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Fonsecaea pedrosoi-induced Th17-cell differentiation in mice is fostered by Dectin-2 and suppressed by Mincle recognition.

Wüthrich M, Wang H, Li M, Lerksuthirat T, Hardison SE, Brown GD, Klein B - Eur. J. Immunol. (2015)

Bottom Line: Here, we investigated whether costimulation by TLR agonists fosters the development of adaptive immune responses, by examining the development of fungus-specific T cells.Subcutaneous infection of mice with F. pedrosoi spores induced the activation, expansion, and differentiation of Ag-specific CD4(+) T cells but TLR costimulation did not further augment these T-cell responses.The Dectin-2/FcRγ/Card9 signaling pathway promoted the differentiation of fungus-specific CD4(+) T cells into Th17 cells, whereas Mincle inhibited the development of this T-helper subset in infected mice.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, WI, USA.

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T‐cell activation and expansion is modestly regulated by Dectin‐1, Dectin‐2, MCL, and Card9. Wild type, Myd88−/−, Card9−/−, FcRγ−/−, Dectin‐1−/−, Dectin‐2−/−, Mincle−/−, and Clec4d+/+ and Clec4d−/− mice adoptively received 105 CD4+ purified, naïve 1807 Tg cells and were infected with 2 × 106 live F. pedrosoi spores or not. At day 7 postinfection, the popliteal lymph nodes were harvested and the (A) number and (B) frequency of activated (CD44+) transferred 1807 (Thy1.1+) and endogenous CD4+ T cells was enumerated by flow cytometry. (A, B) The values over the bars in the histogram indicated the n‐fold change in T‐cell numbers versus the corresponding wild‐type control mice. (C) The dot plots show the sum of concatenated events from five mice per group and the values indicate the mean of endogenous and 1807 CD4+ T cells. Data are expressed as mean + SD of five mice per group from a single experiment representative of two independent experiments. The number and frequency of activated (CD44+) T cells was not statistically significant between infected knockout mice versus wild‐type controls using the Wilcoxon rank test for nonparametric data.
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eji3393-fig-0003: T‐cell activation and expansion is modestly regulated by Dectin‐1, Dectin‐2, MCL, and Card9. Wild type, Myd88−/−, Card9−/−, FcRγ−/−, Dectin‐1−/−, Dectin‐2−/−, Mincle−/−, and Clec4d+/+ and Clec4d−/− mice adoptively received 105 CD4+ purified, naïve 1807 Tg cells and were infected with 2 × 106 live F. pedrosoi spores or not. At day 7 postinfection, the popliteal lymph nodes were harvested and the (A) number and (B) frequency of activated (CD44+) transferred 1807 (Thy1.1+) and endogenous CD4+ T cells was enumerated by flow cytometry. (A, B) The values over the bars in the histogram indicated the n‐fold change in T‐cell numbers versus the corresponding wild‐type control mice. (C) The dot plots show the sum of concatenated events from five mice per group and the values indicate the mean of endogenous and 1807 CD4+ T cells. Data are expressed as mean + SD of five mice per group from a single experiment representative of two independent experiments. The number and frequency of activated (CD44+) T cells was not statistically significant between infected knockout mice versus wild‐type controls using the Wilcoxon rank test for nonparametric data.

Mentions: To investigate which innate recognition and signaling pathways are required to activate and expand antigen‐specific T cells in vivo we enumerated the number of activated (CD44+) 1807 T cells from the skin draining lymph nodes of F. pedrosoi infected wild‐type, CLR‐, and signaling adaptor‐deficient mice. Although not statistically significant, the number of activated (CD44+) 1807 T cells was reduced by 20–40% in infected Dectin‐1−/−, Dectin‐2−/−, Card9−/−, and Clec4d−/− mice versus control wild‐type recipient mice (Fig. 3A+C). Little or no change in 1807 T‐cell activation and expansion was observed in infected Myd88−/−, FcRγ−/−, and Mincle−/− mice versus infected control mice.


