CD4 T淋巴细胞在脑卒中后抑郁发病机制中的研究进展

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Abstract The pathophysiological mechanism of post-stroke depression is unclear. Regarding its neurobiological alterations, available research evidence includes elevated monoamine system (especially serotonin) alterations, hypothalamic pituitary adrenal axis abnormalities, disruption of the prefrontal cortex circuit, alterations in neuroplasticity and glutamate neurotransmission, and excess pro-inflammatory cytokines. The immune inflammatory response may play an important role in the pathophysiological process of post-stroke depression, especially the imbalance of CD4 T lymphocytes and their related cytokines, which may damage the neuroplasticity of T lymphocytes and maintain the function of the nervous system, resulting in the imbalance of the regulation of the immune inflammatory response after stroke, affecting the synthesis of neurotransmitters and the release of metabolism, thus leading to depression.

Key words： Cytokines CD4 T lymphocytes Immune inflammatory response Post-stroke depression

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	ZHANG Linli1 SONG Jinggui2

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ZHANG Linli1 SONG Jinggui2. Research progress of CD4 T lymphocytes in the pathogenesis of post-stroke depression[J]. 中国医药导报, 2020, 17(31): 62-65.

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http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2020/V17/I31/62

[1] Cramer JV，Benakis C，Liesz A. T cells in the post-ischemic brain：troopers or paramedics? [J]. J Neuroimmunol，2019，326：33-37.
[2] Wang Z，Shi Y，Liu F，et al. Diversiform etiologies for post-stroke depression [J]. Front Psychiatry，2019，9：761.
[3] Kisuya J，Chemtai A，Raballah E，et al. The diagnostic accuracy of Th1（IFN-γ，TNF-α，and IL-2）and Th2（IL-4，IL-6 and IL-10）cytokines response in AFB microscopy smear negative PTB- HIV co-infected patients [J]. Sci Rep，2019，9（1）：2966.
[4] Lee GR. The balance of Th17 versus treg cells in autoimmunity [J]. Int J Mol Sci，2018，19（3）：730.
[5] Evans FL，Dittmer M，de la Fuente AG. Protective and regenerative roles of t cells in central nervous system disorders [J]. Front Immunol，2019，10：2171.
[6] Djuretic IM，Levanon D，Negreanu V，et al. Transcription factors T-bet and Runx3 cooperate to activate IFNg and silence IL4 in T helper type 1 cells [J]. Nat Immunol，2007， 8（2）：145-153.
[7] Schiweck C，Valles-Colomer M，Arolt V，et al. Depression and suicidality：a link to premature T helper cell aging and increased Th17 cells [J]. Brain Behav Immun，2020， 87：603-609.
[8] Slyepchenko A，Maes M，Kohler CA，et al. T helper 17 cells may drive neuroprogression in major depressive disorder：proposal of an integrative model [J]. Neurosci Biobehav Rev，2016，64：83-100.
[9] Harrington LE，Hatton RD，Mangan PR，et al. Interleukin 17-producing CD4 effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages [J]. Nat Immunol，2005，6（11）：1123-1132.
[10] Seo KY，Kitamura K，Han SJ，et al. TH17 cells mediate inflammation in a novel model of spontaneous experimental autoimmune lacrimal keratoconjunctivitis with neural damage [J]. Allergy Clin Immunol，2018，142（1）：96.e2-108.e2.
[11] Zhang S. The role of transforming growth factor β in T helper 17 differentiation [J]. Immunology，2018，155（1）：24-35.
[12] Liu X，Hu H，Fan H，et al. The role of STAT3 and AhR in the differentiation of CD4+ T cells into Th17 and Treg cells [J]. Medicine（Baltimore），2017，96（17）：e6615.
[13] Withers DR，Hepworth MR，Wang X，et al. Transient inhibition of ROR-γt therapeutically limits intestinal inflammation by reducing TH17 cells and preserving group 3 innate lymphoid cells [J]. Nat Med，2016，22（3）：319-323.
