4.4 Article

Detection of invariant natural killer T cells in ejaculates from infertile patients with chronic inflammation of genital tract

Journal

Publisher

WILEY
DOI: 10.1111/aji.12671

Keywords

chronic inflammation of male genital tract; interferon-; interleukin-17; invariant natural killer Tcells; spermatozoa

Funding

  1. National Natural Science Foundation of China [81300530]
  2. Science Foundation of Guangdong Province [2016A0202 15024]

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Chronic inflammation of genital tract is thought to play a major role in male fertility disorder. Natural killer (NK) T cells are a heterogeneous group of T cells that share properties of both T cells and NK cells which display immunoregulatory properties. However, little is known regarding the presence and function of NK T cells in ejaculates from patients with chronic inflammation of genital tract. Invariant NK T (iNK T) cells were detected by invariant (V24-JQ) TCR chain in ejaculates from patients suffering from chronic inflammation of genital tract (CIGT) using flow cytometry and immunofluorescence of double staining (n=40). Inflammatory cytokines interleukin (IL)-6, IL-17, and IFN- were detected in cell-free seminal plasma using an enzyme-linked immunosorbent assay (ELISA). The correlation between the percentage of iNK T cells and spermatozoa count, motility, vitality, seminal IL-6, IL-17, and IFN- was investigated. Significant percentages of iNK T cells above 10% were detected in 50% (CIGT-NKT+ group). A negative correlation was detected between the percentage of iNK T cells and spermatozoa count (r=-.5957, P=.0056), motility (r=-.6163, P=.0038), and vitality (r=-.8032, P=.0019) in CIGT-NKT+ group (n=20). Interestingly, a significant correlation of iNK T cells to seminal IL-6 (r=.7083, P=.0005), IFN- (r=.9578, P<.0001) was detected whereas lack of correlation between iNK T cells and IL-17 (r=-.1557, P=.5122) in CIGT-NKT+ group. The proliferative response of iNK T cells could accompany an inflammatory response to spermatozoa and consequently influence sperm quality through secretion of IFN- but not IL-17 under chronic inflammatory condition.

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