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This bidirectional communication is mediated by microglia, astrocytes, peripheral immune cells, and the neurovascular unit through cytokines, chemokines, complement proteins, neurotransmitters, and neuropeptides. At the molecular level, pattern-recognition receptors, including Toll-like receptors and nucleotide-binding oligomerization domain-like receptors, activate NF-\u03baB, MAPK, and JAK\u2013STAT signaling. These pathways regulate cytokine production, oxidative stress, cellular metabolism, and glial phenotypes. NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome activation induces caspase-1-dependent maturation of IL-1\u03b2 and IL-18 and promotes pyroptosis, thereby amplifying neuroinflammation. Complement C1q\/C3\u2013CR3 signaling mediates synaptic pruning, whereas C\u2013C motif chemokine ligand 2 (CCL2)\u2013CCR2 signaling promotes leukocyte recruitment and microglial activation. Cytokines and matrix metalloproteinases disrupt endothelial tight junctions and compromise blood\u2013brain barrier integrity. In addition, calcitonin gene-related peptide (CGRP) and substance P activate neuropeptide receptors to drive neurogenic inflammation. Together, these molecular circuits regulate glial activation, immune-cell trafficking, synaptic remodeling, neuronal excitability, vascular function, and cell survival. Their dysregulation contributes to neurodegenerative, neuroinflammatory, psychiatric, neurodevelopmental, and peripheral diseases through the blood\u2013brain barrier, gut\u2013brain axis, and vagus nerve. This Review summarizes how molecular neuroimmune mechanisms drive disease initiation, progression, and heterogeneity, and discusses emerging therapies targeting inflammasomes, complement, chemokine receptors, neuropeptide signaling, and microbiota to advance biomarker-guided, personalized neuroimmune medicine.<\/jats:p>","DOI":"10.1186\/s43556-026-00565-7","type":"journal-article","created":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T13:27:01Z","timestamp":1788960421000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Neuroimmune interactions: from molecular mechanisms to therapeutic targets"],"prefix":"10.1186","volume":"7","author":[{"given":"Yi-hang","family":"Hao","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rong-jia","family":"Shi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ya-ling","family":"Tang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin-hua","family":"Liang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,9,9]]},"reference":[{"key":"565_CR1","doi-asserted-by":"publisher","first-page":"1473","DOI":"10.1161\/strokeaha.122.036946","volume":"53","author":"E Candelario-Jalil","year":"2022","unstructured":"Candelario-Jalil E, Dijkhuizen RM, Magnus T. 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