CD7 regulates the persistence of terminally exhausted CD8+ T cells during chronic infection
Year: 2025
Type: article
Abstract: CD8 + T cell exhaustion limits immune responses during cancer and chronic infection. We identify CD7 as a tissue-specific regulator of terminally exhausted CD8 + T cells during chronic infection. CD7 expression progressively increases during exhaustion, reaching its highest levels on a subset of CD101 + Tim3 low terminally exhausted cells that arise in the liver. Transcriptomic analysis revealed that CD7-deficient terminally exhausted cells display altered expression of co-stimulatory, translational, and effector genes, correlating with markedly reduced persistence and increased apoptotic susceptibility. Importantly, CD7 is preferentially upregulated on PD-1 + CD39 + tumor-infiltrating lymphocytes in human head and neck squamous cell carcinoma, suggesting that CD7 may play a conserved role in promoting exhausted T cell survival. These findings reveal a function for CD7 in sustaining terminally exhausted CD8 + T cells and demonstrate that CD7 signaling is a critical regulator of T cell persistence during chronic infection.
Source: Cell Reports
Authors: Sean Hyslop, Colby J. Hofferek, Maria V. Stegantseva, Emerald Kan, Kelli A. McCord, Victor M. Alvarez, Amanda Y. Xia, Jacob P. Conarty, Andreas Wieland, William H. Hudson
Language: English
Topic: T-cell and B-cell Immunology
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $5,620
Awards: G251813993, G2727974149, G3102002109, Engineering bZIP family transcription factors for therapeutic T-cell persistence and effector function, G418187648, G4707044273, G4964878375, G5241867077, G5628162970, G863484009, G9000043858, Baylor College of Medicine Cancer Center - Cancer Center Support Grant
OpenAlex ID: W4414382640