Abstract
γδ T cells express several different toll-like receptor (TLR)s. The role of MyD88-dependent TLR signaling in TCR activation of murine γδ T cells is incompletely defined. Here, we report that Pam3CSK4 (PAM, TLR2 agonist) and CL097 (TLR7 agonist), but not lipopolysaccharide (TLR4 agonist), increased CD69 expression and Th1-type cytokine production upon anti-CD3 stimulation of γδ T cells from young adult mice (6-to 10-week-old). However, these agonists alone did not induce γδ T cell activation. Additionally, we noted that neither PAM nor CL097 synergized with anti-CD3 in inducing CD69 expression on γδ T cells of aged mice (21-to 22-month-old). Compared to young γδ T cells, PAM and CL097 increased Th-1 type cytokine production with a lower magnitude from anti-CD3-stimulated, aged γδ T cells. Vγ1+and Vγ4+cells are two subpopulations of splenic γδ T cells. PAM had similar effects in anti-CD3-Activated control and Vγ4+subset-depleted γδ T cells; whereas CL097 induced more IFN-γ production from Vγ4+subset-depleted γδ T cells than from the control group. Finally, we studied the role of MyD88-dependent TLRs in γδ T cell activation during West Nile virus (WNV) infection. γδ T cell, in particular, Vγ1+subset expansion was significantly reduced in both MyD88-And TLR7-deficient mice. Treatment with TLR7 agonist induced more Vγ1+cell expansion in wild-type mice during WNV infection. In summary, these results suggest that MyD88-dependent TLRs provide co-stimulatory signals during TCR activation of γδ T cells and these have differential effects on distinct subsets.
| Original language | English (US) |
|---|---|
| Article number | A1350 |
| Journal | PLoS One |
| Volume | 9 |
| Issue number | 9 |
| DOIs | |
| State | Published - Sep 18 2014 |
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ASJC Scopus subject areas
- Agricultural and Biological Sciences(all)
- Biochemistry, Genetics and Molecular Biology(all)
- Medicine(all)
Cite this
The co-stimulatory effects of MyD88-dependent toll-like receptor signaling on activation of murine γδ T Cells. / Zhang, Jinping; Wang, Jia; Pang, Lan; Xie, Guorui; Welte, Thomas; Saxena, Vandana; Wicker, Jason; Mann, Brian; Soong, Lynn; Barrett, Alan; Born, Willi; O'Brien, Rebecca; Wang, Tian.
In: PLoS One, Vol. 9, No. 9, A1350, 18.09.2014.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The co-stimulatory effects of MyD88-dependent toll-like receptor signaling on activation of murine γδ T Cells
AU - Zhang, Jinping
AU - Wang, Jia
AU - Pang, Lan
AU - Xie, Guorui
AU - Welte, Thomas
AU - Saxena, Vandana
AU - Wicker, Jason
AU - Mann, Brian
AU - Soong, Lynn
AU - Barrett, Alan
AU - Born, Willi
AU - O'Brien, Rebecca
AU - Wang, Tian
PY - 2014/9/18
Y1 - 2014/9/18
N2 - γδ T cells express several different toll-like receptor (TLR)s. The role of MyD88-dependent TLR signaling in TCR activation of murine γδ T cells is incompletely defined. Here, we report that Pam3CSK4 (PAM, TLR2 agonist) and CL097 (TLR7 agonist), but not lipopolysaccharide (TLR4 agonist), increased CD69 expression and Th1-type cytokine production upon anti-CD3 stimulation of γδ T cells from young adult mice (6-to 10-week-old). However, these agonists alone did not induce γδ T cell activation. Additionally, we noted that neither PAM nor CL097 synergized with anti-CD3 in inducing CD69 expression on γδ T cells of aged mice (21-to 22-month-old). Compared to young γδ T cells, PAM and CL097 increased Th-1 type cytokine production with a lower magnitude from anti-CD3-stimulated, aged γδ T cells. Vγ1+and Vγ4+cells are two subpopulations of splenic γδ T cells. PAM had similar effects in anti-CD3-Activated control and Vγ4+subset-depleted γδ T cells; whereas CL097 induced more IFN-γ production from Vγ4+subset-depleted γδ T cells than from the control group. Finally, we studied the role of MyD88-dependent TLRs in γδ T cell activation during West Nile virus (WNV) infection. γδ T cell, in particular, Vγ1+subset expansion was significantly reduced in both MyD88-And TLR7-deficient mice. Treatment with TLR7 agonist induced more Vγ1+cell expansion in wild-type mice during WNV infection. In summary, these results suggest that MyD88-dependent TLRs provide co-stimulatory signals during TCR activation of γδ T cells and these have differential effects on distinct subsets.
AB - γδ T cells express several different toll-like receptor (TLR)s. The role of MyD88-dependent TLR signaling in TCR activation of murine γδ T cells is incompletely defined. Here, we report that Pam3CSK4 (PAM, TLR2 agonist) and CL097 (TLR7 agonist), but not lipopolysaccharide (TLR4 agonist), increased CD69 expression and Th1-type cytokine production upon anti-CD3 stimulation of γδ T cells from young adult mice (6-to 10-week-old). However, these agonists alone did not induce γδ T cell activation. Additionally, we noted that neither PAM nor CL097 synergized with anti-CD3 in inducing CD69 expression on γδ T cells of aged mice (21-to 22-month-old). Compared to young γδ T cells, PAM and CL097 increased Th-1 type cytokine production with a lower magnitude from anti-CD3-stimulated, aged γδ T cells. Vγ1+and Vγ4+cells are two subpopulations of splenic γδ T cells. PAM had similar effects in anti-CD3-Activated control and Vγ4+subset-depleted γδ T cells; whereas CL097 induced more IFN-γ production from Vγ4+subset-depleted γδ T cells than from the control group. Finally, we studied the role of MyD88-dependent TLRs in γδ T cell activation during West Nile virus (WNV) infection. γδ T cell, in particular, Vγ1+subset expansion was significantly reduced in both MyD88-And TLR7-deficient mice. Treatment with TLR7 agonist induced more Vγ1+cell expansion in wild-type mice during WNV infection. In summary, these results suggest that MyD88-dependent TLRs provide co-stimulatory signals during TCR activation of γδ T cells and these have differential effects on distinct subsets.
UR - http://www.scopus.com/inward/record.url?scp=84907218079&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84907218079&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0108156
DO - 10.1371/journal.pone.0108156
M3 - Article
C2 - 25232836
AN - SCOPUS:84907218079
VL - 9
JO - PLoS One
JF - PLoS One
SN - 1932-6203
IS - 9
M1 - A1350
ER -