PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “rejection”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1977

In vitro correlates of rejection. II. Rat mixed lymphocyte reactivity in vitro and cardiac allograft acute rejection, hyperacute or accelerated rejection, and prolongation by active immunization.

The relationship of F1 hybrid to parental strain cardiac allograft rejection rates to mixed lymphocyte reactivity in vitro has been studied in 10 strain combinations crossing the major histocompatibility barrier in three different models of acute rejection, accelerated or hyperacute rejection after skin graft immunization, and attempted active enhancement using 10(7) donor strain bone marrow cells. Although high and low reactivity could be discerned between the F1 hybrid and reciprocal parental strain in three of five instances in the one-way lymphocyte culturr reaction, low reactivity was only associated with prolonged graft survival in one combination. Two strain combinations giving high in vitro lymphocyte responses were associated with easily enhanced grafts. The BN strains was a low responder in vitro in the three combinations tested and as a recipient strain, allografts could not be actively enhanced. After skin graft presensitization, BN recipients rejected grafts hyperacutely in two of three combinations and with a median survival time of 2 days in the third combination. The association of poor in vitro proliferative responses, the inability to induce enhancement, and rapid graft rejection after skin graft presensitization could be related to genetic mechanisms controlling the amount and class or subclass of antibody or to the generation of suppressor cells and remains to be determined.

Animals↗
PubMed1978

The cellular basis of allograft rejection in vivo. I. The cellular requirements for first-set rejection of heart grafts.

The nature of the cells required for first-set graft rejection in vivo was examined by using an adoptive transfer system to restore heart-graft rejection in irradiated rats. Highly purified inocula of peripheral T lymphocytes were shown to quantitatively account for the restorative ability of adoptively transferred cells. These T cells were shown to be long-lived small lymphocytes which are not recently derived from the thymus during adult life. They belong to the pool of T cells which constantly recirculate from blood to lymph as shown by their rapid appearance in the lymph of iradiated syngeneic rats after intravenous injection. Neither B lymphocytes nor antibodies in the circulation or in the graft itself are required for first-set graft rejection.

B-Lymphocytes↗
PubMed1978

The cellular basis of allograft rejection in vivo. II. The nature of memory cells mediating second set heart graft rejection.

An adoptive transfer system was used to study the cellular basis of memory in animals immunized by grafting with major histocompatibility complex incompatible tissue. Memory was characterised by a large (greater than 100 fold) increase in the potency of lymphocytes to precure graft rejection. This increase in potency endured for at least 1 yr after sensitization. The memory cells were shown to be Ig-- small lymphocytes which were long lived and which did not recirculate from blood to lymph in normal recipients although they did home to lymphoid tissue from which they could be recovered several months later. The thymus was not required either for the generation of memory cells or their maintenance. Cells carrying memory for alloantibody synthesis did recirculate normally but alloantibody synthesis was shown not to be required for rejection.

Animals↗
PubMed1977

In vitro correlates of rejection. I. Suppressive effect and specificity in mixed lymphocyte interaction of alloantiserum producing hyperacute rejection.

A hyperimmune antiserum from WfBN F1 hybrid rats primed to hyperacutely reject LBN F1 cardiac allografts has been studied. A large volume of antiserum will cause allograft rejection in less than 1 day. In the in vitro MLI, concentrations of this antiserum as low as 0.05% are markedly suppressive. This suppression is dose-dependent and immunizing-strain-specific at concentrations less than 1%. The suppressive activity is in the globulin fraction. After in vivo absorption, donor-strain specificity is clearly shown, with some cross-reactivity with third-party ACI strain. Moderate suppression of the rat MLI was seen with some normal rat sera, and augmentation of the MLI was seen in some experiments when very dilute concentrations of hyperimmune serum were used. Since suppression or augmentation of the MLI can occur as a function of antiserum dose and presumably antibody concentration, single measurements of MLI blocking factors may be misleading, and MLI suppression is not necessarily a correlate of allograft enhancement.

Animals↗
PubMed1976

[Hyperproduction of the epithelium and its vital rejection in the lumen of the small intestine outside the "rejection zone"].

Whole and histologically-treated biopsy material of the small intestinal mucosa of dogs with a full intestinal fistulae and of dogs with a portion of the small intestine excluded from digestion was studied. An intensive production of the surplus epithelial structures (protrusions, layers) was revealed in the areas of the crypts and the base of the villi. Rejection of these structures into the intestinal lumen occurred outside the "expulsion zone" with the preservation of the intactness of the villar surface. Less marked signs of this process were seen in control material. The data obtained testify to the fact of the existence of another way of development of the crypt cell leaving the crypt-villus system in the composition of the branching and rejecting epithelial structures.

