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,§
*
Department of Medicine, Cleveland Veteran’s Affairs Medical Center, Cleveland, OH 44106;
Case Western Reserve University, Cleveland, OH 44106;
Department of Dermatology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106; and
§
Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106
Allograft rejection has been associated with detection of the type
1 lymphokines, IFN-
and IL-2. The role of type 2 cytokines (IL-4 and
IL-5) remains controversial, as is whether alloreactive
CD4+ and CD8+ T cells behave similarly when
exposed to type 2 cytokine-enhancing manipulations. We studied the
characteristics of alloreactive CD4+ and CD8+ T
cells before and after type 2 immune deviation induced by IL-4 plus
anti-IFN- Ab. Alloreactive T cells from naive mice were low in
frequency, produced only IL-2, and were predominantly CD4+,
while alloreactive T cells from allograft-primed mice were high in
frequency, produced IFN-, IL-2, and IL-4, and were predominantly
CD8+. Type 2 immune deviation of allospecific
CD4+ T cells resulted in IL-4 and IL-5 production without
IFN-, consistent with unipolar type 2 immunity. These T cells
mediated delayed-type hypersensitivity, but not cytotoxicity. Under
identical type 2 cytokine-inducing conditions, allospecific
CD8+ T cells were primed to become IL-4, IL-5, and IFN-
producers, and exhibited cytotoxicity, but not classic delayed-type
hypersensitivity. Adoptive transfer of either cell population into SCID
recipients of allogeneic skin resulted in graft rejection, with stable
allospecific type 2 cytokine production in vivo. Adoptive transfer of
the IL-4/IL-5-producing CD4+ T cells, but not the
CD8+ T cells, induced a distinct histopathology
characterized by marked eosinophilic infiltration of the skin. We
conclude that type 2 immune deviation has differential effects on
CD4+ and CD8+ T cells and results in emergence
of alternate effector mechanisms capable of destroying
allografts.
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