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IL-21 Is Required for Optimal Antibody Production and T Cell Responses during Chronic Toxoplasma gondii Infection
- Source :
- PLoS ONE; May2013, Vol. 8 Issue 5, p1-10, 10p
- Publication Year :
- 2013
-
Abstract
- Previous studies have indicated that Il21r<superscript>−/−</superscript> mice chronically infected with Toxoplasma gondii display a defect in serum IgG; however, the basis for this antibody defect was not defined and questions remain about the role of IL-21 in promoting the production of IL-10, which is required to limit infection-induced pathology during toxoplasmosis. Therefore, Il21<superscript>−/−</superscript> mice were challenged with T. gondii to determine whether IL-21 impacts the parasite-specific CD8<superscript>+</superscript> T cell response, its contribution to thymus-dependent antibody production after infection, and balance between protective and pathogenic responses. Whereas IL-21 has been implicated in the differentiation of IL-10 producing CD4<superscript>+</superscript> T cells no immune-mediated pathology was evident in Il21<superscript>−/−</superscript> mice during the acute response, nor was there a defect in the development of this population in chronically infected Il21<superscript>−/−</superscript> mice. However, Il21<superscript>−/−</superscript> mice displayed a defect in IgG production after infection that correlated with a decrease in GC B cell numbers, the CD4<superscript>+</superscript> and CD8<superscript>+</superscript> T cell numbers in the brain were reduced over the course of the chronic infection leading to a decrease in total IFN-γ production and an increase in parasite numbers associated with susceptibility to toxoplasmic encephalitis. Together, these results identify a key role for IL-21 in shaping the humoral and cellular response to T. gondii, but indicate that IL-21 has a limited role in regulating immunopathology. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 19326203
- Volume :
- 8
- Issue :
- 5
- Database :
- Complementary Index
- Journal :
- PLoS ONE
- Publication Type :
- Academic Journal
- Accession number :
- 88375416
- Full Text :
- https://doi.org/10.1371/journal.pone.0062889