# Neutrophil–Galectin-9 Axis Linking Innate and Adaptive Immunity in ATL, Sézary Syndrome, COVID-19, and Psoriasis: An AI-Assisted Integrative Review

## TL;DR

This paper explores how neutrophils and Galectin-9 connect innate and adaptive immunity in diseases like ATL, Sézary syndrome, COVID-19, and psoriasis using AI-assisted analysis.

## Contribution

It identifies a recurring neutrophil–Galectin-9 regulatory module across multiple diseases using AI-driven literature synthesis.

## Key findings

- Neutrophils show persistent activation and elevated Gal-9 expression across all studied conditions.
- Neutrophil-derived Gal-9 links innate hyperactivation to T-cell exhaustion and IL-17-driven inflammation in COVID-19 and psoriasis.
- AI-assisted synthesis combined with expert validation reveals unifying immunological mechanisms and potential therapeutic targets.

## Abstract

Beyond their traditional role as short-lived antimicrobial cells, neutrophils are increasingly recognized as key regulators of adaptive immunity and tumor progression. This AI-assisted integrative review investigated the neutrophil–T-cell axis, particularly the role of Galectin-9 (Gal-9), across adult T-cell leukemia/lymphoma (ATL), Sézary syndrome (SS), coronavirus disease 2019 (COVID-19), and psoriasis. Leveraging AI tools (GPT-5 and Adobe Acrobat AI Assistant) for literature synthesis (2000–2025) and expert validation, we aimed to identify common immunological mechanisms. Across all conditions, neutrophils displayed persistent activation, elevated Gal-9 expression, and modulated T-cell interactions. In ATL and SS, neutrophilia correlated with poor survival and TCR signaling dysregulation, suggesting Gal-9-mediated immune modulation. In COVID-19 and psoriasis, neutrophil-derived Gal-9-linked innate hyperactivation to T-cell exhaustion and IL-17-driven inflammation. These findings define a recurring neutrophil–Gal-9 regulatory module connecting innate and adaptive immune responses. This study underscores the feasibility of combining AI-driven literature synthesis with expert review to identify unifying immunological mechanisms and therapeutic targets across malignancy and inflammation.