Inflammation-induced disruption of SCS macrophages impairs B cell responses to secondary infection

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Science  06 Feb 2015:
Vol. 347, Issue 6222, pp. 667-672
DOI: 10.1126/science.aaa1300

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Bacterial infection breaks the lymph node barrier

During infections, lymph nodes are command central. Fragments from invading pathogens enter lymph nodes through the lymph. There, specialized cells called subcapsular sinus (SCS) macrophages capture these antigens and use them to initiate humoral immunity. Despite being such important players, Gaya et al. report that in mice, infection throws these organized sentinels into disarray (see the Perspective by Buzsaki). Disrupting SCS macrophages had important consequences: Bacterially infected mice could not respond as efficiently to a subsequent viral infection.

Science, this issue p. 667; see also p. 612


The layer of macrophages at the subcapsular sinus (SCS) captures pathogens entering the lymph node, preventing their global dissemination and triggering an immune response. However, how infection affects SCS macrophages remains largely unexplored. Here we show that infection and inflammation disrupt the organization of SCS macrophages in a manner that involves the migration of mature dendritic cells to the lymph node. This disrupted organization reduces the capacity of SCS macrophages to retain and present antigen in a subsequent secondary infection, resulting in diminished B cell responses. Thus, the SCS macrophage layer may act as a sensor or valve during infection to temporarily shut down the lymph node to further antigenic challenge. This shutdown may increase an organism’s susceptibility to secondary infections.

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