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Peritoneal cavity is dominated by IFNγ-secreting CXCR3+ Th1 cells.

Zygmunt BM, Groebe L, Guzman CA - PLoS ONE (2011)

Bottom Line: The peritoneal cavity environment also results in an increased percentage of memory cells producing cytokines.Up-regulation of IFNγ production occurs mostly in CXCR3(+) cells considered as Th1, whereas the up-regulation of IL-4 affects mostly in CXCR3(-) cells which are considered as Th2.We conclude that the peritoneal cavity does not change the Th-lineage of the cells, but that domination of this anatomic niche by Th1 cells rather results from preferential migration to this compartment.

View Article: PubMed Central - PubMed

Affiliation: Department of Vaccinology and Applied Microbiology, Helmholtz Centre for Infection Research, Braunschweig, Germany.

ABSTRACT
The chemokine receptor CXCR3, which was shown to take part in many inflammatory processes, is considered as a Th1 specific marker. Here, we show in a mouse model that CXCR3 expressing CD4(+) cells preferentially migrate to the peritoneal cavity under steady-state conditions. The peritoneal cavity milieu leads to an up-regulated expression of CXCR3. However, blocking of known ligands of this chemokine receptor did not alter the preferential migration. The peritoneal cavity environment also results in an increased percentage of memory cells producing cytokines. Up-regulation of IFNγ production occurs mostly in CXCR3(+) cells considered as Th1, whereas the up-regulation of IL-4 affects mostly in CXCR3(-) cells which are considered as Th2. We conclude that the peritoneal cavity does not change the Th-lineage of the cells, but that domination of this anatomic niche by Th1 cells rather results from preferential migration to this compartment.

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The PerC environment results in increased expression of CXCR3 on CD4+ T cells.(A) The expression level of CXCR3 on CD4+ cells from spleen (black line) or PerC (grey area) of BALB/c mice was determined by flow cytometry. (B) CXCR3+ and CXCR3− CD4+ T cells were sorted from Sp of donor BALB/c mice and stained with CFSE. Cells were then adoptively transferred to naïve recipient animals by i.v or i.p. route. After 24 h, cells were re-isolated from spleens or peritoneal cavities and re-stained with an anti-CXCR3 antibody. The expression level of CXCR3 on CFSE+ cells was then analyzed by flow cytometry. The differences were statistically significant at P<0.001 (*), n.s. – not significant.
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pone-0018032-g003: The PerC environment results in increased expression of CXCR3 on CD4+ T cells.(A) The expression level of CXCR3 on CD4+ cells from spleen (black line) or PerC (grey area) of BALB/c mice was determined by flow cytometry. (B) CXCR3+ and CXCR3− CD4+ T cells were sorted from Sp of donor BALB/c mice and stained with CFSE. Cells were then adoptively transferred to naïve recipient animals by i.v or i.p. route. After 24 h, cells were re-isolated from spleens or peritoneal cavities and re-stained with an anti-CXCR3 antibody. The expression level of CXCR3 on CFSE+ cells was then analyzed by flow cytometry. The differences were statistically significant at P<0.001 (*), n.s. – not significant.

Mentions: During our experiments we observed that the expression level of CXCR3 is higher on cells isolated from PerC (Figure 3A) than on Sp cells. There are reports showing that the PerC environment can lead to changes in gene expression profiles [10], expression of surface molecules and homing phenotype of B1 cells [11]. Thus, we decided to evaluate if this is also the case for CD4+ cells, thereby resulting the differences in the expression levels of CXCR3 to an imprinting occurring in the PerC. To this end, we sorted CXCR3+ and CXCR3− CD4+ cells from BALB/c mice and stained them with CFSE. Then, the cells were separately injected to recipient animals by i.v. or i.p. route. After 24 h cells were re-isolated from Sp or PerC of i.v. or i.p. injected animals, and after re-staining they were analyzed by flow cytometry. The obtained results showed that CXCR3 is up-regulated on CXCR3+ cells which are exposed to the PerC environment (Figure 3B). However, there was no statistically significant difference in CXCR3 expression between CXCR3− cells isolated from Sp and PerC (Figure 3C). We conclude that the PerC environment increases the expression level of CXCR3 on CD4+ cells positive for this molecule, but it does not affect the frequency of CXCR3+ CD4+ cells.


