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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Impaired neutrophil response and CD4+ T helper cell 1 development in interleukin 6-deficient mice infected with Candida albicans.

To define the role of interleukin (IL)6 in Candida albicans infection, IL-6 deficient mice were assessed for susceptibility to systemic or gastrointestinal infection, as well as for parameters of elicited T helper cell ( Th) immunity. IL-6-deficient mice were more susceptible than wild-type mice to either type of infection caused by virulent C. albicans. In response to systemic challenge with a live vaccine strain of yeast, IL-6-deficient mice failed to mount Th1-associated protective immunity, but the resulting Th2-biased response could be redirected to the Th1 phenotype by IL-10 neutralization. Severe impairment of the macrophage and neutrophil response to infection was observed in IL-6-deficient mice, but administration of IL-6 would increase both neutrophil response and resistance to infection. IL-6 seems to oppose the Th2- promoting role of IL-10 in candidiasis, its early regulatory activity involving effects on neutrophil function.[1]

References

  1. Impaired neutrophil response and CD4+ T helper cell 1 development in interleukin 6-deficient mice infected with Candida albicans. Romani, L., Mencacci, A., Cenci, E., Spaccapelo, R., Toniatti, C., Puccetti, P., Bistoni, F., Poli, V. J. Exp. Med. (1996) [Pubmed]
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