A5056143043- Immune Cell Function and Interaction
- Hepatitis C virus research
- Immune cells in cancer
- Cytomegalovirus and herpesvirus research
- Immune Response and Inflammation
- Inflammation biomarkers and pathways
- Hepatitis B Virus Studies
- MicroRNA in disease regulation
- T-cell and B-cell Immunology
- HIV Research and Treatment
- Galectins and Cancer Biology
- Cancer-related molecular mechanisms research
- interferon and immune responses
- COVID-19 Clinical Research Studies
- Telomeres, Telomerase, and Senescence
- Extracellular vesicles in disease
- Immunotherapy and Immune Responses
- HIV-related health complications and treatments
- Reproductive System and Pregnancy
- DNA Repair Mechanisms
- SARS-CoV-2 and COVID-19 Research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Monoclonal and Polyclonal Antibodies Research
- Signaling Pathways in Disease
- S100 Proteins and Annexins
East Tennessee State University
2016-2025
James H. Quillen VA Medical Center
2015-2025
Ministry of Education of the People's Republic of China
2012-2025
Tianjin Medical University
2006-2025
Second Hospital of Tianjin Medical University
2025
Shandong University
2024
United States Department of Veterans Affairs
2012-2022
Chinese University of Hong Kong
2020
Wuhan Pulmonary Hospital
2020
Fudan University
2020
Hepatitis C virus (HCV) is an important human pathogen that remarkably efficient at establishing persistent infection. The HCV core protein the first expressed during early phase of Our previous work demonstrated suppresses host immune responses, including anti-viral cytotoxic T-lymphocyte responses in a murine model. To investigate mechanism core-mediated immunosuppression, we searched for proteins capable associating with using yeast two-hybrid system. Using as bait, screened T...
Tim-3 and PD-1 are powerful immunoinhibitory molecules involved in immune tolerance, autoimmune responses, antitumor or antiviral evasion. A current model for regulation during responses suggests a divergent function, such that acts synergistically with TLR signaling pathways innate cells to promote inflammation, yet the same molecule terminates Th1 immunity adaptive cells. To better understand how might be functioning we examined kinetics of expression human CD14+ M/M(Ф) relation IL-12, key...
The sepsis initial hyperinflammatory reaction, if not treated early, shifts to a protracted state of immunosuppression that alters both innate and adaptive immunity is associated with elevated mortality. Myeloid-derived suppressor cells (MDSCs) are myeloid progenitors precursors fail differentiate into mature innate-immunity known for their potent immunosuppressive activities. We previously reported murine MDSCs expand dramatically in the bone marrow during late sepsis, induced by cecal...
Abstract Oxidative stress caused by excess reactive oxygen species (ROS) accelerates telomere erosion and mitochondrial injury, leading to impaired cellular functions cell death. Whether oxidative stress‐mediated induces or vice versa, in human T cells—the major effectors of host adaptive immunity against infection malignancy—is poorly understood due the pleiotropic effects ROS. Here we employed a novel chemoptogenetic tool that selectively produces single ( 1 O 2 ) only at telomeres...
T cell immunoglobulin and mucin domain-containing protein 3 (Tim-3) is a newly identified negative immunomodulator that up-regulated on dysfunctional cells during viral infections. The expression function of Tim-3 human innate immune responses HCV infection, however, remains poorly characterized. In this study, we report constitutively expressed resting CD14(+) monocyte/macrophages (M/M(Ø)) functions as cap to block IL-12, key pro-inflammatory cytokine linking adaptive responses....
Hepatitis C virus (HCV) is remarkable at disrupting human immunity to establish chronic infection. Upregulation of inhibitory signaling pathways (such as T cell Ig and mucin domain protein-3 [Tim-3]) accumulation regulatory cells (Tregs) play pivotal roles in suppressing antiviral effector (Teff) responses that are essential for viral clearance. Although the Tim-3 pathway has been shown negatively regulate Teffs, its role regulating Foxp3(+) Tregs poorly explored. In this study, we...
Abstract Hepatitis C virus (HCV) dysregulates innate immune responses and induces persistent viral infection. We previously demonstrated that HCV core protein impairs IL-12 expression by monocytes/macrophages (M/MΦs) through interaction with a complement receptor gC1qR. Because core-mediated lymphocyte dysregulation occurs the negative immunomodulators programmed death-1 (PD-1) suppressor of cytokine signaling-1 (SOCS-1), aim this study was to examine their role in suppression M/MΦs....
Summary Host immune responses must be tightly regulated by an intricate balance between positive and negative signals while fighting pathogens; persistent pathogens may usurp these regulatory mechanisms to dampen host immunity facilitate survival in vivo . Here we report that T im‐3, a signalling molecule expressed on monocytes cells, is up‐regulated natural killer ( NK ) cells individuals chronically infected with hepatitis C virus HCV ). Additionally, the transcription factor ‐bet was also...
