The DOI matches its Crossref record; 67 of the 68 references it cites were found in a registry or an index.
Loss of ‘homeostatic’ microglia and patterns of their activation in active multiple sclerosis
Open accessAbstract
Microglia and macrophages accumulate at the sites of active demyelination and neurodegeneration in the multiple sclerosis brain and are thought to play a central role in the disease process. We used recently described markers to characterize the origin and functional states of microglia/macrophages in acute, relapsing and progressive multiple sclerosis. We found microglia activation in normal white matter of controls and that the degree of activation increased with age. This microglia activation was more pronounced in the normal-appearing white matter of patients in comparison to controls and increased with disease duration. In contrast to controls, the normal-appearing white matter of patients with multiple sclerosis showed a significant reduction of P2RY12, a marker expressed in homeostatic microglia in rodents, which was completely lost in active and slowly expanding lesions. Early stages of demyelination and neurodegeneration in active lesions contained microglia with a pro-inflammatory phenotype, which expressed molecules involved in phagocytosis, oxidative injury, antigen presentation and T cell co-stimulation. In later stages, the microglia and macrophages in active lesions changed to a phenotype that was intermediate between pro- and anti-inflammatory activation. In inactive lesions, the density of microglia/macrophages was significantly reduced and microglia in part converted to a P2RY12+ phenotype. Analysis of TMEM119, which is expressed on microglia but not on recruited macrophages, demonstrated that on average 45% of the macrophage-like cells in active lesions were derived from the resident microglia pool. Our study demonstrates the loss of the homeostatic microglial signature in active multiple sclerosis with restoration associated with disease inactivity.
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“Similarly, microglia in active MS lesions lack Tmem119 (Satoh et al., 2016; Zrzavy et al., 2017).”
From Activated microglia drive demyelination via CSF1R signaling (2021) · cites this paper as Zrzavy et al., 2017
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“Microglial cells within active white matter lesions are characterized by the absence of homeostatic markers such as P2RY12 and an upregulation of CXCR4, indicating a shift to a disease-associated state (31, 41, 42).”
From The role of microglia in multiple sclerosis: implications for treatment with Bruton’s tyrosine kinase inhibitors (2025) · cites this paper as [41]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“TMEM119 is one of the main homeostatic microglia markers that is not expressed on monocyte-derived macrophages and has been shown to be downregulated in active MS lesions and other inflammatory conditions of the brain47–49.”
From CHIT1 at diagnosis predicts faster disability progression and reflects early microglial activation in multiple sclerosis (2024) · cites this paper as [47]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Interestingly, the phenotype of microglia we observed in HDLS is similar to that found in an SOD1 ALS mouse model and in multiple sclerosis patients, in which the molecules associated with the homeostatic microglial phenotype (e.g., P2RY12, CSF-1R) are down-regulated and inflammatory markers are up-regulated [24, 57].”
From Loss of homeostatic microglial phenotype in CSF1R-related Leukoencephalopathy (2020) · cites this paper as [57]
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In the citing paper
“As reported previously (Zrzavy et al., 2017), P2RY12+ cells expressing TSPO were substantially reduced in active lesions (Fig. 2E–H).”
From A quantitative neuropathological assessment of translocator protein expression in multiple sclerosis (2019) · cites this paper as Zrzavy et al., 2017
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In the citing paper
“Thus, in contrast to the pattern of TSPO expression in rodent models, it may not be so specifically associated with pro-inflammatory microglia in multiple sclerosis (Zrzavy et al., 2017).”
From A quantitative neuropathological assessment of translocator protein expression in multiple sclerosis (2019) · cites this paper as Zrzavy et al., 2017
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In the citing paper
“Indeed, most phagocytes initially present in active MS lesions are microglia, and with lesion maturation, more macrophages will infiltrate from the blood47.”
From CHIT1 at diagnosis predicts faster disability progression and reflects early microglial activation in multiple sclerosis (2024) · cites this paper as [47]
The cited source says what the claim attributes to it.
