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Some characteristics of IL-5-producing T cells in mouse liver induced by Schistosoma japonicum infection
Schistosome infection could cause significant liver damage in animal; Th2 cells play an important role in the progress of this disease. In our study, C57BL/6 mice were infected by Schistosoma japonicum and lymphocytes were isolated from the liver to detect some characteristics of interleukin-5 (IL-5...
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Published in: | Parasitology research (1987) 2013-05, Vol.112 (5), p.1945-1951 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Schistosome infection could cause significant liver damage in animal; Th2 cells play an important role in the progress of this disease. In our study, C57BL/6 mice were infected by
Schistosoma japonicum
and lymphocytes were isolated from the liver to detect some characteristics of interleukin-5 (IL-5)-producing T cells by different methods. The results revealed that
S
.
japonicum
infection could induce a large amount of IL-5 in mouse liver T cells by the means of fluorescent bead immunoassay and RT-PCR. Although, mouse liver contained many T cell subsets, such as Th cells, Tc cells, NKT cells, and γδ T cells. Fluorescence activated cell sorting results indicated that Th cells were the main source of IL-5 in the T cell population after phorbol 12-myristate 13-acetate and ionomycin stimulation. Moreover, the percentage of IL-5-producing Th cells continued to increase from 4 to 8 weeks after
S
.
japonicum
infection, which differed from the changes of IFN-γ
+
Th1 cells, IL-4
+
Th2 cells, and IL-17A
+
Th17 cells during
S
.
japonicum
infection. Additionally, cytokines co-expression results demonstrated that 36.2 % of IL-5
+
Th cells could express IL-4, and 10 % of it could produce IFN-γ or IL-17A. Collectively, these findings implied that IL-5-producing Th cells posses some properties which differ from other cytokines secreting Th cells. |
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ISSN: | 0932-0113 1432-1955 |
DOI: | 10.1007/s00436-013-3350-2 |