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,
*
University of Melbourne, Department of Surgery, Royal Melbourne Hospital, Victoria, Australia;
Cardiovascular Biology Laboratory, Harvard School of Public Health, and
Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115; and
§
Monash Medical School, Alfred Hospital, Prahran, Australia
To study the role of IL-4 in tolerance induction and transplant
arteriosclerosis, BALB/c hearts were transplanted into C57BL/6J
wild-type or IL-4 knockout (IL-4-/-) recipients. A
30-day course of anti-CD4/8 mAb was used to induce long term graft
survival. Primary graft survival was 50% (5 of 10) in
IL-4-/- recipients comparable to 63% (5 of 8) in
wild-type recipients. Mice with allografts surviving >80 days were
tested for tolerance by challenge with a second donor or third party
(CBA) heart. Secondary donor-strain heart grafts survived >30 days,
but showed histologic evidence of ongoing alloimmune response. Third
party hearts rejected rapidly. Although immunostaining and
32P RT-PCR assays showed no differences in the mononuclear
cell infiltration and T cell activation between IL-4-/-
and wild-type tolerant recipients, some monokines (IL-12, TNF-
, and
allograft inflammatory factor-1) were up-regulated in grafts from
IL-4-/- recipients. Computer-assisted analysis of
elastin-stained vessels revealed that the severity of vascular
thickening (percentage of luminal occlusion, mean ± SD,
n = 329) was similar in grafts from
IL-4-/- (63.7 ± 16.9%) and wild-type (69.5 ±
17.6%) recipients. Thus, IL-4 deficiency did not alter primary or
secondary graft survival, infiltration, or vascular thickening. The
selective alterations in monokine expression suggests that alternative
pathways are activated and may compensate in IL-4-/-
mice.
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