In the citing paper
“TMEM119 is one of the main homeostatic microglia markers that is not expressed on monocyte-derived macrophages and has been shown to be downregulated in active MS lesions and other inflammatory conditions of the brain47–49.”
From CHIT1 at diagnosis predicts faster disability progression and reflects early microglial activation in multiple sclerosis (2024) · cites this paper as [47]
In the citing paper
“The loss of homeostatic microglial proteins is visible in immunofluorescence double-staining of IBA1 and TMEM119 in terminally sick mice and mock-infected healthy control brains, and shows the reciprocal regulation of both proteins in prion disease (Figure 5A) [55,73,88,89,90,91].”
From Loss of Homeostatic Microglia Signature in Prion Diseases (2022) · cites this paper as [90]
In the citing paper
“since its expression is maintained by resident human microglia in MS lesions and is not expressed by infiltrating immune cells (Zrzavy et al., 2017).”
From Complex cell-state changes revealed by single cell RNA sequencing of 76,149 microglia throughout the mouse lifespan and in the injured brain (2018) · cites this paper as Zrzavy et al., 2017
In the citing paper
“Several of these microglial genes were also observed in human microglia, including P2RY12 and TMEM119 (REFs25,33–36).”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [36]
In the citing paper
“In human MS, microglia lose the expression of the P2RY12 homeostatic microglial marker and adopt a pro-inflammatory phenotype that includes the expression of phagocytic-related markers (macrosialin (also known as CD68)), antigen presentation markers (MHC class I and II molecules and T lymphocyte activation antigen CD86) and proteins involved in the production of reactive oxygen species (cytochrome”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [36]
In the citing paper
“and appears to exhibit stable expression even in response to a variety of inflammatory conditions (9, 96).”
From The Transcriptional Landscape of Microglial Genes in Aging and Neurodegenerative Disease (2019) · cites this paper as [96]
In the citing paper
“Studies have shown that microglial migration, proliferation, and activation are involved in the onset and progression of disease in acute, relapsing, and progressive forms of MS in humans (Zrzavy et al. 2017).”
From MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis (2025) · cites this paper as Zrzavy et al. 2017
In the citing paper
“However, activation conditions are variable and microglial phenotype changes with disease progression (Zrzavy et al. 2017).”
From MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis (2025) · cites this paper as Zrzavy et al. 2017
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Fate Mapping Analysis Reveals That Adult Microglia Derive from Primitive Macrophages
Ginhoux, F., Greter, M., Leboeuf, M., Nandi, S., See, P., Gokhan, S., Mehler, M. F., Conway, S. J., Ng, L. G., Stanley, E. R., et al. (2010) · Science · doi:10.1126/science.1194637 · Cited by 5,175
The M1 and M2 paradigm of macrophage activation: Time for reassessment
Martinez, F. O., & Gordon, S. (2014) · F1000Prime Reports · doi:10.12703/p6-13 · Cited by 4,689
Kettenmann, H., Hanisch, U.-K., Noda, M., & Verkhratsky, A. (2011) · Physiological Reviews · doi:10.1152/physrev.00011.2010 · Cited by 3,547
Identification of a unique TGF-β–dependent molecular and functional signature in microglia
Butovsky, O., Jedrychowski, M. P., Moore, C. S., Cialic, R., Lanser, A. J., Gabriely, G., Koeglsperger, T., Dake, B., Wu, P. M., Doykan, C. E., et al. (2014) · Nature Neuroscience · doi:10.1038/nn.3599 · Cited by 2,543
