Study on the virus clearance mechanism of type I interferon b

Release date: 2015-05-18

Type I interferons play an important role in the innate immunity and acquired immunity of the host against microbial infection. This includes controlling the state of the pathogen, regulating the innate immune response, activating the acquired immune response, and so on. Despite this, some studies have found that type I interferons can increase the severity of infection. Previous studies have found that blockade of type I interferon can promote clearance after viral infection, and this effect is mainly achieved by creating an environment of immunosuppression, including: 1. Promoting some negative regulatory factors such as IL-10. , the production of PD-1; 2, destroy the structure of the spleen; 3, inhibit the migration of lymphocytes to the spleen. However, it is still unclear which type of interferon I has this function.

The type I interferon family mainly includes two types of members: IFN-a and IFN-b, in addition to IFN-e, IFN-w, and the like. The downstream receptors for these factors are all heterodimers composed of IFNAR1 and IFNAR2. Despite this, due to their different mechanisms of action with receptors, the resulting downstream signals also differ.

In a recent study, the Michael BA Oldstone team from the University of Washington School of Medicine reported the regulation of different subtypes of type I interferon in viral infection, and the study was published in the journal cell hostμbe.

First, the authors compared viral proliferative capacity in wild-type mice, IFN-b-deficient mutant mice (IFN-b-/-) and IFN-receptor-mutant mutant mice (IFN-a-/-) in response to LCMV infection. . The results showed that IFN-b-/- mice showed no significant difference in proliferative capacity 24 hours after virus infection compared to wild type mice. The viral load of IFN-a-/- mice was significantly higher than the other two groups. This indicates that IFN-b does not have an inhibitory effect in the early stage of viral infection.

Infection with LCMV destroys the structure of lymph nodes and affects the migration of lymphocytes. The authors want to know if IFN is involved in this process. IFNAR1 and IFN-b were blocked by specific antibodies, and by means of fluorescence imaging, the authors found that both blocking methods can well protect the spleen structure from damage. This result indicates that IFN-b may have a role in the structure of the lymph nodes.

Previous studies used antibodies to block IFNAR1 and found that levels of CD4+ effector T cells were increased after day 5 and day 9 of LCMV infection, whereas levels of CD8+ T cells were not affected. In this study, the authors blocked the function of IFN-b by antibodies and found that the levels of CD4+ T cells and CD8+ T cells were significantly increased after 9 days of infection. Previous studies in the IFNAR1 blockade have been found to be caused by a decrease in immunosuppressive factors such as IL-10 and PD-1, and IL-10 or PD-1 was not found in IFN-b in this study. A decrease in expression occurs after blocking.

To investigate whether this property of IFN-b affects host clearance of the virus. The authors blocked IFN-b or IFN-a in mice and infected LCMV. The viral load in the serum is then continuously monitored over a period of time. In the early stage, blocking IFN-a or IFN-b alone did not inhibit the viral load. However, after 30 days of infection, IFN-b blockade had the same effect as IFNAR1 blockade, whereas IFN- Blocking of a has no effect.

The above results indicate that IFN-b can control the viral load in the later stage of viral infection, but it may have some negative effects on the lymphatic system.

Source: Bio Valley

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