RT Journal Article
SR Electronic
T1 γδ T cells do not contribute to peripheral inflammatory pain
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 390294
DO 10.1101/390294
A1 Jelena Petrović
A1 Jaqueline Raymondi Silva
A1 Julia P. Segal
A1 Abigail S. Marshall
A1 Cortney M. Haird
A1 Ian Gilron
A1 Nader Ghasemlou
YR 2018
UL http://biorxiv.org/content/early/2018/08/13/390294.abstract
AB Circulating immune cells, which are recruited to the site of injury/disease, secrete various inflammatory mediators that are critical to nociception and pain. The role of tissue-resident immune cells, however, remains poorly characterized. One of the first cells to be activated in peripheral tissues following injury are γδ T cells, which serve important roles in infection and disease. Using a transgenic mouse line lacking these cells, we sought to identify their contribution to inflammatory pain. Three distinct models of inflammatory pain were used: intraplantar injection of formalin and incisional wound (as models of acute inflammatory pain) and intraplantar injection of complete Freund’s adjuvant (as a model of chronic inflammatory pain). Our results show that absence of these cells does not alter baseline sensitivity, nor does it result in changes to mechanical or thermal hypersensitivity after tissue injury. These results were consistent in both male and female mice, suggesting that there are no sex differences in these outcomes. This comprehensive characterization suggests that γδ T cells do not contribute to basal sensitivity or the development and maintenance of inflammatory pain.This work was supported by grants from the Canadian Institutes of Health Research, the J. P. Bickell Foundation, and Queen’s University to NG. The authors thank Dr. Michael D. Kawaja for technical support.