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Microglia as a source and target of cytokines
Open accessAbstract
Cytokines constitute a significant portion of the immuno‐ and neuromodulatory messengers that can be released by activated microglia. By virtue of potent effects on resident and invading cells, microglial cyto‐ and chemokines regulate innate defense mechanisms, help the initiation and influence the type of immune responses, participate in the recruitment of leukocytes to the CNS, and support attempts of tissue repair and recovery. Microglia can also receive cyto‐ and chemokine signals as part of auto‐ and paracrine communications with astrocytes, neurons, the endothelium, and leukocyte infiltrates. Strong responses and modulatory influences can be demonstrated, adding to the emerging view that microglial behavior is highly dependent on the (cytokine) environment and that reactions to a challenge may vary with the stimulation context. In principle, microglial activation aims at CNS protection. However, failed microglial engagement due to excessive or sustained activation could significantly contribute to acute and chronic neuropathologies. Dysregulation of microglial cytokine production could thereby promote harmful actions of the defense mechanisms, result in direct neurotoxicity, as well as disturb neural cell functions as they are sensitive to cytokine signaling. GLIA 40:140–155, 2002. © 2002 Wiley‐Liss, Inc.
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“Cellular and molecular mechanisms resulting from injury or infections, underlying the development of proinflammatory cytokines and chemokines in the CNS, are canonically triggered and modulated by astrocytes and microglia (Hanisch, 2002; Murphy et al., 1997)”
From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Hanisch, 2002
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CNS Macrophages and Infant Infections
Oschwald, A., Petry, P., Kierdorf, K., & Erny, D. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.02123 · Cited by 11
Microglial TLR9: Plausible Novel Target for Therapeutic Regime Against Glioblastoma Multiforme
Tiwari, R., Singh, S., Gupta, C. L., & Bajpai, P. (2020) · Cellular and molecular neurobiology · doi:10.1007/s10571-020-00925-z · Cited by 8
“…the glioblastoma-associated microglial (GAMs) and macrophages are worth of special mention as they play a fundamental role in adopting pro-inflammatory state and providing cytotoxic responses against microbial intruders (Hanisch 2002), as well as participate in tumor surveillance (Jaiswal et al.”
BackgroundZheng, N., Liu, X., Zhang, R., Ho, I. H. T., Chen, S., Xu, J., Yao, H., Wang, J., Yue, J., Wang, X., et al. (2018) · The Spine Journal · doi:10.1016/j.spinee.2018.06.354 · Cited by 9
Endogenous Neuronal Replacement in the Juvenile Brain Following Cerebral Ischemia
Rodgers, K. M., Ahrendsen, J. T., Patsos, O. P., Strnad, F. A., Yonchek, J. C., Traystman, R. J., Macklin, W. B., & Herson, P. S. (2018) · Neuroscience · doi:10.1016/j.neuroscience.2018.03.045 · Cited by 9
Nutritional and Nanotechnological Modulators of Microglia
Maysinger, D., & Zhang, I. (2016) · Frontiers in Immunology · doi:10.3389/fimmu.2016.00270 · Cited by 11
Association of ICAM-1 (K469E) and MCP-1 -2518 A>G gene polymorphism with brain abscess.
Mishra, P., Prasad, K., Singh, K., Sahu, R., & Ojha, B. (2016) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2016.01.021 · Cited by 8
Shishkov, R., Chervenkov, T., Yamashima, T., & Tonchev, A. (2013) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2013.02.016 · Cited by 8
“Currently, the best known cells of the central nervous system (CNS) performing immune functions are the glial cells (Raivich et al., 1999; Hanisch, 2002), while much less is known of the immune functions of other CNS cell types such as neurons (Tian et al.”
BackgroundD-β-hydroxybutyrate inhibits microglial activation in a cell activation model in vitro
Xu, X.-D., Zhang, Q., Tu, J., & Ren, Z. (2011) · 中国人民解放军军医大学学报:英文版 · doi:10.1016/s1000-1948(11)60042-7 · Cited by 8
Lee, S., Kim, H. S., Hong, J., Lee, E., Kim, E., Choi, T. Y., Moon, S. W., Sung-Won, J., Yoon, H., Kim, H.-S., et al. (2025) · Asian Journal of Psychiatry · doi:10.1016/j.ajp.2025.104489 · Cited by 7
Schlake, K., Teller, J., Hinken, L., Laser, H., Lichtinghagen, R., Schäfer, A., Fegbeutel, C., Weissenborn, K., Jung, C., Worthmann, H., et al. (2024) · BMC Neurology · doi:10.1186/s12883-024-03580-9 · Cited by 7
“By crossing the blood– brain-barrier they bind to microglial cells, which in turn produce mediators that impair the cholinergic -metabo- lism and alter neurotransmission causing delirious symptoms [12, 14, 15].”
