Essential pathogenic role for endogenous interferon-gamma (IFN-γ) during disease onset phase of murine experimental autoimmune orchitis. I. In vivo studies

We previously found that immunization of CH3/He male mice with syngeneic testicular germ cells (TGC) without the aid of any adjuvants was sufficient to induce DTH to TGC and experimental autoimmune orchitis (EAO). To evaluate the role of endogenous IFN-γ in this model, C3H/He mice immunized subcutaneously with TGC on days 0 and 14 received a single injection of anti-murine IFN-γ MoAb on day 15, 20 or 25. On day 45, DTH to TGC was tested, testis specimens were collected for histological examination, and blood samples collected for IFN-γ measurement. The results showed that whilst MoAb treatment on day 15 or 25 did not influence DTH responses, EAO development, and appearance of IFN-γ in the circulation, treatment on day 20 significantly suppressed all of them. Thus, a single injection with anti-IFN-γ MoAb may successfully down-regulate testicular autoimmunity, provided that the treatment is given at an optimal time point during disease development

Vaccinia virus and Cowpox virus are not susceptible to the interferon-induced antiviral protein MxA

MxA protein is expressed in response to type I and type III Interferon and constitute an important antiviral factor with broad antiviral activity to diverse RNA viruses. In addition, some studies expand the range of MxA antiviral activity to include particular DNA viruses like Monkeypox virus (MPXV) and African Swine Fever virus (ASFV). However, a broad profile of activity of MxA to large DNA viruses has not been established to date. Here, we investigated if some well characterized DNA viruses belonging to the Poxviridae family are sensitive to human MxA. A cell line inducibly expressing MxA to inhibitory levels showed no anti-Vaccinia virus (VACV) virus activity, indicating either lack of susceptibility of the virus, or the existence of viral factors capable of counteracting MxA inhibition. To determine if VACV resistance to MxA was due to a virus-encoded anti-MxA activity, we performed coin-fections of VACV and the MxA-sensitive Vesicular Stomatitis virus (VSV), and show that VACV does not protect VSV from MxA inhibition in trans. Those results were extended to several VACV strains and two CPXV strains, thus confirming that those Orthopoxviruses do not block MxA action. Overall, these results point to a lack of susceptibility of the Poxviridae to MxA antiviral activity. © 2017 Lorenzo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Peer reviewe