Maternal immune tolerance of the semiallogeneic fetus is a complex phenomenon. Macrophages are an abundant cell population in the human decidua, and changes in distribution or phenotype may be involved in the development of preeclampsia. The aim of this study was to assess the distribution and phenotype of macrophages in preterm preeclamptic, preterm control, and term control placentas. Placentas of preterm preeclamptic (n ‫؍‬ 6), preterm control (n ‫؍‬ 5), and term control pregnancies (n ‫؍‬ 6) were sequentially immunohistochemically stained for CD14, CD163, DC SIGN, and IL-10. The distributions of CD14 CD14 and CD163 expression increased significantly in preterm preeclamptic decidua basalis compared with preterm control pregnancies (P ‫؍‬ 0.0006 and P ‫؍‬ 0.034, respectively). IL-10 expression was significantly lower in the decidua parietalis of preterm preeclamptic pregnancies compared with preterm control pregnancies (P ‫؍‬ 0.03). The CD163/CD14 ratio was significantly lower in the decidua basalis (P ‫؍‬ 0.0293) and the DC SIGN/CD14 ratio was significantly higher in the decidua basalis (P < 0.0001) and parietalis (P < 0.0001) of preterm preeclamptic pregnancies compared with preterm control pregnancies. CD14 ؉ macrophages did express Flt-1. Alterations in distribution and phenotype of macrophages in the decidua of preterm preeclamptic pregnancies compared with control pregnancies may contribute to the pathogenesis of preeclampsia. (Am J

Objective. Adipose tissue can secrete soluble mediators (adipokines) with potent immune regulatory functions. Some adipokines have been previously associated with radiographic damage in patients with rheumatoid arthritis (RA). In the present study, we investigated the capacity of baseline adipokine levels to predict radiographic progression over a period of 4 years and studied their contribution relative to that of other known risk factors, such as anti-cyclic citrullinated peptide (anti-CCP) antibodies.Methods. Serum concentrations of leptin, visfatin, resistin, adiponectin, adipsin, tumor necrosis factor ␣ (TNF␣), and interleukin-6 (IL-6) were determined in serum samples obtained at baseline from 253 patients with RA from the Early Arthritis Cohort. The association between levels of these adipokines and radiographic progression was determined using a multivariate normal regression model correcting for age, sex, treatment strategy, body mass index (BMI), and the presence of anti-CCP antibodies.Results. Levels of IL-6, TNF␣, visfatin, and adiponectin were positively associated with radiographic progression over 4 years. This association was independent of BMI. However, only adiponectin levels remained significantly associated with radiographic progression when the model was corrected for the presence of anti-CCP antibodies, whereas a trend was observed for IL-6. The association of both TNF␣ and visfatin with radiographic damage disappeared after correction for the presence of anti-CCP antibodies, which is consistent with the fact that the levels of both cytokines correlated significantly with anti-CCP antibody levels in these patients. Conclusion.Our results indicate that adipokines are predictors of radiographic progression in RA, possibly through distinct underlying biologic mechanisms.

Natural killer (NK)-cell alloreactivity can be exploited in haploidentical hematopoietic stem cell transplantation (HSCT). NK cells from donors whose HLA type includes Bw4, a public epitope present on a subset of HLA-B alleles, can be alloreactive toward recipients whose cells lack Bw4. Serologically detectable epitopes related to Bw4 also exist on a subset of HLA-A alleles, but the interaction of these alleles with KIR3DL1 is controversial. We therefore undertook a systematic analysis of the ability of most common HLA-B alleles and HLA-A alleles with Bw4 serologic reactivity to protect target cells from lysis by KIR3DL1-dependent NK cells. All Bw4(-) HLA-B alleles failed to protect target cells from lysis. All Bw4(+) HLA-B alleles with the exception of HLA-B*1301 and -B*1302 protected targets from lysis. HLA-A*2402 and HLA-A*3201 unequivocally protected target cells from lysis, whereas HLA-A*2501 and HLA-A*2301 provided only weak protection from lysis. KIR3DL1-dependent alloreactive NK clones were identified in donors with HLA-A*2402 but not in donors with HLA-B*1301 or -B*1302. These findings clarify the HLA types that donors and recipients need in haploidentical HSCT and other NK allotherapies in order to benefit from NK alloreactivity.

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