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Blood, 15 September 2006, Vol. 108, No. 6, pp. 1949-1956.
Prepublished online as a Blood First Edition Paper on May 16, 2006; DOI 10.1182/blood-2006-04-016857.
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Submitted January 24, 2006
Accepted May 3, 2006
Do CD8 effector cells need IL-7R expression to become
resting memory cells?
Eva Buentke, Anne Mathiot, Mauro Tolaini, James Di Santo, Rose Zamoyska, and Benedict Seddon*
Cancercenter Karolinska, Karolinska Hospital, Stockholm, Sweden
Division of Immune Cell Biology, National Institute for Medical Research, London, U.K.
Division of Molecular Immunology, National Institute for Medical Research, London, U.K.
Institute Pasteur, 25-27 rue du Docteur Roux, Paris, France
* Corresponding author; email: bseddon{at}nimr.mrc.ac.uk.
The role for IL-7R expression in the differentiation of
effector T cells into resting memory remains
controversial. Here, using a conditional IL-7R transgenic
model, we were able to test directly whether CD8 effector
T cells require IL-7R expression for their differentiation
into resting memory cells. In the absence of IL-7R
expression, effectors cells transferred into ‘ full’ hosts
underwent a protracted and unremitting contraction
compared to IL-7R expressing control cells and were unable
to develop into long-term resting memory cells.
Surprisingly, when the same effector cells were
transferred into empty T cell deficient hosts, they could
generate long lived fully functional resting memory cells
independently of IL-7R expression. Formation of these
latter cells was found to dependent on IL-15, since the
same IL-7R deficient effector cells were rapidly lost from
IL-15 deficient hosts, having a half life of less than 40
hours. Therefore, our data suggest that under
physiological conditions, both IL-7 and IL-15 synergise to
promote the formation of memory cells directly by limiting
the contraction of effectors that occurs following an
immune response and that re- expression IL-7R is a key
check point in the regulation of this process.
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