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Author Notes:


Conceptualization: Craig M. Coopersmith, Mandy L. Ford.

Formal analysis: Katherine T. Fay, Deena B. Chihade, Mandy L. Ford.

Funding acquisition: Craig M. Coopersmith, Mandy L. Ford.

Investigation: Katherine T. Fay, Deena B. Chihade, Ching-Wen Chen, Nathan J. Klingensmith, John D. Lyons, Kimberly Ramonell, Zhe Liang.

Project administration: Craig M. Coopersmith, Mandy L. Ford.

Supervision: Craig M. Coopersmith, Mandy L. Ford.

Writing – original draft: Katherine T. Fay, Mandy L. Ford.

Writing – review & editing: John D. Lyons, Craig M. Coopersmith, Mandy L. Ford.

The authors have declared that no competing interests exist.


Research Funding:

This work was supported by funding from the National Institutes of Health (GM104323, GM109779, and GM113228 to MLF and CMC; and GM072808 and GM095442 to CMC).

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.


  • Science & Technology
  • Multidisciplinary Sciences
  • Science & Technology - Other Topics
  • CD43
  • TH1/TH2

Increased mortality in CD43-deficient mice during sepsis


Journal Title:



Volume 13, Number 9


, Pages e0202656-e0202656

Type of Work:

Article | Final Publisher PDF


CD43 is a large transmembrane protein involved in T cell activation. Previous studies of CD43-/-mice in viral models have demonstrated a role for CD43 in Th1/Th2 skewing, activation of Foxp3+ Treg, and T cell apoptosis. However, the role of CD43 during sepsis has never been tested. Thus, we interrogated the role of CD43 during sepsis using a murine cecal ligation and puncture (CLP) model, and found that CD43-/-mice demonstrated significantly worsened mortality compared to B6 mice following CLP. Phenotypic analysis of splenocytes isolated 24 h after septic insult revealed significantly increased apoptosis of central memory cells in both CD4+and CD8+T cell compartments in CD43-/-septic mice compared to WT septic mice. Furthermore, CD43-/-septic mice exhibited a prominent Th2 skewing following sepsis relative to WT septic mice, as evidenced by a significant decrease in the frequency of IL-2+CXCR3+TH1 cells as a significant increase in the frequency of IL-4+CCR4+TH2 cells. Finally, septic CD43-/-animals contained significantly fewer CD25+Foxp3+TRegcells as compared to WT septic animals. Importantly, depleting CD25+Treg eliminated the increased mortality observed in CD43-/-mice. Taken together, these data demonstrate an important role of CD43 in modulating immune dysregulation and mortality following sepsis.

Copyright information:

© 2018 Fay et al.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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