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• W1990897911 abstract "63 We have shown that mononuclear cells (MNC) localize preferentially in fibronectin (FN)-rich areas in rejecting rat cardiac allografts (Tx). The cellular form of FN (cFN), virtually absent in native hearts, is primarily expressed by infiltrating macrophages and endothelial cells in rejecting Tx. However, macrophages infiltrating cardiac Tx in rats rendered tolerant by treatment with RIB-5/2, a nondepleting CD4 mAb, fail to express cFN. This study was designed to test a hypothesis that the lack of macrophage-derived FN may, in fact, play a functional role in regulating IL-2 and IFN-γ levels in tolerant hosts. In the first series of experiments, we contrasted intra-Tx events in tolerant hosts with those in recipients in which the unresponsive state has been abolished. Adoptive transfer of regulatory spleen cells (100×106) from RIB-5/2-treated LEW recipients of LBNF1 cardiac Tx into syngeneic secondary hosts, confers infectious tolerance to donor-specific test cardiac Tx (AT group). However, concomitant infusion of OX36, a CD4-depleting mAb (2mg/rat i.v. at day 1 and 2 post-Tx), uniformly recreates acute (7-day) rejection of cardiac Tx in otherwise tolerant AT hosts (AT-OX36 group). The OX36-facilitated disruption of the infectious tolerance pathway was associated with enhanced intra-Tx expression of macrophage-derived FN (++/+++ vs −), and increased frequency of IL-2R+ cells (44±10 vs 2±1 p<0.01), T cells (74±2 vs 25±2 p<0.05) and macrophages (138±57 vs 68±9 p<0.05), as determined by immunostaining. Increased deposition of cFN in rejecting cardiac Tx in OX36-AT group was accompanied by a sharp increase in the expression of mRNA coding for IL-2 (2.5-fold) and IFN-γ (5-fold), as compared to AT group. Then, in an attempt to block interactions between FN and MNC in rejecting cardiac Tx, a course of CS1-FN peptides (1mg/day ×6 days i.v.), that specifically block interactions between cFN and its VLA-4 receptor on MNC, was given to AT-OX36 rats (CS1-OX36-AT group). The CS1-VLA-4 blockage decreased the number of T cells by 1/3, without significantly affecting infiltrating IL-2R+ cells (45±4 vs. 73±22 in OX36-AT) or macrophages (>200 in both groups). cFN was densely deposited in both cardiac Tx groups (++/+++), with densitometric ratio of ca. 1.5 in both OX36-AT and CS1-OX36-AT. In contrast, CS1-FN therapy significantly depressed intra-Tx expression of IL-2 and IFN-γ mRNAs, as determined by competitive template RT-PCR. The number of transcripts/μg RNA in CS1-OX36-AT vs OX36-AT group was for IL-2: 4.5×104 vs 12×104 (p<0.05), and for IFN-γ. 6.8×104 vs. 23 × 104 (p<0.02). In conclusion, the functional blockage of FN - VLA-4 interactions plays an important role in the maintenance of transplantation tolerance by preventing local expression of Th1 cytokines that otherwise facilitate acute Tx rejection." @default.
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• W1990897911 date "1999-04-01" @default.
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• W1990897911 title "FIBRONECTIN - VLA-4 INTERACTIONS REGULATE Th1 CYTOKINE NETWORK IN TOLERANT CARDIAC ALLOGRAFT RECIPIENTS" @default.
• W1990897911 doi "https://doi.org/10.1097/00007890-199904150-00091" @default.
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