Self-citationthe Immunological Genome Consortium, Gautier, E. L., Shay, T., Miller, J., Greter, M., Jakubzick, C., Ivanov, S., Helft, J., Chow, A., Elpek, K. G., et al. (2012) · Nature Immunology · doi:10.1038/ni.2419 · Cited by 1,972 · cited 1×
“…to be microglia-specific in comparison to other brain cells (Chiu et al., 2013; Hickman et al., 2013) or in comparison to peripheral myeloid cells (Gautier et al., 2012; Hickman et al., 2013; Butovsky et al., 2014) or to be involved in pro- or anti-inflammatory microglia/macrophage function such…”
BackgroundNew tools for studying microglia in the mouse and human CNS
Bennett, M. L., Bennett, F. C., Liddelow, S. A., Ajami, B., Zamanian, J. L., Fernhoff, N. B., Mulinyawe, S. B., Bohlen, C. J., Adil, A., Tucker, A., et al. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1525528113 · Cited by 1,804
M2 microglia and macrophages drive oligodendrocyte differentiation during CNS remyelination
Miron, V. E., Boyd, A., Zhao, J.-W., Yuen, T. J., Ruckh, J. M., Shadrach, J. L., van Wijngaarden, P., Wagers, A. J., Williams, A., Franklin, R. J. M., et al. (2013) · Nature Neuroscience · doi:10.1038/nn.3469 · Cited by 1,777 · cited 1×
“It has been suggested to stimulate remyelination (Butovsky et al., 2006; Miron et al., 2013) and early stages of remyelination within multiple sclerosis lesions are mainly seen in the core of active lesions (Raine et al., 1981; Prineas et al., 1993; Raine, 2017).”
A polarizing question: do M1 and M2 microglia exist?
Ransohoff, R. M. (2016) · Nature Neuroscience · doi:10.1038/nn.4338 · Cited by 1,573
Microglia in neurodegenerative disease
Perry, V. H., Nicoll, J. A. R., & Holmes, C. (2010) · Nature Reviews Neurology · doi:10.1038/nrneurol.2010.17 · Cited by 1,543
Axonal damage in acute multiple sclerosis lesions
Ferguson, B. (1997) · Brain · doi:10.1093/brain/120.3.393 · Cited by 1,532
Flagged first, then by citations
1 of the 68 references couldn’t be matched to a known paper.
Research works printed but not linked: 2
- Babinski, 1885, Recherches sur l’anatomie pathologique de la sclerose en plaque et étude comparative des diverses variétés de la scleroses de la moelle, Arch Physiol, 5, 186
- Marburg, 1906, Die sogenannte akute multiple Sklerose, J Psychiatric Neurol, 27, 1
Cited by
Sorted by citations
Items 201–300 of 698
Insights into disseminated MS brain pathology with multimodal diffusion tensor and PET imaging
Bezukladova, S., Tuisku, J., Matilainen, M., Vuorimaa, A., Nylund, M., Smith, S., Sucksdorff, M., Mohammadian, M., Saunavaara, V., Laaksonen, S., et al. (2020) · Neurology Neuroimmunology & Neuroinflammation · doi:10.1212/nxi.0000000000000691 · Cited by 49
The role of the complement system in Multiple Sclerosis: A review
Saez-Calveras, N., & Stüve, O. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.970486 · Cited by 51
Garg, N., Padron, E., Rammohan, K. W., & Goodman, C. F. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm11206139 · Cited by 54
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Cubas-Núñez, L., Gil‐Perotín, S., Castillo-Villalba, J., López, V. P., Tarazona, L. R. S., Gasqué-Rubio, R., Carratalà‐Boscà, S., Alcalà-Vicente, C., Miralles, F. C. P., Lassmann, H., et al. (2021) · Neurology Neuroimmunology & Neuroinflammation · doi:10.1212/nxi.0000000000000972 · Cited by 58
Self-citationDynamic Responses of Microglia in Animal Models of Multiple Sclerosis
Plastini, M. J., Desu, H. L., & Brambilla, R. (2020) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2020.00269 · Cited by 48
Nylund, M., Sucksdorff, M., Matilainen, M., Polvinen, E., Tuisku, J., & Airas, L. (2022) · Brain Communications · doi:10.1093/braincomms/fcab301 · Cited by 48
