4.6 Article

IL-17A Controls IL-17F Production and Maintains Blood Neutrophil Counts in Mice

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JOURNAL OF IMMUNOLOGY
卷 183, 期 2, 页码 865-873

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AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0804080

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  1. Deutsche Forschungsgemeinschaft [V1508/1-1]
  2. National Institutes of Health Grant [HL 073361]

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G-CSF, its receptor, and IL-17 receptor A (IL-17RA) are all required to maintain baseline neutrophil counts in mice. In this study, we tested whether IL-17F could compensate and maintain baseline neutrophil counts in the absence of IL-17A. Unlike the reduced neutrophil counts found in IL-17RA-deficient mice, neutrophil counts were mildly increased in IL-17A-deficient (Il17a(-/-)) animals. There was no evidence for infection or altered neutrophil function. Plasma G-CSF and IL-17F levels were elevated in Il17a(-/-) compared with wild-type mice. IL-17F was mainly produced in the spleen and mesenteric lymph nodes, but IL-23 was unaltered in Il17a(-/-) mice. Instead, Il17a(-/-) splenocytes differentiated with IL-6, TGF-beta, and IL-23 ex vivo produced significantly more IL-17F in response to IL-23 than wild-type cells. Adding rIL-17A to Il17a(-/-) splenocyte cultures reduced IL-17F mRNA and protein secretion. These effects were also observed in wild-type but not IL-17RA-deficient cells. We conclude that IL-17A mediated suppression of IL-17F production and secretion requires IL-17RA and is relevant to maintain the normal set point of blood neutrophil counts in vivo. The Journal of Immunology, 2009, 183: 865-873.

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