[14] Moaaz M，Youssry S，Elfatatry A，et al. Th17/Treg cells imbalance and their related cytokines （IL-17，IL-10 and TGF-β） in children with autism spectrum disorder [J]. J Neuroimmunol，2019，337：577071.
[15] Peck A，Mellins ED. Plasticity of T-cell phenotype and function：the T helper type 17 example [J]. Immunology，2010，129（2）：147-153.
[16] Ghosh S，Roy-Chowdhuri S，Kang K，et al. The transcription factor Foxp1 preserves integrity of an active Foxp3 locus in extrathymic Treg cells [J]. Nat Commun，2018，9（1）：4473.
[17] Mayer CT，Floess S，Baru AM，et al. CD8+Foxp3+ T cells share developmental and phenotypic features with classical CD4+Foxp3+ regulatory T cells but lack potent suppressive activity [J]. Eur J Immunol，2015，41（3）：716-725.
[18] Hong M，Zheng J，Ding ZY，et al. Imbalance between Th17 and Treg cells may play an important role in the development of chronic unpredictable mild stress-induced depression in mice [J]. Neuroimmunomodulation，2013，20（1）：39-50.
[19] 剧锦叶.Th17/Treg细胞免疫失衡在卒中后抑郁的作用[D].太原：山西医科大学，2019.
[20] Veldhoen M，Uyttenhove C，van Snick J，et al. Transforming growth factor-beta ‘reprograms’ the differentiation of T helper 2 cells and promotes an interleukin 9-producing subset [J]. Nat Immunol，2008，9（12）：1341-1346.
[21] Kabata H，Moro K，Koyasu S. The group 2 innate lymphoid cell （ILC2） regulatory network and its underlying mechanisms [J]. Immunol Rev，2018，286（1）：37-52.
[22] Abdelaziz MH，Wang H，Cheng J. Th2 cells as an intermediate for the differentiation of na?觙ve T cells into Th9 cells，associated with the Smad3/Smad4 and IRF4 pathway [J]. Exp Ther Med，2020，19（3）：1947-1954.
[23] Koh B，Abdul Qayum A，Srivastava R，et al. A conserved enhancer regulates IL9 expression in multiple lineages [J]. Nat Commun，2018，9（1）：4803.
[24] Horgusluoglu E，Nudelman K，Nho K，et al. Adult neurogenesis and neurodegenerative diseases：a systems biology perspective [J]. Am J Med Genet B Neuropsychiatr Genet，2017，174（1）：93-112.
[25] Singh NP，Hegde VL，Hofseth LJ，et al. Resveratrol（trans-3，5，4′-trihydroxystilbene）ameliorates experimental allergic encephalomyelitis，primarily via induction of apoptosis in T cells involving activation of aryl hydrocarbon receptor and estrogen receptor [J]. Mol Pharmacol，2007， 72（6）：1508-1521.
[26] Dumoutier L，Van Roost E，Ameye G，et al. IL-TIF/IL-22：genomic organization and mapping of the human and mouse genes [J]. Genes Immun，2000，1（8）：488-494.
[27] Yeste A，Mascanfroni ID，Nadeau M，et al. IL-21 induces IL-22 production in CD4+ T cells [J]. Nat Commun，2014， 5（11）：3753.
[28] Xie MH，Aggarwal S，Ho WH，et al. Interleukin（IL）-22，a novel human cytokine that signals through the interferon receptor-related proteins CRF2-4 and IL-22R [J]. J Biol Chem，2000，275（40）：31335-31339.
[29] Sekimata M，Yoshida D，Araki A，et al. Runx1 and RORγt cooperate to upregulate IL-22 expression in Th cells through its distal enhancer [J]. J Immunol，2019，202（11）：3198-3210.
[30] Chea S，Perchet T，Petit M，et al. Notch signaling in group 3 innate lymphoid cells modulates their plasticity [J]. Sci Signal，2016，9（426）：ra45.
[31] Seshadri S，Allan DSJ，Carlyle JR. Bacillus anthracis lethal toxin negatively modulates ILC3 function through perturbation of IL-23-mediated MAPK signaling [J]. PLoS Pathog，2017，13（10）：e1006690.
[32] Zhu X，Ding J，Wang B，et al. Circular RNA DLGAP4 is down-regulated and negatively correlates with severity，inflammatory cytokine expression and pro-inflammatory gene miR-143 expression in acute ischemic stroke patients [J]. Int J Clin Exp Pathol，2019，12（3）：941-948.