Toll-like receptor 4 and CD11b expressed on microglia coordinate eradication of Candida albicans cerebral mycosis

Medical Sciences Amyloid beta-Peptides CD11b Antigen QH301-705.5 Medical Immunology 610 Diseases CP: Immunology Article 3. Good health Fungal Proteins Toll-Like Receptor 4 Mice Immune System Diseases Mycoses Alzheimer Disease Allergy and Immunology CP: Neuroscience 616 Candida albicans Medical Specialties Medicine and Health Sciences Animals Microglia Biology (General)
DOI: 10.1016/j.celrep.2023.113240 Publication Date: 2023-10-17T09:29:41Z
ABSTRACT
The fungal pathogen Candida albicans is linked to chronic brain diseases such as Alzheimer's disease (AD), but the molecular basis of anti-Candida immunity remains unknown. We show that C. enters mouse from blood and induces two neuroimmune sensing mechanisms involving secreted aspartic proteinases (Saps) candidalysin. Saps disrupt tight junction proteins blood-brain barrier (BBB) permit invasion. also hydrolyze amyloid precursor protein (APP) into β (Aβ)-like peptides bind Toll-like receptor 4 (TLR4) promote killing in vitro while candidalysin engages integrin CD11b (Mac-1) on microglia. Recognition Aβ-like promotes clearance brain, disruption recognition through markedly prolongs cerebral mycosis. Thus, cleared innate immune Saps, Aβ, candidalysin, CD11b.
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