BackgroundKristóf, Z., Gál, Z., Török, D., Eszlári, N., Sütöri, S., Sperlágh, B., Anderson, I. M., Deakin, J. F. W., Bagdy, G., Juhász, G., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25020865 · Cited by 7
“…the resident immune cells of the CNS, microglia, become activated, which leads to the release of neuroactive molecules such as adenosine triphosphate (ATP), glutamate, nitric oxide (NO), brain-derived neurotrophic factor (BDNF), and pro-inflammatory cytokines, including TNF-α and IL-1 β [18,19].”
BackgroundIshida, E., Furusho, H., Renn, T., Shiba, F., Chang, H., Oue, H., Terayama, R., Ago, Y., Tsuga, K., & Miyauchi, M. (2023) · Frontiers in Pediatrics · doi:10.3389/fped.2023.1203894 · Cited by 6
Janpaijit, S., Lertpatipanpong, P., Sillapachaiyaporn, C., Baek, S. J., Charoenkiatkul, S., Tencomnao, T., & Sukprasansap, M. (2022) · Heliyon · doi:10.1016/j.heliyon.2022.e11869 · Cited by 6
“…prostaglandins (PGs), and pro-inflammatory cytokines such as interleukin 1β (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α), ultimately resulting in neurodegeneration (Hanisch, 2002; Iizumi et al., 2016; Smith et al., 2012). ao), monruedee.suk@mahidol.ac.th (M. Sukprasansap).”
BackgroundNavarro‐Sempere, A., Martínez-Peinado, P., Rodrigues, A., Garcia, P., Camarinho, R., Garcı́a, M., & Segovia, Y. (2021) · Mediators of Inflammation · doi:10.1155/2021/5891095 · Cited by 8
Song, B., Lee, S.-J., & Kim, C.-H. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22136853 · Cited by 7
Clinical and biological markers of electroconvulsive therapy effectiveness: a narrative review
Zilles‐Wegner, D., von Mücke-Heim, I.-A., Yrondi, A., & Takamiya, A. (2026) · Translational Psychiatry · doi:10.1038/s41398-026-03900-2 · Cited by 7
Gudi, C. R., Wannemuehler, M. J., & Mansell, T. J. (2025) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2025.115650 · Cited by 5
Gan, H. K., Zhang, M., Duan, Y., Palahati, A., He, Q., Tan, J., Li, Y., Zhai, X., & Zhao, J. (2025) · Genes & Diseases · doi:10.1016/j.gendis.2025.101614 · Cited by 4
“48 IL-1 b and IL-1 b antibodies have been reported to reduce cerebral edema and cerebral infarction in the mouse MCAO model.”
Oue, K., Yamawaki, Y., Ouhara, K., Imado, E., Tamura, T., Doi, M., Shimizu, Y., Yoshida, M., Mizuno, N., Morioka, N., et al. (2024) · Journal of Oral Microbiology · doi:10.1080/20002297.2024.2419155 · Cited by 5
“Furthermore, they release bioactive substances such as cytokines, chemokines, and growth factors that are protective to neurons and tissues; they also produce inflammatory factors including reactive oxygen species and inflammatory cytokines that promote damage [51].”
Shigemoto‐Mogami, Y., Nakayama-Kitamura, K., & Sato, K. (2024) · Frontiers in Neuroanatomy · doi:10.3389/fnana.2024.1438190 · Cited by 5
“They also release cytokines, chemokines, and growth factors, thereby affecting brain development (Hanisch, 2002; Kettenmann, 2006; Shigemoto-Mogami and Sato, 2021).”
BackgroundZhang, C., Wei, C., Huang, X., Hou, C., Liu, C., Zhang, S., Zhao, Z., Liu, Y., Zhang, R., Zhou, L., et al. (2023) · BMC Medicine · doi:10.1186/s12916-023-02895-7 · Cited by 7
Tang, J. M., McClennan, A., Liu, L., Hadway, J. A., Ronald, J. A., Hicks, J. W., Hoffman, L., & Anazodo, U. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24087522 · Cited by 7
“, IL-1β, IL-6, TNF-α), it is possible that activated microglia may contribute to the dystrophic brain’s impairment [25,54,55].”
