J Immunol
Department of Surgery, Emory University School of Medicine, Atlanta, GA
Published: May 2021
Sepsis induces significant immune dysregulation characterized by lymphocyte apoptosis and alterations in the cytokine milieu. Because cancer patients exhibit a 10-fold greater risk of developing sepsis compared with the general population, we aimed to understand how pre-existing malignancy alters sepsis-induced immune dysregulation. To address this question, we assessed the impact of tumor-specific CD8 T cells on the immune response in a mouse model of cecal ligation and puncture (CLP)-induced sepsis. Tumor-bearing animals containing Thy1.1 tumor-specific CD8 T cells were subjected to CLP, and groups of animals received anti-Thy1.1 mAb to deplete tumor-specific CD8 T cells or isotype control. Results indicated that depleting tumor-specific T cells significantly improved mortality from sepsis. The presence of tumor-specific CD8 T cells resulted in increased expression of the 2B4 coinhibitory receptor and increased apoptosis of endogenous CD8 T cells. Moreover, tumor-specific T cells were not reduced in number in the tumors during sepsis but did exhibit impaired IFN-γ production in the tumor, tumor draining lymph node, and spleen 24 h after CLP. Our research provides novel insight into the mechanisms by which pre-existing malignancy contributes to increased mortality during sepsis.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8121248 | PMC |
http://dx.doi.org/10.4049/jimmunol.2000865 | DOI Listing |
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