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Results: 1 to 10 of 13

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Focus on Immunology and Proteomics.
Link AJ
(2015) Proteomics Clin Appl 9: 965-6
MeSH Terms: Allergy and Immunology, Proteomics
Added February 15, 2016
0 Communities
1 Members
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2 MeSH Terms
Mechanisms of regulatory T cell counter-regulation by innate immunity.
Yeh H, Moore DJ, Markmann JF, Kim JI
(2013) Transplant Rev (Orlando) 27: 61-4
MeSH Terms: Humans, Immune Tolerance, Immunity, Innate, T-Lymphocytes, Regulatory, Transplantation Immunology
Show Abstract · Added October 24, 2013
One of the most significant advances in the field of immunology in the last decade is delineation of the pivotal role of regulatory T cells (Tregs) in the maintenance of self-tolerance. While Tregs are just now being applied therapeutically in early phase clinical trials, data gleaned from basic and translational studies to-date suggest enormous potential to intervene in human disease. Data from our work and the work of others suggest that the innate immune system plays an important role in the differentiation and function of Tregs, largely through the production of cytokines but also through expression of cell surface ligands. These molecules are expressed differentially depending on whether the stimulus includes trauma, ischemia/necrosis, and microbial infection, and have opposing effects on Tregs, in contrast to those associated with dendritic cell maturation and somatic cell apoptosis, which promote Treg differentiation and function. We refer to the former process as Treg counter-regulation. Since the transplantation procedure involves surgical trauma, organ ischemia, and exposure to environmental microbes, Treg counter-regulation represents a key area of intervention to improve strategies for promoting allograft tolerance.
Copyright © 2013 Elsevier Inc. All rights reserved.
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1 Members
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5 MeSH Terms
Machine learning competition in immunology - Prediction of HLA class I binding peptides.
Zhang GL, Ansari HR, Bradley P, Cawley GC, Hertz T, Hu X, Jojic N, Kim Y, Kohlbacher O, Lund O, Lundegaard C, Magaret CA, Nielsen M, Papadopoulos H, Raghava GP, Tal VS, Xue LC, Yanover C, Zhu S, Rock MT, Crowe JE, Panayiotou C, Polycarpou MM, Duch W, Brusic V
(2011) J Immunol Methods 374: 1-4
MeSH Terms: Algorithms, Allergy and Immunology, Artificial Intelligence, Histocompatibility Antigens Class I, Humans, Peptides, Protein Binding
Added August 6, 2012
0 Communities
1 Members
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7 MeSH Terms
What's New, What's Hot in Solid Organ Transplantation? Summary of the American Transplant Congress 2011.
Karp SJ, Mannon RB
(2011) Am J Transplant 11: 2308-16
MeSH Terms: Graft Rejection, Humans, Immune Tolerance, Immunosuppression, Immunosuppressive Agents, Organ Preservation, Organ Transplantation, Tissue Donors, Transplantation Immunology, Transplantation, Homologous, Treatment Failure
Show Abstract · Added May 22, 2014
Breakthroughs in basic and clinical science in solid organ transplantation were presented at the American Transplant Congress 2011. Key areas of presentation included the pathogenesis of late allograft failure, immune regulation and tolerance, pathways in allograft injury, electing appropriate patients for transplantation, determining the best allocation schemes to maximize effective utilization, organ preservation, monitoring the alloimmune response and immunosuppressive management. In this review, we present highlights of the meeting. These presentations demonstrate the exciting promise in translating from the bench to affect patient care.
©Copyright 2011 The American Society of Transplantation and the American Society of Transplant Surgeons.
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11 MeSH Terms
An unexpected counter-regulatory role of IL-10 in B-lymphocyte-mediated transplantation tolerance.
Zhao G, Moore DJ, Lee KM, Kim JI, Duff PE, O'Connor MR, Hirohashi T, Lei J, Yang M, Markmann JF, Deng S
(2010) Am J Transplant 10: 796-801
MeSH Terms: Adaptive Immunity, Animals, B-Lymphocytes, Graft Survival, Interleukin-10, Mice, Mice, Inbred C3H, Mice, Inbred C57BL, Neutralization Tests, Transplantation Immunology
Show Abstract · Added October 24, 2013
Monoclonal antibody against the CD45RB protein induces stable transplantation tolerance to multiple types of allograft. We have previously established that this tolerance protocol relies on the regulatory function of B lymphocytes for its effect. B lymphocytes have also been reported to participate in immune regulation in several other settings. In most of these systems, the regulatory function of B lymphocytes depends on the production of IL-10. Therefore, we investigated the role of IL-10 in the anti-CD45RB model of B-cell-mediated transplantation tolerance. Surprisingly, using antibody-mediated neutralization of IL-10, IL-10-deficient recipients and adoptive transfer of IL-10-deficient B lymphocytes, we found that IL-10 actually counter-regulates tolerance induced by anti-CD45RB. Furthermore, neutralization of IL-10 reduced the development of chronic allograft vasculopathy compared to anti-CD45RB alone and reduced the production of graft reactive alloantibodies. These data suggest that the participation of regulatory B lymphocytes in transplantation tolerance may be distinct from how they operate in other systems. Identifying the specific B lymphocytes that mediate transplantation tolerance and defining their mechanism of action may yield new insights into the complex cellular network through which antigen-specific tolerance is established and maintained.
