A5014009392- Complement system in diseases
- Fungal Infections and Studies
- Renal Diseases and Glomerulopathies
- Infectious Diseases and Mycology
- Actinomycetales infections and treatment
- Immune Cell Function and Interaction
- Vasculitis and related conditions
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- T-cell and B-cell Immunology
- Immunodeficiency and Autoimmune Disorders
- Antifungal resistance and susceptibility
Chang Gung University
2022-2024
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...
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...