Possible bases for this interaction remain speculative; poststroke depression may be associated with central nervous system (CNS) inflammation that could exacerbate IL-17 expression by T cells when they infiltrate the brain and/or with neurotrophic/neuroprotective deficits that might impair neural resilience to IL-17 mediated neurodegenerative pathways [26]. Here, IL17A is linked to depressive symptom measurement.