Deficit Schizophrenia Is Characterized by Defects in IgM-Mediated Responses to Tryptophan Catabolites (TRYCATs): a Paradigm Shift Towards Defects in Natural Self-Regulatory Immune Responses Coupled with Mucosa-Derived TRYCAT Pathway Activation

摘要: Deficit schizophrenia is accompanied by mucosa-associated activation of the tryptophan catabolite (TRYCAT) pathway, as indicated increased IgA responses to noxious (NOX) TRYCATs, but not regulatory or protective (PRO) suggesting neurotoxic, excitotoxic, inflammatory, and oxidative potential. No previous studies examined IgM-mediated autoimmune TRYCAT pathway in deficit versus nondeficit schizophrenia. We measured IgM NOX namely, quinolinic acid (QA), 3-OH-kynurenine (3HK), picolinic (PA), xanthurenic (XA) acid, PRO including kynurenic (KA) anthranilic (AA), 40 healthy controls schizophrenic patients. computed (QA + PA 3HK XA)/PRO (AA KA) ratio ∆ differences - values NOX/PRO ratio. characterized significantly attenuated all TRYCATs highly ∆IgA compared controls. The negative symptoms are positively associated with directed against KA/3HK findings support view that a distinct subtype may be discriminated from specific defect isotype-mediated pathway. Lowered together mucosa-derived contribute neuroprogression, symptoms, All all, compensatory (anti-)inflammatory reflex system (CIRS), natural responses, underpin