Fonsecaea pedrosoi-induced Th17-cell differentiation in mice is fostered by Dectin-2 and suppressed by Mincle recognition.

Wüthrich M, Wang H, Li M, Lerksuthirat T, Hardison SE, Brown GD, Klein B - Eur. J. Immunol. (2015)

T‐cell activation and expansion is modestly regulated by Dectin‐1, Dectin‐2, MCL, and Card9. Wild type, Myd88−/−, Card9−/−, FcRγ−/−, Dectin‐1−/−, Dectin‐2−/−, Mincle−/−, and Clec4d+/+ and Clec4d−/− mice adoptively received 105 CD4+ purified, naïve 1807 Tg cells and were infected with 2 × 106 live F. pedrosoi spores or not. At day 7 postinfection, the popliteal lymph nodes were harvested and the (A) number and (B) frequency of activated (CD44+) transferred 1807 (Thy1.1+) and endogenous CD4+ T cells was enumerated by flow cytometry. (A, B) The values over the bars in the histogram indicated the n‐fold change in T‐cell numbers versus the corresponding wild‐type control mice. (C) The dot plots show the sum of concatenated events from five mice per group and the values indicate the mean of endogenous and 1807 CD4+ T cells. Data are expressed as mean + SD of five mice per group from a single experiment representative of two independent experiments. The number and frequency of activated (CD44+) T cells was not statistically significant between infected knockout mice versus wild‐type controls using the Wilcoxon rank test for nonparametric data.
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eji3393-fig-0003: T‐cell activation and expansion is modestly regulated by Dectin‐1, Dectin‐2, MCL, and Card9. Wild type, Myd88−/−, Card9−/−, FcRγ−/−, Dectin‐1−/−, Dectin‐2−/−, Mincle−/−, and Clec4d+/+ and Clec4d−/− mice adoptively received 105 CD4+ purified, naïve 1807 Tg cells and were infected with 2 × 106 live F. pedrosoi spores or not. At day 7 postinfection, the popliteal lymph nodes were harvested and the (A) number and (B) frequency of activated (CD44+) transferred 1807 (Thy1.1+) and endogenous CD4+ T cells was enumerated by flow cytometry. (A, B) The values over the bars in the histogram indicated the n‐fold change in T‐cell numbers versus the corresponding wild‐type control mice. (C) The dot plots show the sum of concatenated events from five mice per group and the values indicate the mean of endogenous and 1807 CD4+ T cells. Data are expressed as mean + SD of five mice per group from a single experiment representative of two independent experiments. The number and frequency of activated (CD44+) T cells was not statistically significant between infected knockout mice versus wild‐type controls using the Wilcoxon rank test for nonparametric data.
Mentions: To investigate which innate recognition and signaling pathways are required to activate and expand antigen‐specific T cells in vivo we enumerated the number of activated (CD44+) 1807 T cells from the skin draining lymph nodes of F. pedrosoi infected wild‐type, CLR‐, and signaling adaptor‐deficient mice. Although not statistically significant, the number of activated (CD44+) 1807 T cells was reduced by 20–40% in infected Dectin‐1−/−, Dectin‐2−/−, Card9−/−, and Clec4d−/− mice versus control wild‐type recipient mice (Fig. 3A+C). Little or no change in 1807 T‐cell activation and expansion was observed in infected Myd88−/−, FcRγ−/−, and Mincle−/− mice versus infected control mice.

Bottom Line: Here, we investigated whether costimulation by TLR agonists fosters the development of adaptive immune responses, by examining the development of fungus-specific T cells.Subcutaneous infection of mice with F. pedrosoi spores induced the activation, expansion, and differentiation of Ag-specific CD4(+) T cells but TLR costimulation did not further augment these T-cell responses.The Dectin-2/FcRγ/Card9 signaling pathway promoted the differentiation of fungus-specific CD4(+) T cells into Th17 cells, whereas Mincle inhibited the development of this T-helper subset in infected mice.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, WI, USA.

Show MeSH
Related in: MedlinePlus