Objective: Regulatory T cells (Tregs) contribute to HIV-1 disease progression by impairing antiviral immunity; however, the precise mechanisms responsible for development of Tregs in setting infection are incompletely understood. Design: In this study, we provide evidence that HIV-induced expansion monocytic myeloid-derived suppressor (M-MDSCs) promote differentiation Foxp3+ Tregs. Methods: We measured MDSC induction and cytokine expression flow cytometry analyzed their functions coculturing...
Complement plays a pivotal role in the regulation of innate and adaptive immunity. It has been shown that binding C1q, natural ligand gC1qR, on T cells inhibits their proliferation. Here, we demonstrate direct hepatitis C virus (HCV) core to gC1qR leads impaired Lck/Akt activation T-cell function. The HCV associates with surface specifically via as this is inhibited by addition either anti-gC1qR antibody or soluble gC1qR. affinity constant protein for determined BIAcore analysis, 3.8 x...
Hepatitis C virus (HCV) is remarkably efficient at establishing persistent infection, suggesting that it has evolved one or more strategies aimed evading the host immune response. T cell responses, including interferon-gamma production, are severely suppressed in chronic HCV patients. The core protein been previously shown to circulate bloodstream of HCV-infected patients and inhibit immunity through an interaction with gC1qR. To determine role core-gC1qR modulation inflammatory cytokine we...
HCV is remarkable at disrupting human immunity to establish chronic infection. The accumulation of T reg cells the site infection and upregulation inhibitory signaling pathways (such as T‐cell Ig mucin domain protein‐3 ( im‐3) galectin‐9 G al‐9)) play pivotal roles in suppressing antiviral effector eff) that are essential for viral clearance. While im‐3/ al‐9 interactions have been shown negatively regulate eff cells, their role regulating poorly understood. To explore how ‐mediated reg‐cell...
Hepatitis C virus (HCV) is remarkably efficient at evading host immunity to establish chronic infection. During HCV infection, interleukin-12 (IL-12) produced by monocytes/macrophages (M/Mφ) significantly suppressed. Programmed death-1 (PD-1), an inhibitory receptor on immune cells, plays a pivotal role in suppressing T-cell responses during viral To determine whether PD-1 regulates IL-12 production M/Mφ we examined the expressions of PD-1, its ligand PDL-1, and their relationship with from...
ABSTRACT In this study, we demonstrate that killer cell lectin-like receptor subfamily G member 1 (KLRG1), a transmembrane protein preferentially expressed on T cells, is highly CD56 + NK which are significantly reduced in their numbers and functions the peripheral blood of patients with chronic hepatitis C virus (HCV) infection compared to subjects without infection. KLRG1 expression also upregulated healthy cells exposed Huh-7 hepatocytes infected HCV vitro . Importantly, levels inversely...
Myeloid-derived suppressor cells (MDSCs) increase late sepsis immunosuppression and mortality in mice. We reported that microRNA (miR) 21 miR-181b expression Gr1+CD11b+ myeloid progenitors septic MDSCs mice by arresting macrophage dendritic cell differentiation. Here, we report how regulates miR-21 transcription. In vivo vitro binding studies have shown C/EBPα transcription factor, which promotes normal differentiation, binds both miRNA promoters from sham contrast, bind factors Stat3...
Summary T cells play a pivotal role in controlling viral infection; however, the precise mechanisms responsible for regulating T‐cell differentiation and function during infections are incompletely understood. In this study, we demonstrated an expansion of myeloid‐derived suppressor ( MDSC s), particular monocytic s (M‐ s; CD 14 + 33 11b HLA ‐ DR −/low ), patients with chronic hepatitis C virus HCV ) infection. Notably, ‐induced M‐ express high levels phosphorylated signal transducer...
RUNX1 overlapping RNA (RUNXOR) is a long non-coding and plays pivotal role in the differentiation of myeloid cells via targeting runt-related transcription factor 1 (RUNX1). We others have previously reported that myeloid-derived suppressor (MDSCs) expand inhibit host immune responses during chronic viral infections; however, mechanisms responsible for MDSC suppressive functions, particular RUNXOR–RUNX1, remain unclear. Here, we demonstrated RUNXOR expressions are significantly upregulated...
The hallmark of HIV/AIDS is a gradual depletion CD4 T cells. Despite effective control by antiretroviral therapy (ART), significant subgroup people living with HIV (PLHIV) fails to achieve complete immune reconstitution, deemed as non-responders (INRs). mechanisms underlying incomplete cell recovery in PLHIV remain unclear. In this study, cells from were phenotyped and functionally characterized, focusing on their mitochondrial functions. results show that while total are diminished, cycling...
Abstract Background While the majority of COVID‐19 patients fully recover from infection and become asymptomatic, a significant proportion survivors experience broad spectrum symptoms lasting weeks to months post‐infection, phenomenon termed “post‐acute sequelae (PASC).” The aim this study is determine whether inflammatory proteins are dysregulated can serve as potential biomarkers for systemic inflammation in survivors. Methods We determined levels plasma 22 coronavirus disease 2019...