Animals↗
PubMed1976

Tumour rejection in rats sensitized to embryonic tissue. I. Rejection of tumour cells implanted s.c. and detection of cytotoxic lymphoid cells.

Wistar rats were sensitized to rat embryonic tissue by immunization with irradiated (5000 rad) rat embryo cells (2 X 10(6) s.c. + 1 X 10(6) i.p.) derived from embryos aged 14-15 days, or by implantation of irradiated (5000 rad) tissue grafts from these embryos. Three to five immunizations were given at weekly intervals, and the rats were then challenged subcutaneously 7-10 days after the final inoculum with minimal tumour-producing tumour cell doses. Immunization with irradiated rat embryo cells failed to influence the growth and development of tumour cells prepared from hepatoma D23 and D30, sarcoma Mc57, mammary carcinoma AAF57 or cells prepared from spontaneously arising mammary carcinomata Sp4 and Sp15. Using adoptive transfer techniques, lymphoid cells from embryo-sensitized rats, when used in a 3000 : 1 ratio (lymphoid cells : tumour cells), were shown effectively to retard the growth of hepatoma D23 in 3 out of 7 experiments performed. Similar adoptive transfer procedures proved ineffective in preventing the growth of mammary carcinoma AAF57. Using in vitro cytotoxicity tests, lymph node cells and spleen cells from embryo-immunized rats were shown to be cytotoxic for several rat tumour cell targets : hepatoma D23 (7/10 tests), sarcoma Mc7 (8/12 tests), mammary carcinoma AAF57 (2/2 tests) and Sp4 (3/4 tests), and for 14-15-day-old rat embryo cells (5/10 tests). In comparative tests lymphoid cells were relatively non-cytotoxic for 20-day-old rat embryo cells (1/6 tests) or cells prepared from adult rat lung or kidney (1/10 tests). The role of embryonic antigen(s) in tumour rejection is discussed.

Animals↗
PubMed1977

Cellular components of allograft rejection: identity, specificity, and cytotoxic function of cells infiltrating acutely rejecting allografts.

Functioning mononuclear cells have been harvested from heterotopic rat cardiac allografts during maximal transplant cellular infiltration. T cells, identified by a T cell-specific absorbed rabbit anti-rat brain serum, constituted two-thirds of the total cells recovered. Approximately 20% of the infiltrating cells bear and synthesize surface immunoglobulin. Macrophages, identified by latex ingestion and morphologic and cytochemical techniques, comprise 9% of the graft infiltrate. Donor-specific cytotoxic T lymphocytes are concentrated within the graft. A separate population of Fc receptor-positive recovered cells mediate antibody-dependent LMC (Ab-LMC). Neither effector cell was adherent or phagocytic. These studies have conclusively established that cytotoxic T lymphocytes accumulate within rejecting allografts; however, the enriched presence of cytotoxic T cells within the grafts is not fully dependent upon antigen recognition per se, since Lew animals grafted with both BN and BUF hearts have Lew anti-BN and Lew anti-BUF killer cells in each graft.

Animals↗
PubMed1977

When should the third renal transplant rejection episode be treated?

Recent reports cite better survival when repeatedly rejecting renal allografts are removed and patients returned to hemodialysis. However, the criteria for graft removal remain undefined; although some reports recommend removing all kidneys undergoing a third rejection. In our series (1968-1973) of 316 patients with technically successful first grafts followed 2(1/2)-8 years, graft survival was inversely related to the number of rejection episodes. One hundred per cent of kidneys without rejection are currently functioning or functioned at the time of death compared to 90% with one rejection, 67.4% with two and 21% with three. However, 40% of kidneys having three rejection episodes functioned longer than one year after treatment of the third rejection episode. In an attempt to determine the predictability of one year graft survival or failure following treatment of the third rejection, a formula was developed that correctly predicted in 33 of 38 (87%) patients. The formula was based on information available prior to treatment of the third rejection episode, and represents an index of baseline renal function (serum creatinine after second rejection episode) and two indices of the severity of rejection episodes (serum creatinine change between the first and second rejection episodes; rapidity of sequential rejection).Following its derivation, the formula was applied to a second group (1974) of 19 patients having had three rejection episodes. The formula correctly predicted one year allograft survival or failure following treatment of the third rejection episode in 68% of these patients. A striking finding of our review was a significant difference in current patient survival between those having no rejection episodes (89%) and those having one or more rejection episodes (65%) (p < .00001). There was no significantly greater long-term curtailment in survival if more than one rejection eipsode was treated. Patients having one rejection eipsode seemed to die from varying causes and at varying time periods. Patients dying after two or more rejection episodes had an increased incidence of deaths due to bacterial infection.