BackgroundRubinstein, L., Kiffer, F. C., Puukila, S., Lowe, M. G., Goo, B., Luthens, A., Schreurs, A., Torres, S. M., Steczina, S., Tahimic, C. G. T., et al. (2022) · Life · doi:10.3390/life12111838 · Cited by 7
Shalaby, H. N., Zaki, H. F., Ain-Shoka, A. A., & Mohammed, R. A. (2022) · Molecular Neurobiology · doi:10.1007/s12035-022-02977-2 · Cited by 6
Dysregulated Microglial Cell Activation and Proliferation Following Repeated Antigen Stimulation
Prasad, S., Sheng, W. S., Hu, S., Chauhan, P., & Lokensgard, J. R. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.686340 · Cited by 7
Hazra, I., Sk, O. F., Datta, A., Mondal, S., Moitra, S., Singh, M. K., Chaudhuri, S., Das, P. K., Basu, A. K., Dhar, I., et al. (2018) · Scandinavian Journal of Immunology · doi:10.1111/sji.12733 · Cited by 7
Role of Microbiota in Neurodegenerative Diseases
Sobol, C. V. (2018) · Russian Journal of Developmental Biology · doi:10.1134/s1062360418060061 · Cited by 7
“, 2010), since many proinflammatory agents are neurotoxic (Hanisch, 2002; Glass et al., 2010).”
Background3D Astrogliosis Model with bFGF and GFAP Expression Profiles Corresponding to an MCAO-injured Brain
Min, S., Shim, H., & Shin, H. (2018) · Biotechnology and Bioprocess Engineering · doi:10.1007/s12257-018-0207-7 · Cited by 6
Intrathecal Administration of CXCL1 Enhances Potassium Currents in Microglial Cells
Deftu, A., Ristoiu, V., & Suter, M. R. (2018) · Pharmacology · doi:10.1159/000486865 · Cited by 6
Microglia in the Physiology and Pathology of Brain
Nagayach, A., Patro, N., & Patro, I. K. (2015) · Proceedings of the National Academy of Sciences India Section B Biological Sciences · doi:10.1007/s40011-015-0585-y · Cited by 6
Safety of striatal infusion of siRNA in a transgenic Huntington's disease mouse model
Johnson, E. S., Chase, K., McGowan, S., Mondo, E., Pfister, E., Mick, E., Friedline, R. H., Kim, J. K., Sapp, E., DiFiglia, M., et al. (2015) · Journal of Huntington's Disease · doi:10.3233/jhd-150163 · Cited by 6
Ribavirin shows immunomodulatory effects on activated microglia
Savic, D., Stojiljković, M., Lavrnja, I., Parabucki, A., Bjelobaba, I., Nedeljkovic, N., Herdegen, T., & Peković, S. (2014) · Immunopharmacology and immunotoxicology · doi:10.3109/08923973.2014.971962 · Cited by 6
Amedei, A., Codolo, G., Ozoliņš, D., Ballerini, C., Biagioli, T., Jaunalksne, I., Žilēvica, A., D'Elios, S., de Bernard, M., & D'Elios, M. (2013) · International Journal of Immunopathology and Pharmacology · doi:10.1177/039463201302600409 · Cited by 6
Li, M., Guo, W., Zhu, Y., Fang, S., Zhang, T., & Shen, Y. (2026) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-026-01669-y · Cited by 5
“…is crucial for early pathogen control or injury response but can become maladaptive if sustained, leading to exacerbated tissue damage, chronic inflammation, and barrier dysfunction (Hanisch 2002 ; Kaur et al. 2010 ; Paolicelli et al. 2022; Rayasam et al. 2021; Rodríguez-Gómez et al. 2020 ).”
Meng, J., Luo, W., Zhang, N., Yu, M., He, Y., Chen, C., Shu, H., & Yu, L. (2025) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2025.1616804 · Cited by 5
“Meng et al. 10.3389/fnmol.2025.1616804 Frontiers in Molecular Neuroscience 06 frontiersin.org 2002).”
InfluentialNeuroinflammation as an Integral Component of Neurodegeneration in Parkinson's Disease
Sayfitdinkhuzhaev, Z. F., Zhukova, N., & Baidanova, A. N. (2024) · Personalized Psychiatry and Neurology · doi:10.52667/2712-9179-2024-4-4-26-33 · Cited by 6
Sun, X., Jin, X., Lin, Z., Liu, X., Yang, J., Li, L., Feng, H., Zhang, W., Gu, C., Hu, X., et al. (2024) · Veterinary Research · doi:10.1186/s13567-024-01416-5 · Cited by 6
Steffens, S. K., Mäkinen, H., Stenberg, D., & Wigren, H. (2024) · Glia · doi:10.1002/glia.24617 · Cited by 7
“Prolonged wakefulness triggers the release of various cytokines, some of which are sleep-promoting (Rockstrom et al., 2018) and are also sensed by microglia (Hanisch, 2002).”
