Am J Reprod Immunol 2010; 64: 93–96 Problem Does addition of enoxaparin to sildenafil and etanercept immunotherapy improve IVF outcome? Methods Report of a striking case with 15 IVF failures. Result When enoxaparin was added, the 16th IVF cycle generated a healthy male baby. Conclusions Combination therapy that includes a heparin may allow successful IVF outcome and this issue merits further study. “
“The enzyme-linked immunospot (ELISPOT) assay is a widely used tool for enumeration of antigen-specific memory B cells in several disciplines, such as
vaccination, cancer immunotherapy and transplantation. For the accurate estimation of antigen-specific memory B cell frequencies, a well-defined B cell activation protocol is pivotal. BMS-777607 In this study, we aimed to characterize a polyclonal B cell activation protocol to facilitate optimal monitoring of antigen-specific memory B cell frequencies. Total, naive and memory B cells were activated polyclonally with an α-CD40 monoclonal antibody, cytosine–phosphate–guanine (CPG) oligodeoxynucleotide (ODN) 2006, interleukin (IL)-2, IL-10 and IL-21. Polyclonal activation of B cells resulted in equal cell death ratios in naive and memory B cells. When tested in an antigen-specific
system, immunoglobulin (Ig)G AZD1208 price spots were detected only in the memory fraction. There was no change in B cell polyclonality due to in-vitro Liothyronine Sodium activation. Our data show that the current polyclonal activation protocol may be used reliably to estimate the frequency of memory B cells in ELISPOT assays. “
“Cerebral malaria is a severe complication of Plasmodium falciparum infection. Although T-cell activation and type II IFN-γ are required for Plasmodium berghei ANKA (PbA)-induced murine experimental cerebral malaria (ECM), the role of type I IFN-α/β in ECM development remains unclear. Here, we address the role of the IFN-α/β pathway in ECM devel-opment in response to hepatic or blood-stage PbA infection, using mice deficient
for types I or II IFN receptors. While IFN-γR1−/− mice were fully resistant, IFNAR1−/− mice showed delayed and partial protection to ECM after PbA infection. ECM resistance in IFN-γR1−/− mice correlated with unaltered cerebral microcirculation and absence of ischemia, while WT and IFNAR1−/− mice developed distinct microvascular pathologies. ECM resistance appeared to be independent of parasitemia. Instead, key mediators of ECM were attenuated in the absence of IFNAR1, including PbA-induced brain sequestration of CXCR3+-activated CD8+ T cells. This was associated with reduced expression of Granzyme B, IFN-γ, IL-12Rβ2, and T-cell-attracting chemokines CXCL9 and CXCL10 in IFNAR1−/− mice, more so in the absence of IFN-γR1.