Surface Properties and Functional Characteristics of Infiltrating Cells Harvested From Acutely Rejecting Cardiac Allografts in Inbred Rats

Nl, Tilney; Tb, Strom; Sg, Macpherson; Cb, Carpenter

doi:10.1097/00007890-197510000-00009

Cited by 81 publications

(30 citation statements)

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“…Lymphocytic infiltration is a salient feature. [2][3][4][5] Recently, we and others have used radiolabeled white blood cell elements in experimental animals and patients to identify and localize inflammation accompanying myocardial infarction,6 7 myocarditis,8 or abscess formation. 9 Because methods are now available to facilitate separation and labeling of selected blood cell elements, and because sensitive clinical detection of rejection of cardiac transplants appears likely to become increasingly important, we undertook this study to determine whether sensitive external detection of rejection of cardiac transplants was feasible with lymphocytes labeled with indium-111 ("'In).…”

mentioning

confidence: 99%

Detection of cardiac transplant rejection with radiolabeled lymphocytes.

Bergmann¹,

Lerch²,

Carlson³

et al. 1982

Circulation

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SUMMARY To determine whether rejection of cardiac transplants could be detected specifically and noninvasively by lymphocytes labeled with indium-111 ("1In), we studied 36 allogeneic and 14 isogeneic heterotopic cardiac transplants in rats. Allogeneic grafts accumulated autologous ll'In-lymphocytes, detectable scintigraphically 24 hours after i.v. injection of the labeled cells. At the time of peak histologic rejection, the allogeneic grafts accumulated 9.2 ± 4.8 times more activity than the native hearts (determined by well counting). The tissue-to-blood ratio in the rejecting transplants was 3.7 ± 2.2; total uptake by the graft was 2.9 ± 2.1% of the injected dose. Autoradiography confirmed that graft radioactivity was associated with labeled lymphocytes. In contrast, isogeneic grafts showed no signs of rejection and did not accumulate radioactivity. Because conventionally isolated and labeled lymphocytes are often contaminated with platelets, we prepared both "'In-platelets and purified "'In-lymphocytes for use in additional experiments. Allogeneic grafts accumulated platelets and purified lymphocytes independently. Thus, deposition of immunologically active cells in the rejecting graft representing specific pathophysiologic events can be detected. The results suggest that rejection of cardiac transplants can be detected noninvasively, potentially facilitating objective early clinical detection of rejection and titration of antirejection therapy.EARLY DETECTION of incipient rejection of transplanted organs is an important criterion in titrating antirejection therapy. Clinically, detection is often based on elevated concentrations of macromolecules released into the circulation or into the urine, or on nonspecific manifestations of inflammation, including fever or leukocytosis.' In the case of cardiac transplants, invasive endocardial biopsy has been used to increase the sensitivity of detection of rejection crises.2The rejection process has been characterized extensively in experimental animals and in patients. Lymphocytic infiltration is a salient feature.2-5 Recently, we and others have used radiolabeled white blood cell elements in experimental animals and patients to identify and localize inflammation accompanying myocardial infarction,6 7 myocarditis,8 or abscess formation.9 Because methods are now available to facilitate separation and labeling of selected blood cell elements, and because sensitive clinical detection of rejection of cardiac transplants appears likely to become increasingly important, we undertook this study to determine whether sensitive external detection of rejection of cardiac transplants was feasible with lymphocytes labeled with indium-111 ("'In).The reflected deposition of radiolabeled platelets rather than white cells, because the conventional leukocyte preparations are heavily contaminated with platelets.'' 13 Because accumulation of lymphocytes is a more specific criterion of rejection and indicates specific pathophysiologic processes, we compared the accumulation of labeled lym...

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mentioning

confidence: 99%

Detection of cardiac transplant rejection with radiolabeled lymphocytes.

Bergmann¹,

Lerch²,

Carlson³

et al. 1982

Circulation

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“…Morphologically these cells were divided into three types by electron microscopy (Lindquist et al 1971). Moreover, these infiltrating cells harvested from the rejected cardiac allografts of rats consisted of 35 to 45% of B-lymphocytes, which had no Fc-receptors and were highly cytotoxic against the donor thymocytes (Tilney et al 1975). These active cells have often been detected in lymph flow from renal allografts or in peripheral blood of acute rejection showed T-lymphocytes experimentally in rat renal allografts by immunofluores cent staining using rabbit anti-rat thymocyte sera.…”

Section: Resultsmentioning

confidence: 99%

Identification of T-lymphocytes in human renal allografts and urine by the fluorescent antibody technique using anti-human T-lymphocyte serum (AHTS).

Kunori

Nishihira

Tan

et al. 1978

Tohoku J. Exp. Med.

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“…Cardiac allografts were transplanted in groups of [8][9][10] animals. The procedures used in the collection of infiltrating cells are modifications of techniques previously described (22). At serial intervals after grafting, the hearts were removed and cleaned of surrounding tissue and clot.…”

Section: Methodsmentioning

confidence: 99%

Transfer of specific unresponsiveness to organ allografts by thymocytes. Specific unresponsiveness by thymocyte transfer.

Hendry

Tilney

Baldwin

et al. 1979

The Journal of Experimental Medicine

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Prolonged survival of vascularized organ allografts has been produced in unmodified inbred rats by transfer of thymocytes from enhanced, engrafted, syngeneic animals. For these thymocytes to increase significantly the survival of test allografts they must be harvested 6-9 d after transplantation. Thymectomy of the enhanced, engrafted animals during the same critical period causes acute rejection of othewise long surviving grafts. For optimal effect, the enhanced thymocyte donor must be actively and passively immunized and receive a cardiac allograft. The necessity for erythrocytes in the initial active immunization regimen is noted. Additionally, the antigenic specificity of the suppressor effect has been established with two histoincompatible donor rat strains. Cellular and humoral host responses mounted by test graft recipients after thymocyte transfer from enhanced, engrafted donors are different from those mounted either by unmodifed animals acutely rejecting their grafts or by enhanced rats bearing well-functioning grafts. Numbers of T lymphocytes are reduced in the grafted hearts and in the spleens of test graft recipients, a finding paralleled by the complete absence of specific direct lymphocyte-mediated cytotoxicity. In contrast, cytotoxic antibody production, although delayed, is increased in magnitude, peaking around the time of graft rejection. These studies provide evidence that different biological manipulations can modify separate pathways in the complex cellular and humoral responses towards organ allografts. They demonstrate that cellular immunity is critically involved in immunological enhancement of vascularized organ allografts, a phenomenon hitherto considered primarily humoral. It seems clear that cells with suppressor activity are present within the thymus during the early phases of immunological enhancement.

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Surface Properties and Functional Characteristics of Infiltrating Cells Harvested From Acutely Rejecting Cardiac Allografts in Inbred Rats

Cited by 81 publications

References 0 publications

Detection of cardiac transplant rejection with radiolabeled lymphocytes.

Detection of cardiac transplant rejection with radiolabeled lymphocytes.

Identification of T-lymphocytes in human renal allografts and urine by the fluorescent antibody technique using anti-human T-lymphocyte serum (AHTS).

Transfer of specific unresponsiveness to organ allografts by thymocytes. Specific unresponsiveness by thymocyte transfer.

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