A5089500092- Immunodeficiency and Autoimmune Disorders
- T-cell and B-cell Immunology
- Immune Cell Function and Interaction
- Fungal Infections and Studies
- Antifungal resistance and susceptibility
- Mycobacterium research and diagnosis
- Infectious Diseases and Mycology
- Atherosclerosis and Cardiovascular Diseases
- Monoclonal and Polyclonal Antibodies Research
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Liver physiology and pathology
- Tuberculosis Research and Epidemiology
- Complement system in diseases
- Actinomycetales infections and treatment
- interferon and immune responses
- Renal Diseases and Glomerulopathies
- Cell Adhesion Molecules Research
- Systemic Lupus Erythematosus Research
- Neonatal Respiratory Health Research
- Medical Imaging and Pathology Studies
- Vasculitis and related conditions
- Blood disorders and treatments
- Protease and Inhibitor Mechanisms
- melanin and skin pigmentation
- Pneumocystis jirovecii pneumonia detection and treatment
Chang Gung University
2015-2025
National Taiwan University
2019
Neutralizing anti-interferon-γ autoantibody (nAIGA)-associated immunodeficiency is an emerging medical issue worldwide. In the present study, we describe and discuss clinical features outcomes of patients with nAIGAs disseminated infections by nontuberculous mycobacteria (dNTM). We thoroughly reviewed records all patients. Microorganisms were identified using previously described methods modifications. All data calculated analyzed SPSS software. Among 46 adult dNTM infections, 45 cases...
Talaromyces marneffei causes life-threatening opportunistic infections, mainly in Southeast Asia and South China. T. infects patients with human immunodeficiency virus (HIV) but also individuals without known immunosuppression. Here we investigated the involvement of anti–IFN-γ autoantibodies severe infections HIV-negative patients. We enrolled 58 adults who were otherwise healthy. found a high prevalence neutralizing (94.8%) this cohort. The presence was strongly associated HLA-DRB1*16:02...
Anti-interferon (IFN)–γ autoantibodies (AIGAs) are a pathogenic factor in late-onset immunodeficiency with disseminated mycobacterial and other opportunistic infections. AIGAs block IFN-γ function, but their effects on signaling unknown. Using single-cell capture method, we isolated 19 IFN-γ–reactive monoclonal antibodies (mAbs) from patients AIGAs. All displayed high-affinity (KD < 10−9 M) binding to IFN-γ, only eight neutralized IFN-γ–STAT1 HLA-DR expression. Signal blockade...
Neutralizing anti–interferon-γ (IFN-γ) autoantibodies (nAIGAs) impair IFN-γ–mediated immunity, predisposing patients with nAIGAs to infection by nontuberculous mycobacteria, Talaromyces marneffei , and other intracellular pathogens. Current clinical management relies on continuous antimicrobial therapy, no treatment offering sustained benefits. Here, we developed human chimeric autoantibody receptor (CAAR) T cells targeting autoreactive B expressing nAIGA cell receptors (BCRs) using an IFN-γ...
Dysregulation of pericellular proteolysis usually accounts for cancer cell invasion and metastasis. Isolation a cell-surface protease system lung metastasis is an important issue mechanistic studies therapeutic target identification. Immunohistochemistry tissue array (n = 64) TCGA database 255) were employed to assess the correlation between serine inhibitors (SPIs) adenocarcinoma progression. The role SPI in motility was examined using transwell assays. Pulldown LC/MS/MS performed identify...
Abstract Pathogenic GM-CSF autoantibodies are found in over 90% of people with pulmonary alveolar proteinosis (PAP), a rare autoimmune disease surfactant lipoprotein accumulating alveoli spaces. However, more and have also been identified without PAP phenotype but underlying severe central nervous system (CNS)-involved Cryptococcus gattii or Nocardia spp. infection since 2013, highlighting the pathogenic mechanisms that might differ between individual diseases. We developed single B cell...
Abstract Primary membranous nephropathy (pMN) is an autoimmune disease associated with autoantibody-mediated immune complexes and the deposition of activated complement proteins on glomerulus. The phospholipase A2 receptor 1 (PLA2R) has been identified as a major antigen for autoantibodies in 80% pMN patients. Antibodies IgG1 IgG3, but not IgG4, can activate complement. Unexpectedly, patients, PLA2R are IgG4 predominance, those IgG3 less abundant affected tissues, arguing role pathologies...