Keeping the peace: commensal Cutibacterium acnes trains CD4+ TH17 cells to trap and kill
Diane M. Thiboutot and Amanda M. Nelson
Department of Dermatology, Penn State College of Medicine and Hershey Medical Center, Hershey, Pennsylvania, USA.
Address correspondence to: Amanda Nelson, Penn State University College of Medicine, Department of Dermatology HU14, 500 University Drive, Hershey, Pennsylvania 17033, USA. Phone: 717.531.0003 ext. 284512; Email: anelson@pennstatehealth.psu.edu.
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Department of Dermatology, Penn State College of Medicine and Hershey Medical Center, Hershey, Pennsylvania, USA.
Address correspondence to: Amanda Nelson, Penn State University College of Medicine, Department of Dermatology HU14, 500 University Drive, Hershey, Pennsylvania 17033, USA. Phone: 717.531.0003 ext. 284512; Email: anelson@pennstatehealth.psu.edu.
Find articles by Nelson, A. in: JCI | PubMed | Google Scholar
Published January 19, 2021 - More info
J Clin Invest. 2021;131(2):e145379. https://doi.org/10.1172/JCI145379.
© 2021 American Society for Clinical Investigation
Commensal or pathogenic bacterial communities of the skin interact with the host immune system to preserve homeostasis or sustain disease. In this issue of the JCI, Agak et al. substantially advance our conceptual understanding of TH17 cell biology. The researchers identified IL-26–independent mechanisms by which CD4+ TH17 clones directly kill bacteria. These CD4+ TH17 clones share antimicrobial properties with cytotoxic T cells and granulocytes as evidenced by secretion of granulysin, granzyme B, and histone-laden DNA extracellular traps. Interestingly, these clones emerged following monocyte education by Cutibacterium acnes strains associated with healthy skin, but not those associated with acne. Overall, the antimicrobial mechanisms employed by these TH17 subsets suggest a unique link between innate and adaptive immune responses.
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