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- 저자 : Kwangmin Na (검색결과 3 건)
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EC-SOD Suppresses Contact Hypersensitivity in Mouse Skin by Impairing Langerhans Cell Migration
Na, Kwangmin,Kim, Kyoung-Eun,Park, Sang-Tae,Kim, Tae-Yoon The Society for Investigative Dermatology, Inc 2007 The Journal of investigative dermatology Vol.127 No.8
Extracellular superoxide dismutase (EC-SOD) is primarily a tissue enzyme and has been implicated in the modulation of inflammatory response. The biological role of EC-SOD in skin, however, has rarely been investigated. In this study, we aim to explore the effects of EC-SOD on the inflammatory response in skin by evaluating the contact hypersensitivity response (CHS) in EC-SOD transgenic mice. Transgenic mice with skin-specific expression of EC-SOD were sensitized and challenged with 2,4,6-trinitro-1-chlorobenzene (TNCB), followed by measurement of ear swelling. EC-SOD transgenic mice showed significantly reduced CHS responses compared with wild-type mice. Histological evaluation of the challenged ears of EC-SOD transgenic mice revealed diminished infiltration of inflammatory cells with a failure to induce expression of inflammatory cytokines, such as tumor necrosis factor-α and IFN-γ, on sensitization and challenge with TNCB. Furthermore, Langerhans cell migration to lymph nodes was impaired in EC-SOD transgenic mice. These results indicate that EC-SOD downregulates CHS through inhibition of the inflammatory response, suggesting a possible therapeutic regimen in inflammatory skin diseases.Journal of Investigative Dermatology (2007) 127, 1930–1937; doi:10.1038/sj.jid.5700802; published online 29 March 2007
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Cho, Kwangmin,Jang, You-Jin,Lee, Se-Jong,Jeon, Yu-Na,Shim, Young-Lim,Lee, Ji-Yong,Lim, Da-Som,Kim, Dong-Hou,Yoon, Seung-Yong Elsevier 2020 Biochemical and biophysical research communication Vol.524 No.3
<P><B>Abstract</B></P> <P>β-Amyloid (Aβ) plaque in the brains of patients with Alzheimer’s disease (AD) is mainly caused by impaired clearance of Aβ by glial cells, including microglia and astrocytes. Because microglia play an important protective role in the central nervous system, many efforts have been made to identify agents that effectively improve microglial Aβ phagocytosis. This study found that TLQP-21, which is cleaved from VGF (VGF nerve growth factor inducible) precursor protein, enhanced Aβ phagocytosis and degradation by microglial BV2 cells. TLQP-21 also improved microglial phagocytic activity and promoted fibrillar amyloid-β (fAβ) uptake by microglial BV2 cells via a C3AR1-dependent mechanism. Moreover, TLQP-21 stimulated Aβ degradation by enhancing lysosome activity, thereby enhancing fAβ clearance. These results suggest that treatment with TLQP-21 may be a novel therapeutic strategy to efficiently enhance microglial Aβ clearance in AD.</P> <P><B>Highlights</B></P> <P> <UL> <LI> TLQP-21 increases extracellular fAβ uptake by microglial BV2 cells. </LI> <LI> TLQP-21 enhances phagocytic activity of microglial BV2 cells. </LI> <LI> TLQP-21 increases fAβ uptake by microglial BV2 cells via C3AR1-dependent mechanisms. </LI> <LI> TLQP-21 enhances the degradation of engulfed Aβ by stimulating a lysosomal degradation pathway. </LI> </UL> </P>
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Minha Kim,So-Dam Kim,Kyoung In Kim,전은혜,Min Gee Kim,Yu-Ree Lim,Enkhmaa Lkhagva-Yondon,Yena Oh,Kwangmin Na,정영철,진병관,송윤선,Myung Shin Jeon 한국뇌신경과학회 2021 Experimental Neurobiology Vol.30 No.2
Stroke causes systemic immunosuppression. T lymphocytes are involved in infarct size in the early stages of stroke. However, the phenotypes of T lymphocytes and their functions in peripheral immune organs and the brain have not been well analyzed in the acute and chronic phases of stroke. Here, we investigated pathological phenotypic alterations in the systemic immune response, especially changes in T lymphocytes, from one day to six months after ischemic stroke in mice. Impairment in thymocyte numbers, development, proliferation, and apoptosis were observed for up to two weeks. The number of mature T cells in the spleen and blood decreased and showed reduced interferon-γ production. Increased numbers of CD4- CD8- CD3+ double-negative T cells were observed in the mouse brain during the early stages of stroke, whereas interleukin (IL)-10+ Foxp3+ regulatory T lymphocytes increased from two weeks during the chronic phase. These phenotypes correlated with body weight and neurological severity scores. The recovery of T lymphocyte numbers and increases in IL-10+ Foxp3+ regulatory T lymphocytes may be important for long-term neurological outcomes. Dynamic changes in T lymphocytes between the acute and chronic phases may play different roles in pathogenesis and recovery. This study provides fundamental information regarding the T lymphocyte alterations from the brain to the peripheral immune organs following stroke.
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