# Modulating Post-Stroke Inflammation with FDA-Approved Immunotherapies: A Literature Review

## TL;DR

This paper reviews FDA-approved immunotherapies that could help reduce harmful inflammation after stroke and improve recovery.

## Contribution

The paper systematically reviews FDA-approved immunotherapies for modulating post-stroke inflammation, highlighting their potential and future research directions.

## Key findings

- FDA-approved immunotherapies can target key inflammatory pathways after stroke.
- Microglia and cytokines play critical roles in post-stroke inflammation.
- Future research should focus on optimizing therapy timing and patient selection.

## Abstract

Stroke has been a topic of extensive research due to its debilitating consequences and high mortality. New findings offer a deeper understanding of specific factors that affect post-stroke recovery and identify therapies that may facilitate this process. One such factor is post-stroke neuroinflammation, a complex and time-dependent process in which acute immune responses can cause significant secondary inflammatory damage if the process is prolonged. Microglia are neuronal immune cells that are highly reactive to cytokines in the neuroenvironment and can, in turn, affect the inflammatory cascades that originate after stroke, making them ideal candidates for immunomodulation in the brain. Many FDA-approved immunotherapies have been found to target distinct inflammatory signaling molecules and responders, including IL-6 inhibitors, IL-13 inhibitors, IL-12/IL-23 inhibitors, B-cell modulators, type I interferon inhibitors, CAR T-cell therapy, calcineurin inhibitors, complement inhibitors, and JAK-STAT pathway inhibitors. The FDA-approved immunotherapies discussed in this review demonstrate potential in modulating the immune response after stroke by targeting key inflammatory pathways involved in secondary brain injury. Future research should focus on defining optimal therapeutic windows, identifying suitable patient populations, determining the most appropriate timing of therapy, and targeting specific immune mechanisms to balance the attenuation of harmful inflammation with the preservation of reparative processes.