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Neuroimmune Network
Research Laboratory

What is neuroimmune network

    인체의 신경계(nervous system)와 더불어 한 축을 담당하는 면역계(immune system)는 인체의 모든 외부 환경과 직접적으로 맞닿아 있으며, 신경계와 면역계가 서로 유기적인 상호작용을 하여 인체가 환경에 적응하는데에 있어서 필수적인 역할을 하고 있습니다. 심지어 박테리아와 같은 단순한 단세포 생물 조차도 바이러스 감염에 대항할 수 있는 면역체계(효소 시스템)를 갖추고 있습니다. 면역기능으로 인해 비로소 생명체는 환경에 적응할 수 있고 나아가 진화도 할 수 있는 것입니다.  

Why neuroimmune network

    면역계와 신경계는 인체에서 가장 중요하고 복잡한 두 시스템으로, 감염이나 외부 변화에 대해 적절히 저항하고 적응하여 항상성을 유지하며 생존을 영위해 가는데 가장 중요한 역할을 담당하고 있습니다. 이 두 시스템을 연구 대상으로 하는 신경과학과 면역학은 그 동안 독자적인 영역으로 연구가 진행되어, 각각의 기능과 질환들에 대한 많은 사실이 규명되는 등, 단일 학문으로서 비약적인 발전을 이루었습니다.

Hirrlinger, J. & Nimmerjahn, A., (2022). Glia, 70(8), pp.1554–1580.


in vitro assay



Optogenetics / Animal behaviors


Lastest Publications

Astrocytes can affect animal behavior by regulating tripartite synaptic trans- mission, yet their influence on affective behavior remains largely unclear. Here we showed that hippocampal astrocyte calcium activity reflects mouse affec- tive state during virtual elevated plus maze test using two-photon calcium imaging in vivo. Furthermore, optogenetic hippocampal astrocyte activation elevating intracellular calcium induced anxiolytic behaviors in astrocyte- specific channelrhodopsin 2 (ChR2) transgenic mice (hGFAP-ChR2 mice). As underlying mechanisms, we found ATP released from the activated hippo- campal astrocytes increased excitatory synaptic transmission in dentate gyrus (DG) granule cells, which exerted anxiolyticeffects. Ourdatauncover aroleof hippocampal astrocytes in modulating mice anxiety-like behaviors by reg- ulating ATP-mediated synaptic homeostasis in hippocampal DG granule cells. Thus, manipulating hippocampal astrocytes activity can be a therapeutic strategy to treat anxiety.

Cho WH 2022

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is accompanied by chronic neurological sequelae such as cognitive decline and mood disorder, but the underlying mechanisms have not yet been elucidated. We explored the possibility that the brain-infiltrating SARS-CoV-2 spike protein contributes to the development of neurological symptoms observed in COVID-19 patients in this study. Our behavioral study showed that administration of SARS-CoV-2 spike protein S1 subunit (S1 protein) to mouse hippocampus induced cognitive deficit and anxiety-like behavior in vivo. These neurological symptoms were accompanied by neuronal cell death in the dorsal and ventral hippocampus as well as glial cell activation. Interestingly, the S1 protein did not directly induce hippocampal cell death in vitro. Rather, it exerted neurotoxicity via glial cell activation, partially through interleukin-1β induction. In conclusion, our data suggest a novel pathogenic mechanism for the COVID-19-associated neurological symptoms that involves glia activation and non-cell autonomous hippocampal neuronal death by the brain-infiltrating S1 protein.

Oh J 2022

Although microglia activation plays an important role in the development of nerve injury-induced neuropathic pain, the molecular mechanisms of spinal cord microglia activation in nerve injury are not completely understood. Recently, two injured sensory neuron-derived molecules, colony stimulating factor-1 (CSF-1) and GT1b, were proposed to trigger spinal cord microglia activation, yet their relationship and relative contribution to microglia activation have not been addressed. In the present study, the role of GT1b and CSF-1 in microglia activation and proliferation was characterized. GT1b stimulation upregulated proinflammatory mediators such as IL-1b, TNF-a, and NADPH oxidase 2 (Nox2), without microglia proliferation. Conversely, CSF-1 stimulation induced microglia proliferation with minimal proinflammatory gene induction. Notably, neither GT1b nor CSF-1 induced mechanical hypersensitivity in female mice; however, they induced similar microglial proliferation in both male and female mice. Taken together, our data indicate that injured sensory neuron-derived GT1b and CSF-1 activate spinal cord microglia in concert through distinct activation pathways.

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