Creatinine↗
PubMed1979

Acute rejection episodes and long-term transplant function.

From 1974 to 1976, 114 kidneys transplanted to 108 patients underwent acute rejection episodes. With repeated rejections there was an increased likelihood of recovery without subsequent rejections, eg, 59% of kidneys that had three rejections regained prolonged good function. Repetitive rejections did not increase mortality. Discriminate analysis of the best serum creatinine level or creatinine clearance within 30 days of rejection and the time interval between rejection episodes correctly predicted the outcome of second rejections in 20/25 cases and correctly predicted the outcome of third rejections in 23/29 cases. Treatment of a third rejection was successful in 70% of kidneys if the best serum creatinine level was less than 2 mg/dL after the second rejection and was successful in 77% of kidneys if the time interval between second and third rejections was longer than one month.

Acute Disease↗
PubMed1979

Serum levels of IgM, IgD, IgA and IgG before and during rejection of renal allotransplants.

In recipients of renal allotransplants the relationship of IgM, IgA and IgG serum levels to 26 rejections was investigated, as well as the relationship of IgD and 22 rejection. For IgM and IgG a significant decline was found in the whole group (p less than 0.05) and in the sub-group of rejections after a period longer than one month following transplantation (p less than 0.05 in IgM and p less than 0.02 in IgD). As compared with values before rejection, a decline of IgM occurred in 11 rejections which amounted to more than 20% and a decline of IgD in 10 rejections by more than 50%. Changes of the serum levels of IgA and IgG were not statistically significant (p greater than 0.05). In recipients of renal allotransplants serum immunoglobulin (Ig) levels of the main classes were investigated for two reasons: (1) as part of a check-up of the condition of the graft and screening of rejection and (2) to detect possible deficiencies of humoral immunity with increased liability to infections. As regards monitoring of the risk of the rejection crisis, hitherto assembled experience did not provide an unequivocal answer in which class of Ig the greatest change may be expected, whether a rise or fall, and it is not even clear whether investigations of serum Ig levels will be a positive contribution. There is only agreement on the point that IgA levels are not related to rejection; according to some authors this applies also to IgM and IgG (8, 11). Other authors (1, 15, 17) appreciate in conjunction with rejections the importance of high IgM and IgG levels, while other workers observed a significant decline of IgM (13, 16, 19). IgD levels were investigated in our previous work on the relationship of renal functions and serum Ig levels in recipients of renal allotransplants (7); we found no reports on the relationship between IgD and rejection.

Adolescent↗
PubMed1976

Kidney transplant biopsies in the diagnosis and management of acute rejection reactions.

In 68 consecutive renal transplant biopsies, histopathologic changes and clinical status of the graft recipient, both at the time of biopsy as well as one month later, were evaluated by independent observers. Nine histologic features were graded semiquantitatively (scale, 0 to 4): glomerular endothelial swelling, proliferation, exudation and necrosis; interstitial edema and infiltrate: vascular endothelial edema, infiltration and necrosis. The total score for each biopsy was termed the acute rejection index (ARI). The validity of the ARI as a means of evaluation rejection reactions was established by correlating the ARI with a second, overall histopathologic categorization. Clinical status at the time of biopsy was classified by retrospective analysis of all clinical data except the biopsy. The mean ARI of patients with an acute clinical rejection was significantly higher than those of patients with just a chronic clinical rejection or no clinical rejection. The utility of the biopsy in predicting the response of the graft recipient to therapy was evaluated in those 46 patients in whom an acute rejection was diagnosed clinically and in whom a full and complete course of therapy for the acute clinical rejection was given. Of the 28 patients whom the pathologist predicted would response to therapy, 27 did show substantial improvement of their renal function up to one month following institution of treatment. Of the 18 patients whom the pathologist predicted would not respond to therapy, 15 had no clinical response. The data suggest that the transplant biopsy is helpful in 1) establishing the diagnosis of an acute rejection and 2) indicating whether or not the graft recipient will respond to standard immunosuppressive treatment for an acute rejection,

Acute Disease↗
PubMed1977

Circulating immune complexes after renal transplantation. Correlation of increased 125I-Clq binding activity with acute rejection characterized by fibrin deposition in the kidney.