Cui, B. C., Aksenova, M. V., Sikirzhytskaya, A., Odhiambo, D. A., Korunova, E., Sikirzhytski, V., Ji, H., Altomare, D., Broude, E. V., Frizzell, N., et al. (2024) · Journal of NeuroVirology · doi:10.1007/s13365-024-01216-9 · Cited by 8
“The release of pro-inflammatory cytokines serves as a widely recognized indicator of the detrimental effects associated with microglia activation (Hanisch 2002).”
Migraine and the microbiota. Can probiotics be beneficial in its prevention? - a narrative review
Kiecka, A., & Szczepanik, M. (2024) · Pharmacological Reports · doi:10.1007/s43440-024-00584-7 · Cited by 6
“Moens et al. [ 81 ] conducted an in vitro study on a human intestinal model and they tested the effect of Lactobacillus acidophi - lus NCIMB 30,175, L. plantarum NCIMB 30,173, Lactoba - cillus rhamnosus NCIMB 30,174, and E. faecium NCIMB [ 110 ].”
Tang, H., Zhang, Y., Zhao, S., & Song, C. (2023) · Journal of Affective Disorders Reports · doi:10.1016/j.jadr.2023.100580 · Cited by 6
Okusha, Y., Lang, B. J., Murshid, A., Borges, T. J., Holton, K. M., Clark, J., Doshi, S., Ikezu, T., & Calderwood, S. K. (2022) · Cell Stress and Chaperones · doi:10.1007/s12192-022-01279-9 · Cited by 7
“Inflammation in the confined spaces of the CNS is a potential hazard and is generally kept under strict control (Hanisch 2002). eHsp90α appears to induce a desirable activation state in microglia, in which cytokines and phagocytosis are activated along with protective Nrf2 activation and…”
BackgroundDhankhar, J., Agrawal, N., & Shrivastava, A. (2021) · Preprints.org · doi:10.20944/preprints202109.0277.v1 · Cited by 1
“Activation of microglia can induce neuronal damage via several mechanisms 79 such as production of free radicals, caspase activation, and excitotoxicity (Crotti et al., 2014; 80 Hanisch, 2002; Kim & de Vellis, 2005; Wang et al., 2004).”
BackgroundRamazi, S., آرانی, ف., Safaei, A., Abbasi, Z., Heidari, Z., Nafchi, H. G., Mohammadsadeghi, H., & Karimzadeh, F. (2021) · The Neuroscience Journal of Shefaye Khatam · doi:10.52547/shefa.9.2.119 · Cited by 5
Ravasz, L., Kékesi, K. A., Mittli, D., Todorov, M. I., Borhegyi, Z., Ercsey-Ravasz, M., Tyukodi, B., Wang, J., Bartfai, T., Eberwine, J. H., et al. (2020) · Cerebral Cortex · doi:10.1093/cercor/bhaa195 · Cited by 7
“…of receptors for cytokines, chemokines, and purinergic receptors, normally assumed to be expressed by microglia, astroglia, dendritic cells and to lesser extent by neurons in the PFC (Hanisch 2002; Ambrosini et al. 2005; Kataoka et al. 2009), were found evenly distributed in FS and Pyr neurons.”
BackgroundPeng, S., Jia, J., Sun, J., Xie, Q., Zhang, X., Deng, Y., & Li, Y. (2019) · International Immunopharmacology · doi:10.1016/j.intimp.2019.105963 · Cited by 6
Gashmardi, N., & Edalatmanesh, M. A. (2019) · The Neuroscience Journal of Shefaye Khatam · doi:10.29252/shefa.7.4.89 · Cited by 4
Up-Regulation of TAB3 Is Involved in Neuronal Apoptosis After Intracerebral Hemorrhage
Zhu, L., Cao, M.-H., Ni, Y., Han, L.-J., Dai, A.-H., Chen, R.-R., Ning, X.-J., Liu, X.-R., & Ke, K.-F. (2017) · Cellular and molecular neurobiology · doi:10.1007/s10571-016-0397-5 · Cited by 5
“Scale bars 50 lm inflammation and neuronal death during stroke (Allan and Rothwell 2001; Hanisch 2002).”
