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NK cells inability to produce IFN gamma in MyD88-/- mice contributes to the delayed clearance of Chlamydia muridarum primary genital infection (133.2)

Title: NK cells inability to produce IFN gamma in MyD88-/- mice contributes to the delayed clearance of Chlamydia muridarum primary genital infection (133.2)
Authors: Nagarajan, Uma M; Sikes, James D; Prantner, Daniel; Goodwin, Anna; Darville, Toni
Source: The Journal of Immunology ; volume 182, issue Supplement_1, page 133.2-133.2 ; ISSN 1550-6606 0022-1767
Publisher Information: Oxford University Press (OUP)
Publication Year: 2009
Description: We have previously shown that MyD88-/- mice have delayed clearance of C. muridarum genital infection in comparison to wild type (WT) mice. The goal of the present study was to investigate the specific mechanisms by which MyD88 protects against C.muridarum infection. A 10-fold higher bacterial load was observed in cervical tissues of MyD88-/- mice at day (d) 4-post infection, suggesting impairment in the early innate response. Further, IFNγ levels were undetectable in the genital secretions of MyD88-/- mice until d4-d5 post infection, though they were restored to normal levels by d7 post infection. Interestingly, recruitment of inflammatory cells such as PMNs, macrophages and NK cells to mouse cervix remains mostly unchanged between WT and MyD88-/- mice at d4 post infection. To address this conundrum, NK cells from the cervix of infected mice at d4 post infection were FACS sorted and the levels of IFNγ mRNA assessed. Overall, MyD88-/- NK cells induced 16 fold less IFNγ than WT NK cells. Surprisingly, this defect in IFN gamma production did not translate to T cells isolated at d7 post-infection from iliac nodes of MyD88-/- mice, suggesting cell type specific regulation. The NK cells dysfunction in MyD88-/- mice also led to ineffective suppression of Th2 response, a plausible explanation for the delayed clearance of infection in MyD88-/- mice. Interestingly, MyD88-/- mice resolve a challenge infection of C. muridarum as effectively as WT mice, suggesting that an adaptive memory response is not impaired in the absence of MyD88 signaling.
Document Type: article in journal/newspaper
Language: English
DOI: 10.4049/jimmunol.182.supp.133.2
Availability: https://doi.org/10.4049/jimmunol.182.supp.133.2; https://academic.oup.com/jimmunol/article/182/Supplement_1/133.2/8014183
Rights: https://academic.oup.com/pages/standard-publication-reuse-rights
Accession Number: edsbas.C459F60F
Database: BASE