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The Journal of Neuroscience, August 15, 2007, 27(33):8857-8865; doi:10.1523/JNEUROSCI.1247-07.2007

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Development/Plasticity/Repair
Social Stress Enhances Sympathetic Innervation of Primate Lymph Nodes: Mechanisms and Implications for Viral Pathogenesis

Erica K. Sloan,¹ John P. Capitanio,^3,4 Ross P. Tarara,³ Sally P. Mendoza,³ William A. Mason,³ and Steve W. Cole^1,2

¹Department of Medicine, Division of Hematology–Oncology, University of California Los Angeles (UCLA) School of Medicine, UCLA AIDS Institute, Cousins Center for Psychoneuroimmunology at the Semel Institute of Neuroscience and Human Behavior, ²Jonsson Comprehensive Cancer Center and UCLA Molecular Biology Institute, Los Angeles, California 90095, and ³California National Primate Research Center and ⁴Department of Psychology, University of California Davis, Davis, California 95616

Correspondence should be addressed to Steve W. Cole, Department of Medicine, Division of Hematology–Oncology, 11-934 Factor Building, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA 90095-1678. Email: coles{at}ucla.edu

Behavioral processes regulate immune system function in part via direct sympathetic innervation of lymphoid organs, but little is known about the factors that regulate the architecture of neural fibers in lymphoid tissues. In the present study, we find that experimentally imposed social stress can enhance the density of catecholaminergic neural fibers within axillary lymph nodes from adult rhesus macaques. This effect is linked to increased transcription of the key sympathetic neurotrophin nerve growth factor and occurs predominately in extrafollicular regions of the paracortex that contain T-lymphocytes and macrophages. Functional consequences of stress-induced increases in innervation density include reduced type I interferon response to viral infection and increased replication of the simian immunodeficiency virus. These data reveal a surprising degree of behaviorally induced plasticity in the structure of lymphoid innervation and define a novel pathway by which social factors can modulate immune response and viral pathogenesis.

Key words: stress; sympathetic nervous system; plasticity; NGF; interferon; SIV

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Received Aug. 24, 2006; revised June 26, 2006; accepted July 2, 2007.

Correspondence should be addressed to Steve W. Cole, Department of Medicine, Division of Hematology–Oncology, 11-934 Factor Building, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA 90095-1678. Email: coles{at}ucla.edu

This article has been cited by other articles:

				S. W. Cole Psychosocial Influences on HIV-1 Disease Progression: Neural, Endocrine, and Virologic Mechanisms Psychosom Med, June 1, 2008; 70(5): 562 - 568. [Abstract] [Full Text] [PDF]

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