BackgroundPark, J.-H., Hong, Y.-J., Moon, E., Kim, S., & Kim, S. (2011) · doi:10.4062/biomolther.2011.19.4.425 · Cited by 5
“However, in pathological conditions, microglia are over-activated and produce reactive proinfl ammatory mediators, including nitric oxide (NO), interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α) and prostaglandin E2 (PGE2) (Minghetti and Levi, 1998; Hanisch, 2002).”
BackgroundJung, J., Kim, Y., Cirunduzi, A. C., Yoon, S., Bang, S., & Yang, S. (2026) · CNS Neuroscience & Therapeutics · doi:10.1002/cns.70919 · Cited by 5
Singh, A. S., Naqvi, A. R., & Chanu, M. T. (2026) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2026.01.050 · Cited by 7
Seidel, F., Fluiter, K., Kleemann, R., Worms, N., van Nieuwkoop, A., Caspers, M. P. M., Grigoriadis, N., Kiliaan, A. J., Baas, F., Michailidou, I., et al. (2023) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2023.1205261 · Cited by 3
“Given that the activation state of microglial cells is highly influenced by the cytokine environment (Hanisch, 2002), anti-C5 treatmentmediated changes in IL-33 may be linked to the partial reversal effect of the treatment on the expression of microglia surface markers.”
BackgroundLim, K.-Y., Kim, S.-I., Kim, H., Kang, J., Park, J. W., Won, J., Shin, D., & Park, S.-H. (2022) · BMC Neurology · doi:10.1186/s12883-022-02818-8 · Cited by 4
Neuromodulatory Effect of Plant Metabolites
Barman, D., Dey, N., Sen, S., Kakoti, B. B., & Vanlalhriatpuii, C. (2022) · Sciences of Phytochemistry · doi:10.58920/sciphy01010047 · Cited by 4
Molecular Signature of Neuroinflammation Induced in Cytokine-Stimulated Human Cortical Spheroids
Kleijn, K. M. A. D., Straasheijm, K. R., Zuure, W. A., & Martens, G. J. M. (2022) · Biomedicines · doi:10.3390/biomedicines10051025 · Cited by 4
“These findings are in line with the relatively high sensitivity of microglial populations to cytokines [28,29].”
ResultDietary fats modulate neuroinflammation in mucin 2 knock out mice model of spontaneous colitis
Wenzel, T. J., Haskey, N., Kwong, E. H., Greuel, B. K., Gates, E. J., Gibson, D. L., & Klegeris, A. (2021) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2021.166336 · Cited by 7
Auriemma, R., Sponchioni, M., Palmiero, U. C., Manfredini, N., Dinani, F. S. R., & Moscatelli, D. (2021) · Macromolecular Chemistry and Physics · doi:10.1002/macp.202100223 · Cited by 4
[Role of pyroptosis in bilirubin-induced microglial injury].
Huang, H., He, C.-M., Li, S.-Y., Zhang, Y., & Hua, Z.-Y. (2020) · Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · doi:10.7499/j.issn.1008-8830.2003175 · Cited by 4
“高胆红素血症是新生儿期常见的临床疾病, 胆红素脑病是其严重并发症 ([3-4]),危害患儿健康及 生命,加重家庭和社会负担。目前胆红素脑病的 发病机制尚不清楚,主要与氧化应激、内质网损伤、 钙离子紊乱等相关,均伴有明显的神经炎症 ([18])。 在胆红素脑病模型动物中,抑制炎症可改善模型 动物预后,提示调控炎症对胆红素脑病的防治有 积极作用 ([5])。通常认为,神经元对胆红素刺激最为 敏感 ([18]),但胆红素引起的神经元损伤不伴明显的 炎症因子释放 ([19])。小胶质细胞作为神经系统的天 然免疫细胞,是炎症因子的主要来源 ([20]);小胶质 细胞过度活化释放大量炎症因子,引起炎症级联 反应,对神经炎症损伤起关键作用 ([…”
Iatrogenic Neuropathology of Systemic Therapies
Torre, M., & Feany, M. Β. (2020) · Surgical pathology clinics · doi:10.1016/j.path.2020.01.004 · Cited by 3
Toledo, G. S., Georgiou, M., Reis, J. N. D., Roberton, V. H., Valinhas, A., Wood, R., Phillips, J. B., Mason, C., Li, D., Li, Y., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-49315-6 · Cited by 5
Flavonoids in neuropathic pain management: A new player on an old target
Akbar, S. (2019) · African Journal of Pharmacy and Pharmacology · doi:10.5897/ajpp2019.5023 · Cited by 4
“oxide synthase (iNOS) is enhanced in the microglia as a result of peripheral nerve injury leading to hyper sensitization (Hanisch, 2002).”
