Semaphorins as Drivers of Inflammatory Disease: Setting Immune Cells in Motion
A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Immunology".
Deadline for manuscript submissions: 3 October 2026 | Viewed by 18
Special Issue Editor
Interests: inflammation; innate immunity; chemotatic cues; microvasculature
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Semaphorins serve as integral modulators of inflammation, exerting precise control over both the acute‑phase response and the resolution phase through coordinated signaling that influences immune cell behavior and tissue homeostasis. Inflammation remains a pervasive driver of disease—from autoimmune syndromes and metabolic disorders to neurodegeneration—creating a substantial global health burden characterized by chronic morbidity and high societal costs. Recent insights reveal that semaphorins fine-tune key cellular processes, including directing cell polarization, adhesion dynamics, chemotactic migration, extracellular matrix remodeling, immune cell infiltration, repulsion signaling, apoptosis, and even axonal growth-cone guidance. Their spatial and temporal regulation functions as molecular switches that either propagate inflammatory cascades or restore tissue equilibrium. Central signaling axes have emerged such as the Sema7A–Plexin C1–integrin β1 pathway, which increases endothelial permeability and inflammatory activation—and Sema3E–Plexin D1, which impairs macrophage egress in atherosclerotic plaques via modulation of cytoskeletal, integrin and PI3K signaling alongside Semaphorin 5A activation of PI3K–AKT–mTOR through Plexin‑A1/B3 in synovial fibroblasts, promoting cytokine release, proliferation, migration and survival. Other family members, including various class‑3 semaphorins, regulate PI3K/Akt upstream and downstream pathways and even modulate PTEN activity depending on receptor context. These nodes underscore the therapeutic relevance of ITGA1/integrin signaling, Plexin B1 and C1 receptors, VEGF/neuropilin interfaces, PI3K–AKT axis regulation, and PTEN‑mediated suppression.
Built on this mechanistic foundation, this Special Issue calls for deeper dissection of semaphorin signaling at cell‑type and spatially resolved levels—especially using spatial transcriptomics and single‑cell approaches—to define how tightly regulated semaphorin–plexin/neuropilin engagement orchestrates transitions from inflammation to resolution. The goal is not merely mapping pathways, but leveraging them toward therapeutic modulation. This Special Issue will focus on reaching readers willing to target semaphorin‑dependent crosstalk or receptor‑specific axes—to restore homeostasis and improve care in inflammatory conditions with precision, mechanistic sophistication, and clinical impact.
Dr. Tiago Granja
Guest Editor
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Keywords
- semaphorins
- inflammation
- neuronal guidance proteins
- soluble guidance cues
- cell motility
- cytoskeletal dynamics
- extracellular matrix
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