Anti-CD14 monoclonal antibody, clone NFN-26 [PE-DyLight 594]

Decidualization is a process that involves phenotypic and functional changes of endometrial stromal cells to sustain endometrial receptivity and the participation of immunoregulatory factors to maintain immune homeostasis. In this context, tolerogenic dendritic cells (DCs) can induce regulatory T cells, which are essential to manage the pro- to anti-inflammatory transition during embryo implantation. Recently, Myeloid Regulatory Cells (MRCs) were proposed as immunosuppressants and tolerance-inducer cells, including the DC-10 subset. This novel and distinctive subset has the ability to produce IL-10 and to induce type 1 regulatory T cells (Tr1) through an HLA-G pathway. Here we focus on the impact of the decidualization process in conditioning peripheral monocytes to MRCs and the DC-10 subset, and their ability to induce regulatory T cells. Anin vitromodel of decidualization with the human endometrial stromal cell line (HESC), decidualized by medroxyprogesterone and dibutyryl-cAMP was used. Monocytes isolated from peripheral blood mononuclear cells from healthy women were cultured with rhGM-CSF + rhIL-4 and then, the effect of conditioned media from decidualized (Dec-CM) and non-decidualized cells (Non-dec-CM) was tested on monocyte cultures. We found that Dec-CM inhibited the differentiation to the CD1a(+)CD14(-)immature DC profile in a concentration-dependent manner. Dec-CM also significantly increased the frequency of CD83(+)CD86(low)and HLA-DR(+)cells in the monocyte-derived culture. These markers, associated with the increased production of IL-10, are consistent with a MRCs tolerogenic profile. Interestingly, Dec-CM treatment displayed a higher expression of the characteristic markers of the tolerogenic DC-10 subset, HLA-G and ILT2/CD85j; while this modulation was not observed in cultures treated with Non-dec-CM. Moreover, when monocyte cultures with Dec-CM were challenged with LPS, they sustained a higher IL-10 production and prevented the increase of CD83, CD86, IL-12p70, and TNF-alpha expression. Finally, the DC-10 subset was able to induce a CD4(+)HLA-G(+)regulatory T cells subset. These results suggest that the decidualization process might induce different subsets of MRCs, like DC-10, able to induce regulatory T cells as a novel CD4(+)HLA-G(+)subset which might play an immunoregulatory role in embryo implantation.

Background: The innate immune response is the primary defense against influenza virus infection. Methods: This is a prospective study carried out in children < 18 years of age who were diagnosed with influenza A or influenza B infection. Demographic and clinical data, laboratory findings and cell immunophenotypes on first presentation were compared. Results: With respect to immunophenotype, influenza A infection resulted in a higher fraction of CD14(+) and CD4(+) IL-17A(+) cells compared to children infected with influenza B. By contrast, influenza B infection resulted in a comparatively higher percentage of double-negative CD4(-) CD8(-) lymphocyte subsets. Influenza A infection was associated with comparatively higher percentages of CD4(+)CD25(high)Foxp3(+) and CD4(+)CD25(low)Foxp3(+) cells. By contrast, the percentage of CD8(+)CD25(hig)h and CD8(+) CD25(low) cells was similar among patients with influenza A infection and influenza B infection. Conclusions: An improved understanding of the fraction of regulatory T cells with influenza virus infections may provide further understandings on immune responses.