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Life sciences · Journal article
Frontiers in Neuroscience · October 9, 2026
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Spontaneous intracerebral hemorrhage (ICH) is a devastating cerebrovascular disorder associated with high mortality, severe disability, and substantial clinical burden. Stroke-associated pneumonia (SAP), one of the most common infectious complications after stroke, is increasingly recognized as a major contributor to mortality and poor neurological outcomes after ICH. Emerging evidence from studies of stroke-induced immunosuppression and the lung–brain axis suggests that SAP is not merely a secondary pulmonary complication, but rather a multifactorial consequence of central nervous system injury, peripheral immune remodeling, and impaired pulmonary host defense. Among these processes, T cells serve as a critical immunological relay between the central nervous system and peripheral immunity. During the acute phase of ICH, pro-inflammatory T-cell subsets infiltrate the injured brain and amplify neuroinflammation, blood–brain barrier disruption, cerebral edema, and neuronal injury. As the disease progresses, T-cell hyporesponsiveness and suppression of Th1/Th17-mediated antimicrobial immunity may increase increase susceptibility to SAP. Once SAP develops, pulmonary inflammation, microbiota dysbiosis, bacterial products, and systemic inflammatory mediators may further aggravate central immune dysregulation through the lung–brain axis, thereby establishing a vicious cycle involving ICH, T-cell dysfunction, SAP, and secondary brain injury. This review summarizes the temporal dynamics, trafficking patterns, and functional transitions of T-cell subsets after ICH, with particular emphasis on their potential roles in the bidirectional interactions between SAP and the injured brain along through the lung–brain axis. A better understanding of this T-cell-centered network may reveal potential targets for preventing SAP, restoring post-ICH immune homeostasis, and attenuating secondary neurological injury.