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Summary: Extracellular vesicle (EV) exchange is emerging as a novel method of communication at the maternal–fetal interface. The presence of the EVs has been demonstrated in the preimplantation embryo culture medium from different species, such as bovines, porcines and humans. Preimplantation embryo‐derived EVs have been shown to carry molecules potentially able to modulate the local endometrial immune system. The non‐classical major histocompatibility complex (MHC) class I molecule human leucocyte antigen (HLA)‐G, the immunomodulatory molecule progesterone‐induced blocking factor and some regulatory miRNAs species are contained in embryo‐derived EV cargo. The implanted syncytiotrophoblasts are also well known to secrete EVs, with microvesicles exerting a mainly proinflammatory effect while exosomes in general mediate local immunotolerance. This review focuses on the current knowledge on the potential role of EVs released by the embryo in the first weeks of pregnancy on the maternal immune cells. Collectively, the data warrant further exploration of the dialogue between the mother and the embryo via EVs. [ABSTRACT FROM AUTHOR]

SUMMARY We investigated the effect of N-acetylcysteine (NAC) on normal human B cell functions. We found that NAC significantly inhibited both the induction of the specific antibody response to the T-dependent antigen Candida albicans and T-dependent pokeweed mitogen (PWM)-induced polyclonal Ig production. NAC did not induce either cell death due to a non-specific toxicity or apoptosis. The NAC-induced inhibitory effect might be a functional consequence of: (i) a down-regulation of the expression on the B cell surface of CD40 and CD27 co-stimulatory molecules and (ii) a down-regulation of interleukin (IL-4) production. In contrast, NAC up-regulated interferon-γ (IFN-γ) production. NAC did not induce any effect on the T cell-independent B cell polyclonal activation system. These results indicate that NAC down-regulates T dependent B cell activation and leads to T helper cell type 1 (Th1) polarization. [ABSTRACT FROM AUTHOR]

Previous work from our laboratory demonstrated that a synthetic heptapeptide (Ch 7), corresponding to a conserved sequence of HIV core protein p24 (aa 232-238), was able to specifically abrogate antigen-induced responses in cultures of normal human peripheral blood lymphocytes (PBL). In the present study we show that Ch7 did not inhibit the induction of IFN-γ secreting cells nor the accumulation of IFN-γ mRNA in antigen-stimulated cultures. However, delayed addition of recombinant human IFN-γ to Ch7-suppressed cultures was able to restore fully the capacity to mount an antigen-specific antibody response. Thus, although the Ch7 immunosuppressive effect may not be directly related to a decreased production of IFN-γ, an increased level of this cytokine is certainly able to counteract the negative effect of the peptide. [ABSTRACT FROM AUTHOR]