BackgroundTesting the Neuroprotective Properties of PCSO-524® Using a Neuronal Cell Cycle Suppression Assay
Zhu, B., Zhang, Y., & Herrup, K. (2019) · Marine Drugs · doi:10.3390/md17020079 · Cited by 5
Correlation between MCP-1-2518A/G polymorphism and the risk of Alzheimer’s disease
Wang, Y., Huang, S., Wu, X., Wang, Y., & Jiang, D. (2018) · Journal of Neural Transmission · doi:10.1007/s00702-018-1936-7 · Cited by 4
“Activated microglial cells produce and release potentially toxic products, including interleukin (IL), tumor necrosis factor alpha (TNF-α) and monocyte chemotactic protein-1 (MCP-1), which could damage neighboring neurons (Hanisch 2002).”
BackgroundHIV-1 Tat alters neuronal intrinsic excitability
Francesconi, W., Berton, F., & Marcondes, M. G. (2018) · BMC Research Notes · doi:10.1186/s13104-018-3376-8 · Cited by 4
Esclerosis múltiple: aspectos inmunológicos actuales
Cuevas-García, C. (2017) · Revista Alergia México · doi:10.29262/ram.v64i1.253 · Cited by 8
Bruno, P., Ins, M., Caetana, M., & Ins, M. (2012) · InTech eBooks · doi:10.5772/30723 · Cited by 4
“The production of cytokines and other molecules by activated microglial cells with implications in cellular processes has been demonstrated in many studies based on in vitro models (Banati et al., 1993; Minghetti and Levi, 1998; Gebicke-Haerter et al., 2001; Hanisch, 2002; Hausler et al., 2002).”
BackgroundKhan, A., Ronan, P. J., & Rahman, S. (2026) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-026-10279-w · Cited by 4
“Our data indicate that intraperitoneal injection of LPS markedly increased the production of proinflammatory cytokines in the hippocampus and prefrontal cortex likely through microglial activation, as microglia are a primary source of proinflammatory cytokines in the brain (Hanisch 2002 ).”
Brain Gamma-Stimulation: Mechanisms and Optimization of Impact
Lushnikov, K. V., Serov, D. A., Astashev, M. E., Козлов, В. А., Melerzanov, A., & Vedunova, M. V. (2025) · Biology · doi:10.3390/biology14121722 · Cited by 4
Neuro-immune interactions in memory
Stewart, E., & Ryan, T. J. (2025) · Neurobiology of Learning and Memory · doi:10.1016/j.nlm.2025.108077 · Cited by 3
“…microglia are an important source of cytokines and chemokines and possess phagocytic capacities used to engulf debris, pathogens or necrotic and apoptotic cells to maintain tissue homeostasis throughout the lifespan (Stence, Waite and Dailey, 2001; Hanisch, 2002; Ransohoff and Perry, 2009).”
A mathematical model of microglia glucose metabolism and lactylation with positive feedback
Larripa, K., & Rǎdulescu, A. (2025) · Journal of Theoretical Biology · doi:10.1016/j.jtbi.2025.112049 · Cited by 2
Metadata
- Authors
- Hanisch, U.
- Affiliations
- Max Delbrück Center (DE)
- Corresponding author
- Hanisch, Uwe‐Karsten
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2002-10-04
- Volume
- 40
- Issue
- 2
- Pages
- 140-155
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- OpenAlex
- W2090804892
- Cited by
- 1,645
- References
- 0
- Citations by year
- 2026: 29 · 2025: 39 · 2024: 62 · 2023: 59 · 2022: 68 · 2021: 85 · 2020: 82 · 2019: 76 · 2018: 85 · 2017: 79 · 2016: 70 · 2015: 81 · 2014: 86 · 2013: 94 · 2012: 93
- FWCI
- 4.22
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- microglia, cytokines, chemokines, microglial activation, neuroinflammation, neuroprotection, astrocyte-microglia interaction, tissue repair, neurotoxicity, neuropathology, innate immunity
- MeSH terms
- Animals, Cell Communication, Endocrine System, Endothelium, Vascular, Humans, Neuroglia, Neurons, Cytokines, Microglia
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