Journal
INFECTION AND IMMUNITY
Volume 79, Issue 10, Pages 4210-4217Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.05286-11
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Funding
- Swedish Research Council, Torsten
- Ragnar Soderbergs Foundation
- Karolinska Institutet
- Swedish Foundation for Strategic Research
- German Research Foundation [1273]
- Magnus Bergwall
- Ake Wibergs
- DA Hagelens Foundation
- ALF-bidrag from Stockholm City Council
- Stockholm City Council
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Streptococcus pneumoniae is a leading cause of bacterial pneumonia, meningitis, and sepsis in children. Human immunity to pneumococcal infections has been assumed to depend on anticapsular antibodies. However, recent findings from murine models suggest that alternative mechanisms, dependent on T helper cells, are also involved. Although the immunological events in which T helper cells contribute to acquired immunity have been studied in mice, little is known about how these responses are generated in humans. Therefore, we examined bacterial and host factors involved in the induction of Th1 and Th17 responses, using a coculture model of human monocytes and CD4(+) T cells. We show that monocytes promote effector cytokine production by memory T helper cells, leading to a mixed Th1/Th17 (gamma interferon [IFN-gamma]/interleukin-17 [IL-17]) profile. Both T helper cytokines were triggered by purified pneumococcal peptidoglycan; however, the balance between the two immune effector arms depended on bacterial viability. Accordingly, live pneumococci triggered a Th1-biased response via monocyte production of IL-12p40, whereas heat-killed pneumococci triggered a Th17 response through TLR2 signaling. An increased understanding of human T helper responses is essential for the development of novel pneumococcal vaccines designed to elicit cell-mediated immunity.
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