiers in Neuroscience · doi:10.3389/fnins.2019.00840 · Cited by 23
Immunology primer for neurosurgeons and neurologists part 2: Innate brain immunity
Blaylock, R. L. (2013) · Surgical Neurology International · doi:10.4103/2152-7806.118349 · Cited by 23
“[99] Mice lacking CD200 receptors demonstrate an exaggerated proinflammatory release following stimulation with LPS or other CNS or systemic immune activators and deficiencies in CD200 are linked to Alzheimer’s dementia and Parkinson’s syndrome.[165,170,182] Aged mice were found to have less CD200R on the surface of t…”
Result
Neuronal CD200 Signaling Is Protective in the Acute Phase of Ischemic Stroke
Mamun, A. A., Ngwa, C., Qi, S., Honarpisheh, P., Datar, S. S., Sharmeen, R., Xu, Y., McCullough, L. D., & Liu, F. (2021) · Stroke · doi:10.1161/strokeaha.120.032374 · Cited by 21
CD200 attenuates methamphetamine-induced microglial activation and dopamine depletion
Yue, X., Qiao, D., Wang, A., Tan, X.-H., Li, Y., Liu, C., & Wang, H. (2012) · Journal of Huazhong University of Science and Technology [Medical Sciences] · doi:10.1007/s11596-012-0072-0 · Cited by 21
Aerobic Physical Exercise as a Non-medical Intervention for Brain Dysfunction: State of the Art and Beyond
Jia, Y., Yao, Y., Zhuo, L., Chen, X., Yan, C., Ji, Y., Tao, J., & Zhu, Y. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.862078 · Cited by 21
“When the body endures a pathological injury, the microglia can be activated by pro-inflammatory factors (97) to mediate downstream signaling pathways that trigger inflammatory reactions and aggravate inflammation (98), or inhibited by anti-inflammatory factors that restore the body to homeostasis (99–101).”
Background
Agonistic CD200R1 DNA Aptamers Are Potent Immunosuppressants That Prolong Allogeneic Skin Graft Survival
Prodeus, A., Cydzik, M., Abdul‐Wahid, A., Huang, E., Khatri, I. A., Gorczynski, R. M., & Gariépy, J. (2014) · Molecular Therapy — Nucleic Acids · doi:10.1038/mtna.2014.41 · Cited by 20
Behavioral and Neurochemical Deficits in Aging Rats with Increased Neonatal Iron Intake: Silibinin’s Neuroprotection by Maintaining Redox Balance
Chen, H.-Q., Wang, X., Wang, M., Liu, Y., Yan, Z., Zhang, Y., & Liu, Z. (2015) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2015.00206 · Cited by 19
“…to environmental toxins, immune/inflammatory factors, genetic predisposition, and innate characteristics of the nigrostriatal dopaminergic system in the brain (Olanow and Tatton, 1999; Kidd, 2000; Gao et al., 2003; Wang et al., 2005a,b, 2007a,b, 2011; Zhang et al., 2011; Connolly and Lang, 2014).”
BackgroundSelf-citation
The role of N-glycosylation of CD200-CD200R1 interaction in classical microglial activation
Liu, C., Shen, Y., Tang, Y., & Gu, Y. (2018) · Journal of Inflammation · doi:10.1186/s12950-018-0205-8 · Cited by 19

Authors: Zhang, S., Wang, X.-J., Tian, L.-P., Pan, J., Lu, G.-Q., Zhang, Y.-J., Ding, J.-Q., & Chen, S.-D.
Affiliations: Shanghai Jiao Tong University (CN)
ORCID: Pan, Jing
Venue: Journal of Neuroinflammation
Publisher: Springer Science and Business Media LLC
Published: 2011-11-06
Volume: 8
Issue: 1
Pages: 154-154
ISSN: 1742-2094 (ISSN-L)
DOI: 10.1186/1742-2094-8-154
PMC: PMC3226566
OpenAlex: W2033271712
Cited by: 154
References: 85
Citations by year: 2026: 3 · 2025: 7 · 2024: 13 · 2023: 12 · 2022: 8 · 2021: 11 · 2020: 10 · 2019: 13 · 2018: 10 · 2017: 8 · 2016: 10 · 2015: 8 · 2014: 16 · 2013: 16 · 2012: 8
FWCI: 7.24
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
Locations: Journal of Neuroinflammation (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
Keywords: Parkinson's disease, microglial activation, dopaminergic neuron loss, 6-hydroxydopamine lesion, substantia nigra, neuroinflammation, inflammatory cytokines, monoamine levels, motor impairment, striatum, neuroprotection, rat model
MeSH terms: Animals, Behavior, Animal, Disease Models, Animal, Dopamine, Humans, Male, Nerve Degeneration, Receptors, Immunologic, Antigens, CD, Oxidopamine, Rats, Sprague-Dawley, Microglia, Antibodies, Blocking, Parkinsonian Disorders, Rats, Dopaminergic Neurons

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CD200-CD200R dysfunction exacerbates microglial activation and dopaminergic neurodegeneration in a rat model of Parkinson's disease

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