Central role of B cells in interleukin-23 dependent neuroinflammation in the GF-IL23 model. Issue 13 (18th July 2022)

• Record Type: Journal Article
• Authors: Nitsch, Louisa; Petzinna, Simon; Zimmermann, Julian; Getts, Daniel R.; Becker, Albert; Müller, Marcus
• Is Part Of: NeuroReport. Volume 33:Issue 13(2022)
• Page Start: 577
• Page End: 582
• Publication Date: 2022-07-18
• Subjects: B cells -- interleukin 23 -- neuroinflammation; Neurosciences -- Periodicals; Nervous system -- Periodicals; Neurophysiology -- Periodicals; Nervous System Diseases -- Periodicals; Nervous System Physiological Phenomena -- Periodicals; Neurosciences -- Periodicals; 616.805
• DOI: 10.1097/WNR.0000000000001818
• Languages: English
• ISSNs: 0959-4965

Abstract

Abstract : Interleukin (IL)-23 is one of the critical cytokines in autoimmune neuroinflammation. To further clarify the local function of IL-23 on the course of neuroinflammation, we recently established a transgenic mouse model with astrocyte-specific expression of IL-23 (GF-IL23). The GF-IL23 mice spontaneously developed a progressive ataxic phenotype with cerebellar infiltration with high amounts of B cells most prominent in the subarachnoid and perivascular space. To enlighten the B cell role in GF-IL23 mice, we generated GF-IL23 mice on a B cell knockout (k.o.) background (GF-IL23 B cell k.o. ). GF-IL23 B cell k.o. mice compared with GF-IL23 mice had no infiltrates or only minor infiltration, and no antibody deposition was detected in the cerebellum. Furthermore, microglia, astrocyte activation, hypervascularization and demyelination were reduced in GF-IL23 B cell k.o. mice compared with GF-IL23 mice. Cytokines and chemokine receptors like IL-12a, cerebrospinal fluid 2 and CXCR3 were downregulated. Our study indicates that B cells are essential in IL-23–dependent neuroinflammation in the GF-IL23 model.