Seung Hee Hong

Blood-brain barrier (BBB) disintegration is a key contributor to neuroinflammation; however, the biological processes governing BBB permeability under physiological conditions remain unclear. Here, we investigate the role of NLRP3 inflammasome in BBB disruption following peripheral inflammatory challenges. Repeated intraperitoneal lipopolysaccharide administration causes NLRP3-dependent BBB permeabilization and myeloid cell infiltration into the brain. Using a mouse model with cell-specific hype

BACKGROUND: Efforts to profile atopic dermatitis (AD) tissues have intensified, yet comprehensive analysis of systemic immune landscapes in severe AD remains crucial. METHODS: Employing single-cell RNA sequencing, we analyzed over 300,000 peripheral blood mononuclear cells from 12 severe AD patients (Eczema area and severity index (EASI) > 21) and six healthy controls. RESULTS: Results revealed significant immune cell shifts in AD patients, including increased Th2 cell abundance, reduced NK cell

Upon antigenic stimulation, naïve CD4+ T cells can give rise to phenotypically distinct effector T helper cells and long-lived memory T cells. We computationally reconstructed the in vivo trajectory of CD4+ T cell differentiation during a type I inflammatory immune response and identified two distinct differentiation paths for effector and precursor central memory T cells arising directly from naïve CD4+ T cells. Unexpectedly, our studies revealed heterogeneity among naïve CD4+ T cells, which ar

The clearance of human immunodeficiency virus-1 (HIV-1) remains a significant public health challenge due to impaired cellular immune responses and HIV-1 maintenance during acute infection. However, the genetic and epigenetic changes influencing the immune response on host infected cells remain unclear. Here, this study analyzes HIV-1 infected CD4+ T cells from peripheral blood mononuclear cells from people living with HIV-1 (PLWH) during early infection (<6 months) using single-cell RNA and ATA

The clearance of human immunodeficiency virus-1 (HIV-1) remains a significant public health challenge due to impaired cellular immune responses and HIV-1 maintenance during acute infection. However, the genetic and epigenetic changes influencing the immune response on host infected cells remain unclear. Here, this study analyzes HIV-1 infected CD4+ T cells from peripheral blood mononuclear cells from people living with HIV-1 (PLWH) during early infection (<6 months) using single-cell RNA and ATA

Abstract Programmed cell death protein and its ligand (PD-1 / PD-L1) blockades have been approved for the treatment of metastatic non-small cell lung cancer (NSCLC). PD-L1 binds to PD-1 and functions as a co-inhibitory factor. It is well known that in cancer, PD-L1 is highly expressed hence cancer cells can evade the host immunity in the tumor microenvironment (TME). Although PD-1 / PD-L1 blockades have been clinically utilized, the biological factors determining treatment outcome remain convolu

Abstract Recent studies suggest that injury-induced dedifferentiation, which leads to the formation of ‘injury-responsive cells’, contributes significantly to tissue repair across various organs, including the liver. Utilizing Yamanaka factors (Oct4, Sox2, Klf4, and c-Myc: OSKM) for in vivo partial reprogramming generates ‘injury-responsive cells’ in the intestine, mirroring those derived from injury-induced dedifferentiation. Thus, the transgene induction of OSKM or viral delivery of Oct4, Sox2