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Natural killer (NK) cells are the most abundant lymphocyte population in the decidua. These cells express killer immunoglobulin-like receptors (KIRs), which upon recognition of HLA class I molecules on tropho- blasts may either stimulate NK cells (activating KIRs) or inhibit them (inhibitory KIRs) to produce soluble factors necessary for the maintenance of pregnancy. KIR genes exhibit extensive haplotype polymorphism; individuals differ in both the number and kind (activating vs. inhibitory) of KIR genes. This polymorphism affects NK cell reactivity and susceptibility to diseases, including gynecological disorders. Therefore we ATR-genotyped 149 spontaneously aborting women and 117 control multiparae (at least 2 healthy-born children). Several genotypes (i.e. combinations of various KIR genes) were differently distributed among the patients and control subjects. Differences were observed in the numbers and the ratios of activating to inhibitory KIRs between patients and healthy women: (i) genotypes containing 6 activating KIR genes were less frequent and those containing 6 inhibitory KIR genes were more frequent in patients than in control subjects, and (ii) an excess of inhibitory KIRs (activating-to-inhibitory KIR gene ratios of 0.33 to 0.83) was associated with miscarriage, whereas ratios close to equilibrium (0.86-1.25) seemed to be protective. In addition, the results suggest for the first time that sporadic and recurrent spontaneous abortions as well as miscarriage in the presence or absence of autoantibodies may have different KIR genotypie backgrounds.
 Natural killer (NK) cells play a major role in the initial control of many viral pathogens and in the rejection of tumors. Consistent with their roles as immune sentinels, NK cells are found in inflamed skin, including lichen planus, psoriasis and atopic dermatitis (AD) lesions. In oral lichen planus lesions, the recruitment as well as intradermal colocalization of NK cells and pDC (plasmacytoid dendritic cells) appear to be mediated by chemerin, a recently identified protein ligand for chemokine-like receptor 1 (CMKLR1), a chemoattractant receptor expressed by both cell types. Dendritic cells can regulate NK cell activity, and NK cells can regulate DC-mediated responses. Since chemerin was recently implicated in recruitment of pDC to psoriatic skin, in this work we determined whether chemerin facilitates interactions between NK and pDC in psoriatic plaques through controlling influx of NK cells to diseased skin. We demonstrate that circulating NK cells from normal donors as well as psoriasis and AD patients respond similarly in functional migration assays to chemerin. However, differences in the distribution of NK cells and pDC in skin lesions suggest that recruitment of both NK cells and pDC is unlikely to be controlled solely by chemerin.
In the present study, infection experiments of E. krijgsmanni using various hosts were conducted to elucidate the host specificity among some animals and the infectivity to mouse strains. According to the results, the infection was not found in most animals, except for rats, in which some oocyst shedding was detected, and there was no significant difference in infectivity among mouse strains. Additionally, oocyst shedding was hardly detectable in a secondary infection to immunocompetent mice, although it was found in immunodeficient mice. These results indicated that only immunocompetent mice could develop adaptive immunity against reinfection by stimuli of the primary infection. Furthermore, the infection experiments were performed with splenic macrophage (Mφ)-depleted mice with a reagent and Beige (Bg) mice known to be a strain of mice with low NK cell activity. No significant effect was found in primary or secondary infections in the Mφ-depleted mice, whereas the mortality rate was clearly increased in Bg mice inoculated with a large number of oocysts. Their oocyst shedding was similar to that of immunocompetent hosts. Taken together, these results suggested that Mφ has only a minor role in the immune response, but the NK cell has an important function in resistance to primary infection of E. krijgsmanni.
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