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,§,
*
The Committee on Developmental Biology;
The Committee on Immunology;
The Ben May Institute and The Department of Pathology;
§
The Department of Medicine, The Gwen Knapp Center for Lupus and Immunology Research, The Howard Hughes Medical Institute, and The Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637
CD28 signaling is critical for IL-2 production by established Th1
clones, but CD28 does not appear to play a role in the activation of
established Th2 clones. To determine the role of CD28 in the generation
of polarized T cells, clones were derived using cells from
CD28-deficient (CD28-/- mice, which had been bred with
mice that express the DO11.10 transgene, a CD4+ TCR-
ß
receptor that recognizes OVA peptide 323–339 bound to
I-Ad. Most T cell clones derived from CD28+/+
mice survived multiple stimulations, while T cell clones derived from
CD28-/- mice survived only if they were derived initially
in the presence of IL-4 or both IL-2 and IL-4. Signaling through the
CD28 molecule did not appear to be important in the initial activation
of T cell clones, as the precursor frequency of clones derived from
normal (CD28+/+) and CD28-/- mice was
similar. Primary stimulation in the presence of IL-4 increased cell
number and viability of both CD28+/+ and
CD28-/- T cells in primary culture. However, the survival
of CD28-/- cells is more dependent on IL-4 than is the
survival of CD28+/+ cells. The continued presence of
anti-IL-4 mAb dramatically decreased the number of viable cells in
the CD28-/- cultures but had little effect on the
viability of the CD28+/+ clones. Thus, initial culture with
IL-4 allows the isolation of CD28-/- T cell clones that
produce IL-4. In these clones, IL-4 acts as both an autocrine growth
and survival factor.
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