A gammaherpesvirus provides protection against allergic asthma by inducing the replacement of resident alveolar macrophages with regulatory monocytes

Machiels, B. et al.

Nat Immunol. 2017 Dec;18(12):1310-1320.

Speaker:  Yu-Ting Shao (邵郁婷)             Time:13:10-14:00, Apr. 25, 2018

Commentator: Po-Lin Chen,Ph.D.( 陳柏齡 醫師)             Place: Room 601

Abstract:

The hygiene hypothesis proposes that the increase in allergic diseases in affluent countries is linked to reduced exposure to infections during early childhood. Early-life infection of children with Epstein-Barr virus (EBV) is suggested to protect the children against persistent sensitization to immunoglobulin E (IgE). Accordingly, the closely related virus murid herpesvirus 4 (MuHV-4) has been shown to alter immunity to bacteria and vaccines. Authors found that respiratory infection with MuHV-4 conferred strong and prolong protection against airway allergy through the replacement of resident alveolar macrophages (AMs) with the recruitment of regulatory monocytes from bone marrow (BM) origin. Authors showed that infection with MuHV-4 induced the death of lung resident AMs and repopulation of the emptied alveolar niche by BM-derived monocytes that rapidly differentiated into AMs. These AMs were able to block the ability of DCs to trigger an HDM-specific TH2 response. As AMs are targeted by many infections and are long-lived, these results might provide a mechanistic explanation for the observation that infections during early childhood can orientate the immune response to heterologous antigens such as allergens in the long term. Their results indicate that replacement of embryonic AMs by regulatory monocytes is a major mechanism underlying the long-term training of lung immunity after infection.

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