Disease relevance of Graft Rejection

• Additionally, the negative regulatory role of CTLA-4 in autoimmune diseases and graft rejection supports a dynamic but complex process of immune regulation that is prominent in the control of self-reactivity [1].
• In others factors such as electrolyte disturbances, steroid treatment for graft rejection, and cerebral infarction may have contributed to the development of the fits [2].
• Letter: Increased serum creatinine resulting from hyperglycemia, mimicking transplant rejection [3].
• Inflammation in asthma, sepsis, transplant rejection, and many neurodegenerative diseases associates an up-regulation of NO synthesis with increased protein nitration at tyrosine [4].
• Thus, chemokine receptor expression may be used for immunologic staging of MS and potentially for other chronic autoimmune/inflammatory processes such as rheumatoid arthritis, autoimmune diabetes, or chronic transplant rejection [5].

High impact information on Graft Rejection

• Thus, unlike the classical MHC antigens, the hemopoietic histocompatibility (Hh) antigens relevant in marrow graft rejection are inherited in a recessive pattern [6].
• At six months, the rate of biopsy-confirmed acute graft rejection in the seronegative group was 52 percent among placebo recipients and 26 percent among valacyclovir recipients (P=0.001) [7].
• To determine the effect of cyclosporine on renal function and graft rejection, we conducted a retrospective analysis of data on 1663 renal-transplant recipients at six centers [8].
• Because Tac chains are expressed only on a small fraction of activated lymphocytes, monoclonal antibodies against the interleukin-2 receptor may offer a more specific means of immunosuppression than polyclonal antilymphocyte globulin in prophylaxis against graft rejection [9].
• Prevention of acute graft rejection by the prostaglandin E1 analogue misoprostol in renal-transplant recipients treated with cyclosporine and prednisone [10].

Chemical compound and disease context of Graft Rejection

• Methotrexate and cyclosporine were used to prevent graft rejection and as graft-versus-host disease (GVHD) prophylaxis [11].
• The use of nicardipine was not associated with an increased incidence of graft rejection or CsA toxicity episodes [12].
• Leflunomide is a novel immunosuppressive and antiinflammatory agent currently being tested for treatment of autoimmune diseases and transplant rejection [13].
• They may be used to mimic the genetic deficiency of the enzyme, in lymphoproliferative disorders or immunosuppressive therapy (i.e., in graft rejection), to potentiate the effect of antileukemic or antiviral nucleosides, and, together with adenosine kinase, to reduce breakdown of adenosine in inflammation, hypertension, and ischemic injury [14].
• Indium-111 antimyosin scans were used to assess myocardial damage in patients with suspected myocarditis and cardiac transplant rejection [15].

Biological context of Graft Rejection

• An understanding of its biological functions has begun to emerge from DNA studies of individuals with partial Y chromosomes, coupled with molecular characterization of genes implicated in gonadal sex reversal, Turner syndrome, graft rejection and spermatogenic failure [16].
• The products of minor histocompatibility (H) loci are serious barriers to tissue transplantation even among major histocompatibility complex (MHC) identical individuals, frequently causing chronic graft rejection and graft versus host disease [17].
• Mixed chimerism induced without lethal conditioning prevents T cell- and anti-Gal alpha 1,3Gal-mediated graft rejection [18].
• The roles that granzyme B plays in human pathologies, such as transplant rejection, viral immunity and particularly tumor immune surveillance, remain a topic for vigorous debate and conjecture [19].
• GA was effective in amelioration of graft rejection in two systems by prolongation of skin graft survival and inhibition of functional deterioration of thyroid grafts, across minor and major histocompatibility barriers [20].

Anatomical context of Graft Rejection

• Class I HLA (histocompatibility locus antigen) molecules are the targets of allospecific cytolytic T lymphocytes (CTL) in graft rejection, and constitute the restricting elements necessary for the interaction between antiviral CTL and virus-infected cells [21].
• Cell membrane modification for rapid display of proteins as a novel means of immunomodulation: FasL-decorated cells prevent islet graft rejection [22].
• Tolerance to the host appeared to be virtually complete in four assay systems: (a) primary mixed lymphocyte reactions (MLR) of purified lymph node (LN) CD8+ cells (+/- IL-2); (b) primary MLR of CD4+ (CD8-) thymocytes; (c) skin graft rejection; and (d) induction of lethal graft-vs.-host disease by CD4+ cells [23].
• In renal-transplant patients in whom azathioprine therapy was withdrawn early because of bone-marrow suppression no rebound graft rejection was noted [24].
• Although triple-drug immunosuppression with cyclosporine, prednisone, and azathioprine has reduced the incidence of acute graft rejection after cardiac transplant, its effect on the development of coronary artery disease is unknown [25].

Associations of Graft Rejection with chemical compounds

• Local synthesis of complement component C3 regulates acute renal transplant rejection [26].
• Carbon monoxide suppresses arteriosclerotic lesions associated with chronic graft rejection and with balloon injury [27].
• No evidence of graft rejection was seen, either during treatment or in the 2 years after cyclosporin was withdrawn [28].
• Mycophenolate mofetil to rescue children with acute renal transplant rejection [29].
• Deoxyspergualin for liver graft rejection [30].

Gene context of Graft Rejection

• Our findings indicate that good HLA-A and B matching is highly dependent on a system for sharing organs among institutions, and results in decreased graft rejection, better long-term graft function, and less need for post-transplantation immunosuppression [31].
• We used three in vivo models to demonstrate a role for CXCR3 in the development of transplant rejection [32].
• During acute and chronic transplant rejection, ligands for CCR5 are upregulated, and the graft is infiltrated by CCR5-positive mononuclear cells [33].
• Recent data implicates a role for the CD40-CD40 ligand (CD40L) pathway in graft rejection [34].
• For BM graft rejection studies, IL-10 was infused into sublethally irradiated recipients of anti-Thy 1.2 + C' T-cell-depleted, fully allogeneic BM grafts [35].

Analytical, diagnostic and therapeutic context of Graft Rejection

• Common risk factors for coronary disease and HLA mismatch are probably not important in the pathogenesis of coronary atherosclerosis after cardiac transplantation, whereas the risk for coronary artery disease may be increased by acute graft rejection and pretransplant idiopathic cardiomyopathy [25].
• These findings suggest that antimyosin scintigraphy is a sensitive and early indicator of cardiac transplant rejection and that it could be useful as a noninvasive method for assessing the efficacy of cyclosporine treatment [36].
• Heart transplant rejection monitored by signal-averaged electrocardiography in patients receiving cyclosporine [37].
• Early graft rejection was seen in one unrelated transplant recipient conditioned with TBI plus thiotepa plus Cy [38].
• Morphologic features of spleen allografts in rats. Graft rejection, acceptance, or lethal graft-versus-host disease in the same donor-recipient pairing [39].

References