Interferon β-Mediated Protective Functions of Microglia in Central Nervous System Autoimmunity
Scheu, S., Ali, S., Mann‐Nüttel, R., Richter, L., Arolt, V., Dannlowski, U., Kuhlmann, T., Klotz, L., & Alferink, J. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20010190 · Cited by 49
The aging mouse CNS is protected by an autophagy-dependent microglia population promoted by IL-34
Berglund, R., Cheng, Y., Piket, E., Adzemovic, M. Z., Zeitelhofer, M., Olsson, T. P., Guerreiro‐Cacais, A. O., & Jagodic, M. (2024) · Nature Communications · doi:10.1038/s41467-023-44556-6 · Cited by 49
Microglia-derived exosomes modulate myelin regeneration via miR-615-5p/MYRF axis
Ji, X., Guo, Y., Wang, L., Wu, W., Wang, J., He, J. M., Gao, R., Rasouli, J., Gao, M.-Y., Wang, Z., et al. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03019-5 · Cited by 50
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Mirarchi, A., Albi, E., & Arcuri, C. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252010951 · Cited by 52
Ni, R., Mu, L., & Ametamey, S. M. (2018) · Acta Pharmacologica Sinica · doi:10.1038/s41401-018-0035-5 · Cited by 50
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Lin, S.-S., Tang, Y., Illés, P., & Verkhratsky, A. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.627760 · Cited by 51
Morgan, B. P., Gommerman, J. L., & Ramaglia, V. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2020.600656 · Cited by 51
Borucki, D. M., Toutonji, A., Couch, C., Mallah, K., Rohrer, B., & Tomlinson, S. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.566892 · Cited by 46
Purinergic receptors in multiple sclerosis pathogenesis
Domercq, M., Zabala, A., & Matute, C. (2018) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2018.11.018 · Cited by 46
Chen, M., Yang, L.-L., Hu, Z.-W., Qin, C., Zhou, L., Duan, Y.-L., Bosco, D. B., Wu, L., Zhan, K., Xu, S.-B., et al. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-02020-y · Cited by 49
Ju, H., Park, K. W., Kim, I., Cave, J. W., & Cho, S. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02552-5 · Cited by 49
Bo, W., Cheng, G., Bi, Q., Lu, C. C., Sun, Q., Li, L., Chen, N., Hu, M., Lu, H., Xu, X., et al. (2024) · Immunity · doi:10.1016/j.immuni.2024.07.011 · Cited by 50
Pathology of inflammatory diseases of the nervous system: Human disease versus animal models
Lassmann, H. (2019) · Glia · doi:10.1002/glia.23726 · Cited by 44
Self-citationIlarregui, J. M., Kooij, G., Rodríguez, E., van der Pol, S. M. A., Koning, N., Kalay, H., van der Horst, J. C., van Vliet, S. J., García-Vallejo, J. J., de Vries, H. E., et al. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1522-4 · Cited by 45
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Korf, J. M., Honarpisheh, P., Mohan, E. C., Banerjee, A., Blasco-Conesa, M. P., Honarpisheh, P., Guzman, G. U., Khan, R., Ganesh, B. P., Hazen, A. L., et al. (2022) · The Journal of Immunology · doi:10.4049/jimmunol.2100884 · Cited by 44
The Possible Role of Neural Cell Apoptosis in Multiple Sclerosis
Kennedy, P. G. E., George, W., & Yu, X. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23147584 · Cited by 42
Zhou, L., Dong, M., Hu, Z., Tang, Y., Chu, Y., Chen, M., Yang, S., Chen, Z., Wu, L., Wang, W., et al. (2022) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2209990120 · Cited by 42
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Chauveau, F., Winkeler, A., Chalon, S., Boutin, H., & Becker, G. (2024) · Molecular Psychiatry · doi:10.1038/s41380-024-02656-9 · Cited by 43
