Immune Downregulation rationale.

Whitnall whitnall at usuhsb.usuhs.mil
Fri Mar 3 14:32:53 EST 1995


Roederer at Darwin.Stanford.Edu (Mario Roederer) wrote:
>
> In article <3iu7p2$8qr at usenet.srv.cis.pitt.edu>, karol+ at pitt.edu (Karol W.
> Gieszczykiewicz) wrote:
> 
> > Hello
..
.. -- 
> 
> I think that stress is a response to a "fight or flight" situation--one in
> which all a body's metabolic energies should be directed to fighting or
> fleeing (immediate threat), not to gearing up B and T cells to fight off
> an infection (which might be dealt with later without incurring death).  

The present consensus is that the adaptive value of glucocorticoid
inhibition of immune and inflammatory responses is to prevent
overreaction of these systems, which can be quite destructive.
Glucocorticoids are also thought to prevent overreaction of other
physiological systems during stress, although the evidence for this
is not as clear cut as for autoimmune disorders and sepsis.

See the classic reference:
Munck, A., Guyre, P.M. and Holbrook, N.J. Physiological functions 
of glucocorticoids in stress and their relation to pharmacological 
actions. Endocrine Reviews 5: 25-44, 1984.

as well as:

Sternberg, E.M. The stress response and the regulation of
inflammatory disease. Annals of Internal Medicine 117: 
854-866, 1992.

Zuckerman, S.H. and Qureshi, N. (1992) In vivo inhibition of lipopolysaccharide-
induced lethality and tumor necrosis factor synthesis by Rhodobacter 
sphaeroides diphosphoryl lipid A is dependent on corticosterone induction. 
Infection and Immunity 60, 2581-2587.



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