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,¶
Departments of
*
Urology and
Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195;
Department of Urology, Hokkaido University School of Medicine, Sapporo, Japan;
§
Department of Urology, Tokyo Women’s Medical College, Tokyo, Japan; and
¶
Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44195
Chemokines direct leukocyte recruitment into sites of tissue
inflammation and may facilitate recruitment of leukocytes into
allografts following transplantation. Although the expression of
chemokines during rejection of MHC-disparate allografts has been
examined, chemokine expression in MHC-matched/multiple minor
histocompatibility Ag-disparate allografts has not been tested. The
intraallograft RNA expression of several C-X-C and C-C chemokines was
tested during rejection of full thickness skin grafts from B10.D2
donors on control Ig-, anti-CD4 mAb-, and anti-CD8 mAb-treated
BALB/c recipients. In all recipients, two patterns of intragraft
chemokine expression were observed during rejection of these grafts: 1)
macrophage-inflammatory protein-1
, macrophage-inflammatory
protein-1ß, GRO- (KC), JE, and IFN-
-inducible protein (IP-10)
were expressed at equivalent levels in allo- and isografts for 2–4
days posttransplant and then returned to low or undetectable levels;
and 2) IP-10 and monokine induced by IFN- (Mig) were expressed in
the allografts 3 days before rejection was completed, suggesting a
possible role in recruiting primed T cells into the allograft. Three
days before completion of rejection, intraallograft IP-10 protein was
restricted to the epidermis, whereas Mig was located in the lower
dermis and associated with the intense infiltration of mononuclear
cells. Treatment of B10.D2 recipients with rabbit antiserum to Mig, but
not to IP-10, delayed rejection of the allografts 3–4 days. The
results suggest that Mig mediates optimal recruitment of T cells into
MHC-matched/multiple minor histocompatibility Ag-disparate allografts
during rejection.
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