de Jong, C. G. H. M., Gabius, H., & Baron, W. (2019) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-019-03327-7 · Cited by 44
Morris, G., Puri, B. K., Maes, M. H. J., OLIVE, L. S., Berk, M., & Carvalho, A. F. (2020) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2020.109858 · Cited by 42
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Geladaris, A., Häusler, D., & Weber, M. S. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22073461 · Cited by 44
Radandish, M., Khalilian, P., & Esmaeil, N. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.667705 · Cited by 41
Xue, S., Lozinski, B. M., Ghorbani, S., Ta, K., D’Mello, C., Yong, V. W., & Dong, Y. (2023) · Journal of Neuroscience · doi:10.1523/jneurosci.2312-22.2023 · Cited by 44
Chinnathambi, S., & Das, R. R. (2021) · Cell & Bioscience · doi:10.1186/s13578-023-01028-0 · Cited by 45
Olejnik, P., Roszkowska, Z., Adamus, S., & Kasarełło, K. (2024) · Pharmacological Reports · doi:10.1007/s43440-024-00642-0 · Cited by 49
Li, F., Xu, D., Hou, K., Gou, X., & Li, Y. (2020) · Journal of Thrombosis and Thrombolysis · doi:10.1007/s11239-020-02098-4 · Cited by 40
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Chu, C., Uruno, A., Katsuoka, F., & Yamamoto, M. (2024) · Antioxidants · doi:10.3390/antiox13121529 · Cited by 43
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Kleijn, K. M. A. D., & Martens, G. J. M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21124229 · Cited by 41
Wang, X., Li, B., Liu, L., Zhang, L., Ma, T., & Guo, L. (2020) · International Immunopharmacology · doi:10.1016/j.intimp.2020.107092 · Cited by 40
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Self-citationBrain incoming call from glia during neuroinflammation: Roles of extracellular vesicles
D’Egidio, F., Castelli, V., d’Angelo, M., Ammannito, F., Quintiliani, M., & Cimini, A. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106663 · Cited by 41
Imitola, J., Rasouli, J., Watanabe, F., Mahajan, K., Sharan, A. D., Ćirić, B., Zhang, G., & Rostami, A. M. (2017) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2017.12.017 · Cited by 38
Electroconvulsive stimulation attenuates chronic neuroinflammation
Goldfarb, S., Fainstein, N., & Ben‐Hur, T. (2020) · JCI Insight · doi:10.1172/jci.insight.137028 · Cited by 41
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Barkaway, A., Attwell, D., & Korte, N. (2022) · Neurophotonics · doi:10.1117/1.nph.9.3.031914 · Cited by 38
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Cong, H., Zhang, M., Chang, H., Du, L., Zhang, X., & Yin, L. (2020) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2020.173523 · Cited by 37
Rahman, M. H., Rana, H. K., Peng, S., Kibria, M. G., Islam, M. Z., Mahmud, S. M. H., & Moni, M. A. (2021) · Computers in Biology and Medicine · doi:10.1016/j.compbiomed.2021.104859 · Cited by 37
Joseph, K., Kirsch, M., Johnston, M., Münkel, C., Stieglitz, T., Haas, C. A., & Hofmann, U. (2021) · Biomaterials · doi:10.1016/j.biomaterials.2021.121230 · Cited by 36
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Meyer‐Arndt, L., Kerkering, J., Kuehl, T., Infante, A. G., Paul, F., Rosiewicz, K. S., Siffrin, V., & Alisch, M. (2023) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-023-10059-w · Cited by 45
Roodselaar, J., Zhou, Y., Leppert, D., Hauser, A. E., Urich, E., & Anthony, D. C. (2021) · Neurology Neuroimmunology & Neuroinflammation · doi:10.1212/nxi.0000000000000975 · Cited by 35
Kaniowska, D., Wenk, K., Rademacher, P., Weiss, R., Fabian, C., Schulz, I., Guthardt, M., Lange, F., Greiser, S., Schmidt, M., et al. (2022) · Stem Cell Reviews and Reports · doi:10.1007/s12015-021-10261-4 · Cited by 35
