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At least 1,063 records · Page 59Linked to original sources
PubMed1972

Functional maturation of thymic lymphocyte populations in vitro.

Mouse thymocytes were cultured for short periods of time either alone or with one of two supporting cell populations, splenic adherent cells or thymic epithelial cells. The thymus-derived (T) cell activity of thymocytes cultured on supporting cell populations increased dramatically during 2 days of culture, as assayed in the mixed lymphocyte interaction (MLI), response to phytomitogens, and helper cell activity in the in vitro antibody response. The level of activity attained was equal to that of spleen and lymph node lymphocytes and greater than that of steroid-resistant thymocytes. The cultured thymocytes had surface antigens characteristic of mature T lymphocytes with regard to theta and H-2. The appearance of functionally active lymphocytes in vitro depended upon cell division. Most of the active cultured cells arose from cells already undergoing maturation, i.e., from cells with reduced theta determinants and increased H-2 determinants. We therefore have generated a population of thymocytes indistinguishable from peripheral T lymphocytes using simple in vitro techniques. The extent to which the production of these active lymphocytes depends upon in vitro differentiation is discussed.

Animals↗
PubMed1988

Long-term residence of a graft is an insufficient stimulus for the induction of tolerance. Investigating the role of cyclosporine in class I-disparate heart grafts in the rat.

This study demonstrates that the induction of tolerance is possible across a class I only antigenic barrier that fails to produce heart graft rejection. However, the long-term residence alone of such a graft per se, does not necessarily lead to the establishment of systemic tolerance in the recipient. The important finding in this study with regard to the biology of allograft tolerance, is that while the class I antigen provides the stimulus, its presence alone is not sufficient for the induction of tolerance; indeed, the action of the Cyclosporine A (CyA) is a necessary adjunct to its induction.

Animals↗
PubMed1990

T cell requirements for the rejection of renal allografts bearing an isolated class I MHC disparity.

This study has examined the cellular and humoral responses underlying the rejection of rat renal allografts bearing an isolated RT1Aa class I MHC disparity. RT1Aa disparate kidneys were rejected promptly by high responder RT1u but not by low responder RT1c recipients (median survival time 10 d and greater than 100 d, respectively). The magnitude and phenotype of the cellular infiltrate were similar in rejecting and nonrejecting RT1Aa disparate kidneys. Paradoxically, graft infiltrating cells and spleen cells from RT1u recipients showed minimal ability to lyse donor strain lymphoblasts in vitro, whereas effector cells from RT1c recipients showed modest levels of cytotoxicity. Injection of RT1u rats with MRC OX8 mAb was highly effective at selectively depleting CD8+ cells from graft recipients but had no effect in prolonging the survival of RT1Aa disparate grafts despite the complete absence of CD8+ cells from the graft infiltrate, which included numerous CD4+ T cells and macrophages. RT1u, but not RT1c, recipients mounted a strong alloantibody response against RT1Aa disparate kidneys. Immune serum obtained from RT1u recipients that had rejected a RT1Aa disparate graft was able, when injected into cyclosporin-treated RT1u recipients, to restore their ability to reject a RT1Aa, but not a third-party RT1c, kidney. These results suggest that CD8+ cells in general and CD8+ cytotoxic effector cells in particular are unnecessary for the rapid rejection of RT1Aa class I disparate kidney grafts by high responder RT1u recipients. By implication, CD4+ T cells alone are sufficient to cause prompt rejection of such grafts and they may do so by providing T cell help for the generation of alloantibody.

Animals↗
PubMed2000

Genes of the class II and class III major histocompatibility complex are associated with typhoid fever in Vietnam.

