Nance · Brain, behavior, and immunity 2007 · narrative review · n=?

Autonomic innervation and regulation of the immune system (1987-2007).

Cited 861 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Narrative review of neuroanatomical and mechanistic literature without human trial data.

PubMed 17467231 · doi:10.1016/j.bbi.2007.03.008 · record verified 2026-08-26

What was done

This review summarized neuroanatomical and functional literature published between 1987 and 2007 regarding the autonomic innervation of primary and secondary immune organs and the molecular pathways by which neurotransmitters modulate immune cell function.

What was found

The abstract reports no numerical data or statistical measures. The qualitative findings reported are: - All primary and secondary immune organs receive substantial postganglionic sympathetic innervation. - Thymus and spleen receive no sensory neural innervation, whereas lymph nodes and bone marrow receive sensory innervation from dorsal root ganglia. - No neuroanatomical evidence supports direct parasympathetic or vagal innervation of any immune organ. - Sympathetic nervous system (SNS) signaling via norepinephrine (NE) predominantly inhibits innate immune cell activity, while exerting bidirectional (enhancing or inhibiting) effects on adaptive immune cells. - Innate immune cells express alpha- and beta-adrenergic receptors, whereas T and B lymphocytes exclusively express beta2-adrenergic receptors (except murine Th2 cells, which lack adrenergic receptors).

Why it matters

This synthesis outlines the direct neuroanatomical architecture connecting the nervous system to lymphoid tissues, identifying the sympathetic-noradrenergic pathway as the primary neural regulator of immune gene expression and cellular activity.

Limits

The abstract describes a narrative review without explicit systematic search criteria, quality appraisal, or quantitative meta-analysis. Findings rely heavily on preclinical animal models (e.g., murine Th2 receptor distribution), and no human clinical data or sample sizes are reported in the abstract.

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