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Signals From Nervous System Influence Immune System, Study Shows

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    Signals From Nervous System Influence Immune System, Study Shows

    Signals From Nervous System Influence Immune System, Study Shows

    In a discovery that demonstrates a clear link between the mind and body at a
    molecular level, scientists have shown that a chemical signal which normally
    allows nerve cells to communicate with each other -to alter sleep cycles,
    for example -- can also re-direct actions of the immune system.
    The research in mice confirms mounting evidence from studies of cultured
    cells that the nervous system directly influences the immune system. It has
    prompted new experiments to determine if the nerve-generated signal or its
    receptors in the immune system might make good drug targets to control
    asthma or allergies.

    "This is the first clue of a practical pharmacological approach to using the
    nervous system for both improving immune defenses and damping harmful immune
    responses at their roots in diseases as diverse as arthritis and asthma,"
    said Edward Goetzl, MD, professor of medicine and immunology at the
    University of California, San Francisco.

    Goetzl is lead author on a scientific paper on the research in the November
    20 issue of the Proceedings of the National Academy of Sciences. The work is
    a collaboration between UCSF and the University of Edinburgh. Goetzl is also
    senior author on a companion paper on the research in FASEB Journal. (FASEB
    stands for the Federation of the American Societies for Experimental
    Biology.)

    The finding is based on experiments with "knockout" mice whose immune cells
    can't receive the normal neuropeptide signal known as vasoactive intestinal
    peptide, or VIP.

    In the nervous system, VIP normally stimulates nerve cell signaling and
    survival, and regulates neural biological clocks. The scientists found that
    VIP also affects the migration of the immune system's T cells and T cell
    secretion of protein signals for other immune cells, both of which are
    central to the body's normal defense against infection. Through its action
    on T cells, VIP can affect the process in which the immune system turns
    against the body, such as in asthma and arthritis.

    In the PNAS paper and in the companion paper in the FASEB Journal, the
    researchers showed that the strength of the VIP signal received by the T
    cells regulates the balance between two types of immune T cells, Th1 and
    Th2. Th1 is normally involved with protection from bacterial invasion and
    other defenses, but Th1 in excess can lead to autoimmune disorders. Th2
    protects from parasitic infections and autoimmunity, but in excess can lead
    to allergies.

    The researchers discovered the effect of VIP on the Th1/Th2 balance by
    examining the relative production of the Th cells' protein products, known
    as cytokines. When the balance is tipped toward Th1 in knockout mice lacking
    a critical form of a VIP receptor, allergy is suppressed and resistance to
    some types of infections is boosted, along with other reactions, they found.

    The research did not determine if the impact of the neuropeptide VIP is
    sufficient to change the course of infections, inflammation or autoimmune
    disease in which T cells are involved.

    The researchers caution that VIP has such broad effects on immune function
    that blocking its action with drugs might risk triggering one kind of immune
    malady while it relieves another. However, the new findings clearly
    demonstrate the potential of neuroregulation of T cell functions and suggest
    the potential value of developing VIP-like drugs with greater immune
    selection than VIP itself, Goetzl added.

    Senior author on the PNAS paper is Anthony Harmar, PhD, professor of
    neurosciences at University of Edinburgh. Co-authors are post-doctoral
    fellows Julia K Voice, PhD, and Glenn Dorsam, PhD, in the UCSF medicine and
    immunology departments; and Yvonne Kong, research assistant in the same
    departments. Also on the study are post-doctoral fellows Sanbing Shen, PhD;
    Katrine M. West, PhD; and Christine F. Morrison, PhD, all at University of
    Edinburgh.

    The research was funded by the National Institutes of Health and the Medical
    Research Council of the United Kingdom.


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    Note: This story has been adapted from a news release issued by University
    Of California - San Francisco for journalists and other members of the
    public. If you wish to quote from any part of this story, please credit
    University Of California - San Francisco as the original source. You may
    also wish to include the following link in any citation:

    http://www.sciencedaily.com/releases...1116064459.htm
    __________________________________________________ __
    Maksim (Max) Bily
    mail to : imax@odyssee.net
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