Experimental autoimmune encephalomyelitis revealed tafta4's role in promoting macrophage and neutrophil recruitment, suggesting its relevance in neuroinflammation.
Description TAFA4, also known as Fam19a4, is a neuropeptide secreted by C-low-threshold mechanoreceptors (C-LTMRs) and has been reported to attenuate inflammation-induced mechanical hypersensitivity. However, its immunological role in the central nervous system (CNS) remains unclear. We found that TAFA4 is predominantly expressed in the CNS, including C-LTMRs, the habenula-fasciculus retroflexus, hypothalamus, and olfactory bulb. In experimental autoimmune encephalomyelitis (EAE), TAFA4-knockout (TAFA4-/-) mice exhibited reduced disease severity, characterized by decreased immune cell infiltration and demyelination in the spinal cord, suggesting a pro-inflammatory role for TAFA4 in EAE progression. Further analysis revealed that TAFA4 promotes the recruitment of monocytes, macrophages, and neutrophils—but not CD4+ T cells—via the formyl peptide receptor 1 (Fpr1), as shown by in vitro migration assays. Intraperitoneal injection of TAFA4 also recruited neutrophils within 5 hours. Additionally, TAFA4 treatment increased Akt, Erk, and Fak phosphorylation in macrophages, highlighting its role in chemotaxis and inflammatory signaling. In conclusion, our study identifies a novel mechanism by which TAFA4 exacerbates neuroinflammation by promoting immune cell migration in CNS diseases, such as multiple sclerosis. Funding Sources X Topic Categories Neuroimmunology (NEUR)
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Yeh et al. (2025) studied this question.
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