To assess the role of circulating immune complexes in the pathogenesis of acute rejection, sera were measured for such complexes by the (125)I-C1(q) binding assay in 45 normal subjects, 24 allografted patients undergoing acute rejection, and in 11 allografted patients in a quiescent phase. Increased C1(q)-binding activity (C1(q)-BA) was detected in 14 patients with acute rejection, 9 of whom had renal biopsies showing fibrin deposition in the vasculature together with cellular infiltrates in the tubulo-interstitial structures; renal histology was not available in the other 5 patients. The other 10 patients with acute rejection, whose biopsies showed only cellular infiltrates, and the 11 patients in a quiescent phase posttransplantation did not have increased levels of serum C1(q)-BA. Of the group with increased serum C1(q)-BA, serial studies in eight patients showed a correlation between increased serum C1(q)-BA and the occurrence of rejection; with reversal by therapy, serum C1(q)-BA returned to within normal levels. Complexes from six patients were analyzed by sucrose density gradient ultracentrifugation to have sedimentation coefficients ranging from 15S to 18.4S. After acid dissociation and analysis by double-diffusion techniques, C1(q)-reactive complexes were shown to contain IgG. Immunofluorescent studies done in five renal biopsies from this group revealed granular deposits of immunoglobulin, and (or) less frequently, of complement in the glomeruli or the tubular basement membranes. The findings suggest that circulating immune complexes may mediate the type of acute rejection characterized by fibrin deposition in the kidney. The role of circulating immune complexes arising from the recipient's original kidney disease could be excluded in 10 patients with humoral rejection, inasmuch as the underlying renal pathology was of a "nonimmunologic" nature; this was corroborated by sequential studies in six patients in whom circulating immune complexes could not be demonstrated before rejection. The participation of administered antilymphocyte globulin (ALG) as an antigen also appears to be excluded in four patients, two who were not given ALG, and in two of whom episodes of rejection occurred unrelated temporally to ALG administration.

Antigen-Antibody Complex↗
PubMed1976

The importance of lipase determinations in the detection of pancreaticoduodenal allograft rejection.

In canine pancreaticoduodenal allografts, the exocrine pancreas is rejected earlier that endocrine islets. Lipase levels prove to be a good parameter of the rejection onset, occurring before other parameters showed any changes. Moreover there is a good correlation between the lipasemia and the functional condition of the exocrine pancreas in periods before and after the rejection crisis. Variations in other parameters which occur during rejection and consequently can sustain the diagnosis of rejection, are an amylase rise, a leucocytosis, a fasting insulin decrease and glucose increase. These changes however are less striking than lipase variations; besides they do not occur constantly and can also be seen in other circumstances. In this way they not only lack rejection specificity but likewise do not allow the functional evolution during and after the rejection crisis. The insulinemia, after glucose loading, is the only one of the mentioned parameters which gives an adequate idea of the endocrine graft function and which consequently has a prognostic value after the rejection crisis, with regard to the function and the survival of the graft. Cool storage preservation of the grafts using a Largiadèr solution proved to have no detrimental effects on the pancreas, as judged by the graft function, the postoperative survival time of the dogs and the rejection pattern of the transplants.

Amylases↗
PubMed1976

Anti-donor immune responses in prediction of transplant rejection.

We assessed various immune responses against donor tissue to determine their value in the diagnosis and prediction of clinical rejection episodes. Twenty-six consecutive clinical renal-transplant recipients were examined. Cell-mediated lymphocytotoxicity preceded and accompanied 41 of 45 rejection episodes (P less than 0.001). Complement-dependent antibody was present in 12 of 15 rejections (P less than 0.002)--four not accompanied by, and eight in association with, cell-mediated lymphocytotoxicity. Mixed lymphocyte reactivity or nonreactivity and inhibition by autologous serum occurred equally often in rejection and quiescence. Lymphocyte-dependent antibody occurred during both rejection episodes and quiescent phases, with a greater frequency during quiescence (P = 0.05). Cell-mediated lymphocytotoxicity was the best predictor of rejection (P less than 0.05). Cell-mediated lymphocytotoxicity was the best predictor of rejection (P less than 0.001), and was more easily suppressed by standard immunosuppressive therapy, than complement-dependent antibody. If specific cell-mediated lymphocytotoxicity, with or without antibody, recurred after rejection therapy, the graft underwent further rejection.

Antigen-Antibody Reactions↗