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Research publication by Dr. Vladimir Badovinac's research group earns press release

Dr. Badovinac’s laboratory
Pictured left to right:  Derek Danahy, Isaac Jensen, Dr. Scott Anthony and Dr. Vladimir Badovinac

A recent manuscript published in PLOS Pathogens by Dr. Badovinac’s laboratory has been highlighted by the journal and selected for a press release. The study is titled Polymicrobial sepsis impairs bystander recruitment of effector cells to infected skin despite optimal sensing and alarming function of skin resident memory CD8 T cells. The first author is Derek Danahy, a graduate student in the laboratory, and contributors are Dr. Scott Anthony, Isaac Jensen, Stacey Hartwig, Dr. Qiang Shan, Dr. Hai-Hui Xue, Dr. John Harty and Dr. Thomas Griffith, in addition to Dr. Badovinac. A summary of the key findings is below.


Press Release

Sepsis impairs previously-immunized hosts protection to secondary skin infections

Infections are generally contained in host barrier tissues, however, infectious pathogens can enter the bloodstream resulting in a septic state that results in tissue damage and death. Despite clearance of the septic pathogen, patients often display increased susceptibility to secondary infections resulting from sepsis-induced numerical and functional changes in the immune response. Previously, we and others have shown that sepsis reduces the quantity (number) and quality (functional capacity) of memory CD8 T cells within the host, contributing to the state of immunoparalysis after sepsis onset. Our study in PLoS Pathogens directly examined sepsis impact on tissue resident memory CD8 T cells (TRM) restricted to barrier tissues and provide rapid protection to localized infections in a non-septic environment. In contrast to memory T cells found within lymphoid tissues, the number and function of TRM in non-lymphoid peripheral tissue (such as skin) was maintained during sepsis suggesting a protective position for memory CD8 T cells within barrier tissues of septic hosts. However, the capacity of TRM to provide protection upon skin re-infection was greatly diminished in septic hosts, which we attributed to a sepsis-induced defect in TRM-extrinsic factors. Thus, our report further supports the notion that therapeutic attempts designed to rescue number and function of CD8 T cells may not be sufficient to fully restore the protective capacity of TRM, if sepsis-induced lesions in T cell-extrinsic factors are not therapeutically treated as well.