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Pilotto, E., Miante, S., Torresin, T., Puthenparampil, M., Frizziero, L., Federle, L., Gallo, P., & Midena, E. (2020) · Ophthalmology · doi:10.1016/j.ophtha.2020.03.024 · Cited by 33
Considering patient age when treating multiple sclerosis across the adult lifespan
Jakimovski, D., Eckert, S. P., Zivadinov, R., & Weinstock‐Guttman, B. (2021) · Expert Review of Neurotherapeutics · doi:10.1080/14737175.2021.1886082 · Cited by 34
Immunopathology of Tumefactive Demyelinating Lesions-From Idiopathic to Drug-Related Cases
Vakrakou, A. G., Brinia, M.-E., Svolaki, I. P., Argyrakos, T., Stefanis, L., & Kilidireas, C. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.868525 · Cited by 32
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Paolicelli, R. C., Sierra, A., Stevens, B., Tremblay, M., Aguzzi, A., Ajami, B., Amit, I., Audinat, É., Bechmann, I., Bennett, M. L., et al. (2022) · SSRN Electronic Journal · doi:10.2139/ssrn.4065080 · Cited by 33
Self-citationBeliën, J., Swinnen, S., D’hondt, R., Verdú de Juan, L., Dedoncker, N., Matthys, P., Bauer, J., Vens, C., Moylett, S., & Dubois, B. (2024) · Nature Communications · doi:10.1038/s41467-024-49312-y · Cited by 32
“Indeed, most phagocytes initially present in active MS lesions are microglia, and with lesion maturation, more macrophages willin fi ltratefromtheblood 47 .”
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Oost, W., Huitema, A. J., Kats, K., Giepmans, B. N. G., Kooistra, S. M., Eggen, B. J. L., & Baron, W. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01598-7 · Cited by 30
Arnold, D. L., Elliott, C., Martin, E. C., Hyvert, Y., Tomic, D., & Montalban, X. (2024) · Neurology · doi:10.1212/wnl.0000000000208058 · Cited by 30
Rahman, M. H., Peng, S., Hu, X., Chen, C., Uddin, S., Quinn, J. M. W., & Moni, M. A. (2019) · IEEE Access · doi:10.1109/access.2019.2960037 · Cited by 30
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Stankoff, B., Poirion, É., Tonietto, M., & Bodini, B. (2018) · Brain Pathology · doi:10.1111/bpa.12641 · Cited by 28
Gilbert, E. A. B., Livingston, J. M., Flores, E. G., Khan, M., Kandavel, H., & Morshead, C. M. (2023) · Brain Research · doi:10.1016/j.brainres.2023.148648 · Cited by 29
Berki, P., Cserép, C., Környei, Z., Pósfai, B., Szabadits, E., Domonkos, A., Kellermayer, A., Nyerges, M., Wei, X., Módy, I., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-49773-1 · Cited by 35
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Self-citationSpiteri, A. G., Terry, R. L., Wishart, C. L., Ashhurst, T. M., Campbell, I. L., Hofer, M. J., & King, N. J. C. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02214-y · Cited by 29
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Pontieri, L., Blinkenberg, M., Bramow, S., Papp, V., Rasmussen, P. V., Kant, M., Schäfer, J., Mathiesen, H. K., Jensen, M. B., Sirakov, G. P., et al. (2021) · European Journal of Neurology · doi:10.1111/ene.15142 · Cited by 29
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Smith, B. C., Tinkey, R. A., Brock, O. D., Mariam, A., Habean, M. L., Dutta, R., & Williams, J. L. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02917-4 · Cited by 27
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Qin, C., Yang, S., Chen, M., Dong, M., Zhou, L., Chu, Y., Shen, Z., Bosco, D. B., Wu, L., Tian, D., et al. (2023) · iScience · doi:10.1016/j.isci.2023.106588 · Cited by 28
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Carrier, M., Robert, M.-È., Ibáñez, F. G., Desjardins, M., & Tremblay, M. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.00903 · Cited by 28