The influence of genes of the major histocompatibility complex (MHC) class II and class III loci on typhoid fever susceptibility was investigated. Individuals with blood culture-confirmed typhoid fever and control subjects from 2 distinct geographic locations in southern Vietnam were genotyped for HLA-DRB1 and HLA-DQB1 alleles, the gene that encodes tumor necrosis factor (TNF)-alpha (TNFA [-238] and TNFA [-308]), the gene that encodes lymphotoxin-alpha, and alleles of the TNF-alpha microsatellite. HLA-DRB1*0301/6/8, HLA-DQB1*0201-3, and TNFA*2 (-308) were associated with susceptibility to typhoid fever, whereas HLA-DRB1*04, HLA-DQB1*0401/2, and TNFA*1 (-308) were associated with disease resistance. The frequency of all possible haplotypes of the 3 individually associated loci were estimated and were found to be significantly different in typhoid case patients and control subjects (chi2=55.56, 32 df; P=.006). Haplotypes that were either protective (TNFA*1 [-308].DRB1*04) or predisposed individuals to typhoid fever (TNFA*2 [-308].DRB1*0301) were determined. This report identifies a genetic association in humans between typhoid fever and MHC class II and III genes.

Alleles↗
PubMed2005

Systemic lupus erythematosus and the extended major histocompatibility complex--evidence for several predisposing loci.

OBJECTIVE: Systemic lupus erythematosus (SLE) is an autoimmune disease reported to be associated with several alleles in the HLA complex. The purpose of this study was to systematically examine the extended HLA complex (xMHC) in order to get an overview of the primary predisposing genetic factors. MATERIALS AND METHODS: One hundred and sixty-four SLE patients and 254 healthy, unrelated controls were genotyped for HLA-DRB1, -B and -A alleles, as well as 13 microsatellites markers covering the xMHC. Moreover, we selected 335 additional controls matched with the patients for the HLA haplotypes showing the strongest associations, in order to look for additional predisposing loci. RESULTS: Two regions of the xMHC showed associations: the region covering DRB1 to B, and the extended class I region. Explicitly, DRB1*03 and B*08 displayed strong associations with SLE, which seem to be independent of each other. Furthermore, associations were seen with alleles at microsatellites D6S2225 and D6S2223, located about 3.6 Mb telomeric of HLA-B, and these were not secondary to the associations found with DRB1*03 and B*08. CONCLUSION: Both the DRB1*03 and the B*08 alleles display disease association, either implicating involvement of both alleles or caused by another yet unidentified gene(s) in linkage disequilibrium. The associations found in the extended class I region could be markers for a 'novel' predisposing locus (loci) in SLE, adding to the risk conferred by DRB1*03 and B*08. Interestingly, this region has been shown to also be associated with other autoimmune diseases, hence the gene(s) might confer a general propensity for autoimmunity.

Adolescent↗
PubMed1997

The alloimmunized patient: monitoring and therapeutics.

The sensitization of renal transplant patients in the form of antihuman leukocyte antigen antibodies often constitutes significant risk to allograft function. Testing for these antibodies is done before, at the time of, and after renal transplantation. Correct interpretation of the results necessitates an understanding of the principles of the tests and of the clinical factors in the patients, especially those receiving another transplant. Treatment remains difficult, although preliminary trials with intravenous gamma globulin have shown promising results in some patients.

Cytotoxicity Tests, Immunologic↗
PubMed1981

Clinical significance of antimonocyte antibody in kidney transplant recipients.

Monocytes appear to contain an antigen system very similar to the "cell-specific" antigen system previously identified on the vascular endothelial cell (VEC). By using a crossmatch technique with monocytes as the target cell, we tested for the presence of antibody to donor vascular endothelial cell antigens in kidney transplantation recipients, as well as performed mixed lymphocyte cultures, and T and B cytotoxicity testing. This technique detected clinically significant sensitization in some (living related) donor-recipient combinations not detected with standard T and B lymphocyte techniques. Patients with positive monocyte crossmatches but negative T or B lymphocyte crossmatches have a very high incidence of severe rejection and graft failure.

Antibodies↗
PubMed1985

Lymphocytotoxic antibodies in leukemic patients treated with bone marrow transplantation.

