Nervous System Communication to the Immune System

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The endocrine and autonomic systems exert their effects by secreting molecules that interact with lymphocytes and macrophages (Wrona 2006). The biologically active molecules secreted by the nervous system interact at specific receptors on cells of the immune system (Table 1.2; see also Blalock and Costa (1990), Carr (1991), Clarke and Bost (1989), DeSouza (1993), Gala and Shevach (1993), Harbour, Leon, Keating, and Hughes (1990), Harbour and Hughes (1991), Johnson, Downs, and Pontzer (1992), O'Neal, Schwarz, and Yu-Lee (1991), and Roupas and Herington (1989)).

The interaction may affect a wide range of immune cell activities, including cytokine and antibody production, cell proliferation, and lytic activity and migration (for recent review see Wrona (2006)). Norepinephrine (NE)-induced inhibition of natural killer (NK) cytotoxicity has been shown to occur at several levels, including an influence on NK cell receptor ligation to target cells, NK cell cytokine secretion, and inhibition of the cytotoxic mechanisms in NK cells (Gan, Zhang, Solomon, and Bonavida 2002). Catecholamines have been shown to enhance (Dhabhar and McEwen 1999) or suppress (Dobbs, Vasquez, Glaser, and Sheridan 1993) immune cell function. Thus, catecholamines can enhance the expression of cell-surface differentiation antigens (Singh 1985) and inhibit macrophage-mediated lysis of tumor cells and complement activation (Koff and Dunnegan 1986). Recently, NE and dopamine (DA) were shown to increase lymphocyte activation with augmented T-helper 1 (Th1) and T-helper 2 (Th2)-type cytokine production while the action of NE with dexamethasone resulted in immunosuppression (Torres, Antonelli, Souza, Teixeira, Dutra, and Gollob 2005). Neuropeptides have also been shown to be present in nerve terminals in primary and secondary lymphoid organs and influence immune cell function (Bellinger, Lorton, Romano, Olschowka, Felten, and Felten 1990). For example, in activated macrophages, vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating polypeptide (PACAP) inhibit the expression of proinflammatory cytokines through effects on the nuclear translocation of transcription-factors-like nuclear factor kappa beta (NF-kB) (Ganea, Rodriquez, and Delgado 2003).

They also promote the survival of Th2 effectors (Delgado, Gonzalez-Rey, and Ganea 2004). Substance P (SP) facilitates lymphocyte migration, proliferation, production of immunoglobulin-A (IgA), and phagocytosis (Feistritzer et al. 2003). Recently, it has been shown that the expression and function of full-length and truncated receptors for SP in acute monocytic leukemia cells (THP-1) demonstrate unique signaling pathways between undifferentiated and differentiated cells and ligand interaction (Lai et al. 2006).

There are also data that support a role for the parasympathetic nervous system in influencing the immune system. Both muscarinic and nicotinic acetylcholine (Ach) receptors have been detected on T lymphocytes and macrophages (Tracey 2002). The cholinergic anti-inflammatory pathway, via the vagus nerve, may control the inflammatory response by inhibiting cytokine release from macrophages bearing nicotinic Ach receptors (Pavlov, Wang, Czura, Friedman, and Tracey 2003). Thus, since lymphoid tissues are innervated with sympathetic and parasympathetic fibers and contain specific receptors on their cell surfaces, it seems reasonable to perceive a mechanism by which the nervous system may communicate or regulate specific aspects of the immune response.

Table 1.2. Receptors for neuropeptides hormones on cells of the immune system.

Receptor

Binding cell type

References

Adrenocorticotropin

ß-Endorphin

Thyrotropin

Prolactin

Growth hormone

Growth hormone releasing hormone

Corticotropin releasing factor

Thyrotropin releasing hormone

Luteinizing hormone releasing hormone

Arginine vasopressin

Somatostatin

Substance P

Calcitonin gene-related peptide

Vasoactive intestinal peptide

Rat spleen T and B cells Spleen

Neutrophils, monocytes, B cells

Human and mouse T and B cells

Rat, mouse, human PBL, spleen, thymus

Rat spleen, human PBL Human PBL

T cell line

Rat thymocytes

Human PBL Mouse T and B cells Rat T and B cells

T cells

Johnson et al. 1992 Carr 1991 Harbour 1990

O'Neal et al. 1991; Gala and Shevach 1993

Suzuki et al. 1990; Roupas and Herington 1989

Guarcello et al. 1991

De Souza 1993

Harbour and Hughes 1991

Blalock and Costa 1990

Johnson et al. 1992 Hiruma et al. 1990 Pascual et al. 1991 McGillis et al. 1991

Ottaway and Greenberg 1984

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