Sympathetic neurons control adaptive immunity in response to Streptococcus pneumoniae infection by regulating T cell and B cell effector function
Zhu, F.; Davis, K.; Acharya, S.; Sekar, J.; Aguilar, D.; Kalpage, N.; Akbari, O.; Swaminathan, S.; Jorth, P.; Swidergall, M.; Jendzjowsky, N.
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This study investigated how lung-innervating sympathetic neurons regulate adaptive immunity. We demonstrate that the nucleus tractus solitarius is activated following Streptococcus pneumoniae pre-exposure and infection, and rostral ventral lateral medulla project sympathetic neurons to the lungs to evoke norepinephrine release. Lung-specific sympathetic neuron depletion reduced B memory and resident memory cells, and antigen-specific IgG. This was phenocopied in Adrb1-/-Adrb2-/- mice (lack {beta}-adrenergic receptors). When B cells from Adrb1-/-Adrb2-/-mice were adoptively transferred into Ighm-/- mice, the bacterial burden was higher than in Ighm-/- mice that received wild-type B cells. Depletion of T cells in Ighm-/- mice that received Adrb1-/- Adrb2-/- B cells had a further increase in bacterial burden compared to adoptively transferred Ighm-/-+ Adrb1-/- Adrb2-/- B cells with intact T cells; interferon-{gamma} release was suppressed with T cell depletion. Sensory neurons stimulate sympathetic brainstem centers to evoke norepinephrine release which stimulate T cells to release interferon-{gamma}, and norepinephrine + interferon-{gamma} co-stimulate B cells to increase antigen-specific IgG production coordinating an adaptive immune response to reduce S. pneumoniae infection. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=129 SRC="FIGDIR/small/706205v1_ufig1.gif" ALT="Figure 1"> View larger version (21K): org.highwire.dtl.DTLVardef@4b2f9corg.highwire.dtl.DTLVardef@22bc5aorg.highwire.dtl.DTLVardef@7bf54dorg.highwire.dtl.DTLVardef@25c4be_HPS_FORMAT_FIGEXP M_FIG C_FIG
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