Peritoneal cavity is dominated by IFNγ-secreting CXCR3+ Th1 cells.

Zygmunt BM, Groebe L, Guzman CA - PLoS ONE (2011)

The PerC environment results in increased expression of CXCR3 on CD4+ T cells.(A) The expression level of CXCR3 on CD4+ cells from spleen (black line) or PerC (grey area) of BALB/c mice was determined by flow cytometry. (B) CXCR3+ and CXCR3− CD4+ T cells were sorted from Sp of donor BALB/c mice and stained with CFSE. Cells were then adoptively transferred to naïve recipient animals by i.v or i.p. route. After 24 h, cells were re-isolated from spleens or peritoneal cavities and re-stained with an anti-CXCR3 antibody. The expression level of CXCR3 on CFSE+ cells was then analyzed by flow cytometry. The differences were statistically significant at P<0.001 (*), n.s. – not significant.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3138734&req=5

pone-0018032-g003: The PerC environment results in increased expression of CXCR3 on CD4+ T cells.(A) The expression level of CXCR3 on CD4+ cells from spleen (black line) or PerC (grey area) of BALB/c mice was determined by flow cytometry. (B) CXCR3+ and CXCR3− CD4+ T cells were sorted from Sp of donor BALB/c mice and stained with CFSE. Cells were then adoptively transferred to naïve recipient animals by i.v or i.p. route. After 24 h, cells were re-isolated from spleens or peritoneal cavities and re-stained with an anti-CXCR3 antibody. The expression level of CXCR3 on CFSE+ cells was then analyzed by flow cytometry. The differences were statistically significant at P<0.001 (*), n.s. – not significant.
Mentions: During our experiments we observed that the expression level of CXCR3 is higher on cells isolated from PerC (Figure 3A) than on Sp cells. There are reports showing that the PerC environment can lead to changes in gene expression profiles [10], expression of surface molecules and homing phenotype of B1 cells [11]. Thus, we decided to evaluate if this is also the case for CD4+ cells, thereby resulting the differences in the expression levels of CXCR3 to an imprinting occurring in the PerC. To this end, we sorted CXCR3+ and CXCR3− CD4+ cells from BALB/c mice and stained them with CFSE. Then, the cells were separately injected to recipient animals by i.v. or i.p. route. After 24 h cells were re-isolated from Sp or PerC of i.v. or i.p. injected animals, and after re-staining they were analyzed by flow cytometry. The obtained results showed that CXCR3 is up-regulated on CXCR3+ cells which are exposed to the PerC environment (Figure 3B). However, there was no statistically significant difference in CXCR3 expression between CXCR3− cells isolated from Sp and PerC (Figure 3C). We conclude that the PerC environment increases the expression level of CXCR3 on CD4+ cells positive for this molecule, but it does not affect the frequency of CXCR3+ CD4+ cells.

Bottom Line: The peritoneal cavity environment also results in an increased percentage of memory cells producing cytokines.Up-regulation of IFNγ production occurs mostly in CXCR3(+) cells considered as Th1, whereas the up-regulation of IL-4 affects mostly in CXCR3(-) cells which are considered as Th2.We conclude that the peritoneal cavity does not change the Th-lineage of the cells, but that domination of this anatomic niche by Th1 cells rather results from preferential migration to this compartment.

View Article: PubMed Central - PubMed

Affiliation: Department of Vaccinology and Applied Microbiology, Helmholtz Centre for Infection Research, Braunschweig, Germany.

ABSTRACT
The chemokine receptor CXCR3, which was shown to take part in many inflammatory processes, is considered as a Th1 specific marker. Here, we show in a mouse model that CXCR3 expressing CD4(+) cells preferentially migrate to the peritoneal cavity under steady-state conditions. The peritoneal cavity milieu leads to an up-regulated expression of CXCR3. However, blocking of known ligands of this chemokine receptor did not alter the preferential migration. The peritoneal cavity environment also results in an increased percentage of memory cells producing cytokines. Up-regulation of IFNγ production occurs mostly in CXCR3(+) cells considered as Th1, whereas the up-regulation of IL-4 affects mostly in CXCR3(-) cells which are considered as Th2. We conclude that the peritoneal cavity does not change the Th-lineage of the cells, but that domination of this anatomic niche by Th1 cells rather results from preferential migration to this compartment.

Show MeSH
Related in: MedlinePlus