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이시영,최동기,곽아름,김시내,Tam Thanh Nguyen,길가애,김은혜,유광하,김인애,이영민,전현정,Edward D. Chan,Xiyuan Bai,김현우,김용성,김수현 대한면역학회 2017 Immune Network Vol.17 No.2
The induction of interleukin (IL)-32 in bone marrow (BM) inflammation is crucial in graft versus host disease (GvHD) that is a common side effect of allogeneic BM transplantation. Clinical trials on a-1 antitrypsin (AAT) in patients with GvHD are based on the preliminary human and mouse studies on AAT reducing the severity of GvHD. Proteinase 3 (PR3) is an IL-32-binding protein that was isolated from human urine. IL-32 primarily induces inflammatory cytokines in myeloid cells, probably due to PR3 expression on the membrane of the myeloid lineage cells. The inhibitory activity of AAT on serine proteinases may explain the anti-inflammatory effect of AAT on GvHD. However, the anti-inflammatory activity of AAT on BM cells remains unclear. Mouse BM cells were treated with IL-32g and different inflammatory stimuli to investigate the anti-inflammatory activity of AAT. Recombinant AATFc fusion protein inhibited IL-32g-induced IL-6 expression in BM cells, but failed to suppress that induced by other stimuli. In addition, the binding of IL-32g to PR3 was abrogated by AAT-Fc. The data suggest that the specific antiinflammatory effect of AAT in mouse BM cells is due to the blocking of IL-32 binding to membrane PR3.
Sinae Kim,Jong Ho Lee,Siyoung Lee,Saerok Shim,Tam T. Nguyen,Jihyeong Hwang,Heijun Kim,Yeo-Ok Choi,Jaewoo Hong,Suyoung Bae,Hyun Jhung Jhun,Hokee Yum,이영민,Edward D. Chan,Liping Yu,Tania Azam,Yong-Dae Kim 대한면역학회 2020 Immune Network Vol.20 No.5
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) is a positive-sense single-stranded RNA (+ssRNA) that causes coronavirus disease 2019 (COVID-19). The viral genome encodes twelve genes for viral replication and infection. The third open reading frame is the spike (S) gene that encodes for the spike glycoprotein interacting with specific cell surface receptor – angiotensin converting enzyme 2 (ACE2) – on the host cell membrane. Most recent studies identified a single point mutation in S gene. A single point mutation in S gene leading to an amino acid substitution at codon 614 from an aspartic acid 614 into glycine (D614G) resulted in greater infectivity compared to the wild type SARS-CoV2. We were interested in investigating the mutation region of S gene of SARS-CoV2 from Korean COVID-19 patients. New mutation sites were found in the critical receptor binding domain (RBD) of S gene, which is adjacent to the aforementioned D614G mutation residue. This specific sequence data demonstrated the active progression of SARS-CoV2 by mutations in the RBD of S gene. The sequence information of new mutations is critical to the development of recombinant SARS-CoV2 spike antigens, which may be required to improve and advance the strategy against a wide range of possible SARS-CoV2 mutations.
Lee, Siyoung,Choi, Dong-Ki,Kwak, Areum,Kim, Sinae,Nguyen, Tam Thanh,Gil, Gaae,Kim, Eunhye,Yoo, Kwang Ha,Kim, In Ae,Lee, Youngmin,Jhun, Hyunjhung,Chan, Edward D.,Bai, Xiyuan,Kim, Hyunwoo,Kim, Yong-Sung 한국조명·전기설비학회 2017 한국조명·전기설비학회 학술대회논문집 Vol. No.
<P>The induction of interleukin (IL)-32 in bone marrow (BM) inflammation is crucial in graft versus host disease (GvHD) that is a common side effect of allogeneic BM transplantation. Clinical trials on α-1 antitrypsin (AAT) in patients with GvHD are based on the preliminary human and mouse studies on AAT reducing the severity of GvHD. Proteinase 3 (PR3) is an IL-32-binding protein that was isolated from human urine. IL-32 primarily induces inflammatory cytokines in myeloid cells, probably due to PR3 expression on the membrane of the myeloid lineage cells. The inhibitory activity of AAT on serine proteinases may explain the anti-inflammatory effect of AAT on GvHD. However, the anti-inflammatory activity of AAT on BM cells remains unclear. Mouse BM cells were treated with IL-32γ and different inflammatory stimuli to investigate the anti-inflammatory activity of AAT. Recombinant AAT-Fc fusion protein inhibited IL-32γ-induced IL-6 expression in BM cells, but failed to suppress that induced by other stimuli. In addition, the binding of IL-32γ to PR3 was abrogated by AAT-Fc. The data suggest that the specific anti-inflammatory effect of AAT in mouse BM cells is due to the blocking of IL-32 binding to membrane PR3.</P>