Re: What role does cytokine play in the immune response to the Ebola Virus?

	There is really no such thing as "cytokine".  Cytokine is the name for a
whole group of proteins or peptides.  Your question is similar to asking
"What is the role of woman in running the government of the State of
Texas?".  Just as there are women who play many different roles in running
a state government, from social workers and policewomen to senators and
lobbyists; there are individual chemokines and cytokines that are involved
in control of all levels of the immune system.  

The Online Medical Dictionary I use
(http://cancerweb.ncl.ac.uk/cgi-bin/omd?query=cytokine&action=Search+OMD)
has this to say about "cytokine":
---------------
cytokine

 Small proteins or biological factors (in the range of 5-20
kD) that are released by cells and have specific effects on cell-cell
interaction, communication and behaviour of other cells. 

Not really different from hormones, but the term tends to be used as a
convenient generic shorthand for interleukins, lymphokines and several
related signalling molecules such as TNF and interferons. 

Generally growth factors would not be classified as cytokines, though TGF
is an exception. Rather an imprecise term. Chemokines are a subset of
cytokines. 
--------------

	So anyway, cytokines and chemokines are molecular signalling molecules
that are released by one cell or group of cells and then bind to other
cells in order to tell the other cells what to do.  For example human
growth hormone tells many bone and muscle cells to grow and divide.  There
are hundreds of cytokines and chemokines that help to coordinate the
mammalian immune system.  Some cause inflamation which helps macrophages to
escape out of the blood vessels into the infected tissue.  Some are
attractants that cause certain types of immune cells to move toward the
site of infection.  
	You are on the right track, to have heard that Ebola virus presents a
particular problem in regard to chemokines.  Ebola virus (EBOV) infections
are characterized by dysregulation of normal host immune responses. Insight
into the mechanism came from recent studies in nonhuman primates, which
showed that EBOV infects cells of the mononuclear phagocyte system (MPS),
resulting in apoptosis (self-inflicted death) of bystander lymphocytes.
	So here you have a virus that attacks the cells of the immune system
itself.  Ebola is not the only virus to do this, human immunodeficiency
viruses (HIV-1 and HIV-2), human T-cell leukemia viruses (HTLV-I and
HTLV-II) and many other viruses cause problems largely because they attack
the immune system itself.
	It is not yet clear exactly which of the hundreds of immune system
chemokines and cytokines get "messed up" by Ebola virus.  Nor is it exactly
clear what all these signalling molecules do in the normal immune system. 
The tools researchers use to study these molecules are still being
developed, so we learn more about this type of intercellular and
intracellular communication each year.  But there is still a lot more
territory to explore, than has already been mapped.

	To learn more about Ebola and chemokines, you would have to go to a
medical library and read papers such as this one:
-----------
Virology 2001 May 25;284(1):20-5
Monocyte-derived human macrophages and peripheral blood 
mononuclear cells infected with ebola virus secrete MIP-1alpha and
TNF-alpha and inhibit poly-IC-induced IFN-alpha in vitro.
Gupta M, Mahanty S, Ahmed R, Rollin PE.
Emory Vaccine Center, Emory University School of Medicine, 
Atlanta, Georgia 30322, USA.
Ebola virus infection of humans is associated with high 
levels of circulating inflammatory chemokines and cytokines. We
demonstrate that direct infection of human PBMC results in 
the induction of MCP-1, MIP-1alpha, RANTES, and
TNF-alpha as early as 24 h p.i. in response to live virus. 
Monocyte-derived macrophages infected with live Ebola-virus
secreted MIP-1alpha and TNF-alpha specifically while RANTES 
and MCP-1 were secreted by with both live or inactivated
virus stimulation and do not require viral replication. Type 
I interferons (IFN-alpha and -beta), IL-1beta and IL-10, were
not induced by Ebola virus. Furthermore, live virus infection 
of both PBMCs and monocytes-derived macrophages inhibited
IFN-alpha induced by double-stranded RNA in vitro. These data 
provide the first direct evidence of a role for macrophages
in the pathogenesis to Ebola virus and suggest that Ebola virus 
can inhibit cellular antiviral mechanisms mediated by type I
interferons. Copyright 2001 Academic Press.
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    But that would most likely be far beyond what a high-school student
should be expected to be able to understand.