Duan, R., Yang, C.-L., Du, T., Ai, L., Wang, A.-R., Sun, W.-J., Li, X., Li, J.-X., Yan, C., & Liu, Q. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02193-0 · Cited by 28
Mitchell, D. K., Shireman, J. M., Potchanant, E. A. S., Lara-Velazquez, M. A., & Dey, M. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.716947 · Cited by 27
Manouchehri, N., Salinas, V. H., Yeganeh, N. R., Pitt, D., Hussain, R. Z., & Stüve, O. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.854390 · Cited by 26
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Uff, C. E. G., Patel, K., Yeung, C., & Yip, P. K. (2022) · Biomolecules · doi:10.3390/biom12050603 · Cited by 26
Sanjay, S., Park, M., & Lee, H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23137300 · Cited by 28
Ahmad, S. F., Nadeem, A., Ansari, M. A., Bakheet, S. A., Shahid, M., Al‐Mazroua, H. A., Sobeai, H. M. A., Alasmari, A. F., Alanazi, M. M., Alhamed, A. S., et al. (2022) · Cellular Immunology · doi:10.1016/j.cellimm.2022.104580 · Cited by 26
Macrophage activation contributes to diabetic retinopathy
Zhang, Y., & Zhou, A. (2024) · Journal of Molecular Medicine · doi:10.1007/s00109-024-02437-5 · Cited by 27
Bell, O. H., Copland, D. A., Ward, A., Nicholson, L. B., Lange, C. A. K., Chu, C. J., & Dick, A. D. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2019.03033 · Cited by 25
Magliozzi, R., Hametner, S., Mastantuono, M., Mensi, A., Karimian, M., Griffiths, L., Watkins, L. M., Poli, A., Berti, G. M., Barusolo, E., et al. (2024) · Brain Pathology · doi:10.1111/bpa.13322 · Cited by 28
Self-citationAlemán-Villa, K. M., Armienta-Rojas, D. A., Camberos-Barraza, J., Rábago-Monzón, Á. R., Camacho-Zamora, A., Osuna‐Ramos, J. F., Magaña‐Gómez, J. A., Guadrón‐Llanos, A. M., Calderón-Zamora, L., Norzagaray-Valenzuela, C. D., et al. (2025) · NeuroImmunoModulation · doi:10.1159/000548021 · Cited by 34
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Spinal cord microglia in health and disease
Kolos, E. A., & Korzhevsky, D. (2020) · Acta Naturae · doi:10.32607/actanaturae.10934 · Cited by 25
Metadata
- Authors
- Zrzavy, T., Hametner, S., Wimmer, I., Butovsky, O., Weiner, H. L., & Lassmann, H.
- Affiliations
- Medical University of Vienna (AT)
- Brigham and Women's Hospital (US)
- Corresponding author
- Lassmann, Hans
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2017-05-24
- Volume
- 140
- Issue
- 7
- Pages
- 1900-1913
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC6057548
- OpenAlex
- W2620266814
- Cited by
- 684
- References
- 68
- Citations by year
- 2026: 62 · 2025: 65 · 2024: 78 · 2023: 87 · 2022: 92 · 2021: 116 · 2020: 71 · 2019: 60 · 2018: 43 · 2017: 10
- FWCI
- 39.52
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Brain (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- NIH (R01NS088137)
- National Multiple Sclerosis Society (5092A1)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- multiple sclerosis, microglia, macrophages, homeostatic microglia, microglial activation, P2Y12 receptor, TMEM119, normal-appearing white matter, demyelination, neurodegeneration, lesion activity, disease duration, pro-inflammatory phenotype, anti-inflammatory phenotype, phagocytosis, oxidative damage, antigen presentation, T cell costimulation, microglial origin
- MeSH terms
- Adult, Aged, Aged, 80 and over, Aging, Demyelinating Diseases, Female, Homeostasis, Humans, Macrophage Activation, Male, Membrane Proteins, Middle Aged, Multiple Sclerosis, Nerve Degeneration, Case-Control Studies, Microglia, Receptors, Purinergic P2Y12, White Matter
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