JC July, 1994 - IL12 and HIV

Erik Robert Wilson erwg0233 at uxa.cso.uiuc.edu
Sun Jul 17 12:04:29 EST 1994


[previous discussion deleted]

>: In the latest Science, Fauci and another group present papers stating that they
>: did not observe a loss in TH1 profiles.  Il-12 was not addressed (at least not 
>: noticed in my first skim!).  Gets more and more confusing all the time....

>: The quest marches on.....


>This is amazing. This finding is in Direct contradiction to Dr Jonas Salk
>and Dr Peter Bretscher ( my Good old immunology professor back in
>Saskatchewan) who showed evidence that as asymptomatic HIV-seropositive
>individuals progress towards AIDS , there is a shift from Th1-mediated
>cytokine production to a Th2-mediated one( Science Vol260:1270 28 may 1993).
> This would have correlated with
>the decrease in IL-12 production as the Predomninace of Th2-mediated
>cytokines produces IL-10 which is a -ve regulator of IL-12.
>I am gonna get a hold of last week's Science.

To grossly oversimplify the 2 articles in the 8 July Science (Maggi et al
and Graziosi et al) and the perspective by Mosmann (p193), it may be true
that HIV promotes a shift toward Th2 (and Th0) patterns of cytokine
production but HIV seems to replicate mainly in those same Th2 and Th0
cells.  Therefore HIV may promote its own progression by inducing a
shift toward the cell types that it replicates in, but having ablated those
cells may leave the relative proportion of Th1/Th2+Th0 constant.  There
is some speculation over the possibility that HIV may not itself be
causing the shift in cytokine production and may simply be taking
advantage of a shift caused by other agents (parasitic infections for
example).  This may indicate that individuals with a strong Th1 response
may indeed control the infection and may only become susceptable once
other environmental agents cause a shift toward a Th2 response which
lends some support to the search for viable methods to promote a shift
to Th1 responses in HIV infected individuals.
	Another interesting point is that since HIV seems to replicate
preferentially in activated Th2 cells, it is destroying "recall-antigen"
specific cells and thus eliminating usefull memory cells that had been
guarding against opportunistic infections.  Once they are gone, the way
is paved for these opportunistic infections to appear and (perhaps) tilt
the patients cytokine profile toward a Th2 response.

>When will these confusing findings stop? when you get all excited about an
>aspect of immunology of HIV, there comes a study to contradict it.
> :Matt
>: MBUCHANAN at opus.mco.edu

>Cheers.
>-- 
>Shahram Mori					   _/\_
>Program in Molecular Biology			  _\  /_
>Dept. of chemistry and Biochemistry Box 3C	  \_  _/
>NMSU  Las Cruces NM				    ||
-- 
|    \   o IO             | "If we do not find     | Erik Wilson              |
|-----|      o GANYMEDE   |anything pleasant, at   | University of Illinois   |
|   O |    o EUROPA       |least we will find      | (217) 359-7547           |
|----/         o CALLISTO |something new" -Voltaire| erikred at uiuc.edu         |



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