The source of TAFA4 and its role in CNS immune cell recruitment during neuroinflammation

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Presentation Time: 08:30 AM - 08:45 AM
Abstract ID: 4215 - B

Presenting Author:
Hwa-Sung Tso , research assistant at Natl. Taiwan Univ. Col. of Med.

Abstract:

TAFA4, also known as Fam19a4, has been reported to be secreted by C-low-threshold mechanoreceptors (C-LTMRs) and alleviate mechanical pain hypersensitivity. However, its immunological function in the central nervous system (CNS) remains incompletely understood. Our study aims to elucidate the wider source of TAFA4 in the CNS and its role in CNS inflammation. We generated lines of TAFA4-knockout (KO)-reporter mice, wherein the TAFA4 gene is deleted and replaced with a membrane-bound green fluorescent protein (GFP) and secretable nano-luciferase. We discovered that TAFA4 expression extended beyond C-LTMRs, encompassing neurons in the habenula-fasciculus retroflexus, hypothalamus, and olfactory bulb. Notably, the kinetics of TAFA4 expression followed a decreased trend during EAE-induced inflammation by nano-luciferase assay. Furthermore, we showed that mice with TAFA4 deficiency exhibited diminished immune cell infiltration and reduced demyelination in the spinal cord after EAE induction. These results underscore the involvement of TAFA4 in pro-inflammatory responses during EAE pathogenesis. Additionally, we showed that TAFA4 acted with chemoattractant properties towards M1 macrophages and neutrophils but not T cells by trans-well analysis. In summary, our study revealed the diverse sources of TAFA4 within the CNS and unveiled its inflammatory role during EAE inflammation. We propose that TAFA4 is potentially involved in CNS immune cell recruitment and inflammation.