Lymphocytotoxic antibodies were studied sequentially in a series of 42 patients with leukemia who received a bone marrow graft. Of these patients, 38% had cytotoxic antibodies before bone marrow transplantation (BMT). After BMT the antibody status changed with time, but 62% of the patients had antibodies at some time after BMT. During the first 10 weeks after BMT, 40% of the patients had antibodies. Thereafter the frequency rose to 50% and remained at that level beyond one year after BMT. In successful grafts the gamma globulins are of donor origin six months after BMT; thus donor B cells are capable of forming lymphocytotoxic antibodies even when the immune system is suppressed by cyclosporine. The antibodies had recognizable HLA specificity in about half the cases before and after BMT. When donor and patient were HLA-identical, HLA specificity did not correspond to donor/recipient antigens. In two cases in which the donor was matched for only one haplotype, antibodies formed by recipient cells, active against donor HLA antigens, were found.

Antilymphocyte Serum↗
PubMed1987

Expression of major histocompatibility complex antigens and replacement of donor cells by recipient ones in human liver grafts.

The disappearance of certain cell populations of donor origin and their replacement by recipient-specific cells constitutes a possible explanation for the relatively mild course of acute rejection despite lack of MHC compatibility in human orthotopic liver transplantation (OLT). In the present report, graft biopsies of 12 OLT patients from a total of 42 patients were studied for expression of MHC antigens after transplantation using monoclonal antibodies to HLA-ABC and HLA-DR. The patients were selected based upon donor-recipient mismatching for HLA-A2, B7, Drw52, or DQw1. Monoclonal antibodies to these 4 polymorphic HLA antigens and monoclonal antibodies to HLA-ABC and -DR were applied to frozen tissue sections and visualized using an immunoperoxidase technique. Expression of HLA-ABC and -DR on, respectively, hepatocytes and bile duct epithelium were observed in posttransplant graft conditions such as viral infections, cholangitis, and acute rejection. However, no specific pattern of MHC antigen distribution was observed for these various pathological graft conditions. Disappearance of DR-positive Kupffer cells of donor origin and immigration of recipient ones was encountered in the early posttransplant biopsies. This Kupffer cell replacement coincided with a reversible episode of acute rejection. The disappearance of highly immunogenic cellular components as HLA-DR positive Kupffer cells of graft origin may be one of the mechanisms contributing to the mild rejection response observed in human liver transplantation.

Antibodies, Monoclonal↗
PubMed1991

Induction of kidney transplantation tolerance across major histocompatibility complex barriers by bone marrow transplantation in miniature swine.

Previous studies from our laboratory have shown that permanent lymphohematopoietic chimerism can be induced in MHC-disparate miniature swine by bone marrow transplantation after lethal total-body irradiation. The purpose of the present study was to determine in this large animal model whether such chimerism would lead to permanent tolerance to a vascularized allograft without a requirement for exogenous immunosuppression. Eight miniature swine that had received MHC-mismatched BMT more than five months earlier underwent kidney transplantation (KTx) from a donor MHC matched (n = 5) or MHC mismatched (n = 3) with the BMT donor. All animals had regained in vitro responsiveness to third-party MHC antigens, as measured by mixed lymphocyte reaction (MLR), before KTx but remained nonresponsive to MHC antigens of the BMT donor and self. All three animals that received KTx mismatched for BMT donor MHC rejected promptly (mean survival time 7.0 days). Of the five animals that received KTx matched for BMT donor MHC, four showed no evidence of rejection and have functioning KTx greater than 200 days after KTx. The fifth animal had excellent renal function for 60 days but then developed a slowly rising BUN and serum creatinine, and died 75 days after KTx. The course of this animal's rejection is consistent with that previously described for rejection due to minor antigen disparities. The difference in survival of KTx matched or mismatched for the MHC of the BMT donor was statistically significant (P = 0.0062). The survival of KTx matched for the MHC of the BMT donor was significantly different from that of control animals without BMT receiving KTx mismatched for MHC (P = 0.0018). We therefore conclude that BMT is an effective means for induction of tolerance to an MHC mismatched KTx in this large animal model.

Animals↗