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10 MeSH Terms
Distinct epitopes for anti-glomerular basement membrane alport alloantibodies and goodpasture autoantibodies within the noncollagenous domain of alpha3(IV) collagen: a janus-faced antigen.
Wang XP, Fogo AB, Colon S, Giannico G, Abul-Ezz SR, Miner JH, Borza DB
(2005) J Am Soc Nephrol 16: 3563-71
MeSH Terms: Adult, Anti-Glomerular Basement Membrane Disease, Antibodies, Autoantibodies, Biopsy, Needle, Collagen, Collagen Type IV, Disease Progression, Enzyme-Linked Immunosorbent Assay, Epitopes, Fatal Outcome, Female, Graft Rejection, Humans, Immunohistochemistry, Isoantibodies, Kidney Failure, Chronic, Kidney Transplantation, Nephritis, Hereditary, Risk Assessment, Transplantation Immunology
Show Abstract · Added August 21, 2013
Alport posttransplantation anti-glomerular basement membrane (GBM) nephritis is mediated by alloantibodies against the noncollagenous (NC1) domains of the alpha3alpha4alpha5(IV) collagen network, which is present in the GBM of the allograft but absent from Alport kidneys. The specificity of kidney-bound anti-GBM alloantibodies from a patient who had autosomal recessive Alport syndrome (ARAS) and developed posttransplantation nephritis was compared with that of Goodpasture autoantibodies from patients with autoimmune anti-GBM disease. Allograft-eluted alloantibodies reacted specifically with alpha3alpha4alpha5 NC1 hexamers, targeting their alpha3NC1 and alpha4NC1 subunits, and recognized a noncontiguous alloepitope formed jointly by the E(A) and E(B) regions of alpha3NC1 domain. In contrast, human Goodpasture autoantibodies recognized the separate E(A) and E(B) autoepitopes of alpha3NC1 but not the composite alloepitope. Molecular modeling of alpha3NC1 revealed that the alloepitope is more accessible within the NC1 hexamers than the partially sequestered Goodpasture autoepitopes. Overall, the specificity of alloantibodies indicated a selective lack of immune tolerance toward the alpha3 and alpha4(IV) collagen chains not expressed in patients with ARAS. Using COL4A3 knockout mice, a model of ARAS, it was shown further that acid-dissociated rather than native alpha3alpha4alpha5 NC1 hexamers elicited murine anti-GBM antibodies most closely resembling human ARAS alloantibodies. In contrast, alpha3NC1 monomers elicited Goodpasture-like murine antibodies, targeting the E(A) and E(B) autoepitopes. Thus, the identity of alpha3NC1 epitopes targeted by anti-GBM antibodies is strongly influenced by the molecular organization of the immunogen. These findings suggest that different isoforms of alpha3(IV) collagen may be implicated in the pathogenesis of ARAS posttransplantation anti-GBM nephritis and Goodpasture disease.
1 Communities
3 Members
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21 MeSH Terms
Experience with cyclosporine.
Langone AJ, Helderman JH
(2004) Transplant Proc 36: 59S-63S
MeSH Terms: Cyclosporine, Graft Rejection, Humans, Immunosuppressive Agents, Kidney Transplantation, Survival Analysis, Transplantation Immunology
Added March 4, 2014
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1 Members
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7 MeSH Terms
Molecular profiling of the role of the NF-kappaB family of transcription factors during alloimmunity.
Finn PW, He H, Ma C, Mueller T, Stone JR, Liou HC, Boothby MR, Perkins DL
(2002) J Leukoc Biol 72: 1054-62
MeSH Terms: Algorithms, Animals, Cytokines, Gene Expression Profiling, Graft Rejection, Graft Survival, Heart Transplantation, I-kappa B Proteins, Kinetics, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, NF-kappa B, NF-kappa B p50 Subunit, Proto-Oncogene Proteins c-rel, RNA, Messenger, Transplantation, Transplantation Immunology
Show Abstract · Added December 10, 2013
Allograft rejection involves a complex network of multiple immune regulators and effector mechanisms. In the current study, we focused on the role of nuclear factor (NF)-kappaB/Rel. Previous studies had established that deficiency of the p50 NF-kappaB family member prolonged allograft survival only modestly. However, because of its crucial role in signal transduction in inflammatory and immune responses, we hypothesized that other NF-kappaB/Rel family members may produce more profound effects on alloimmunity. Therefore, in addition to p50, we analyzed the role of c-Rel, which is expressed predominantly in lymphocytes. Also, to investigate NF-kappaB activation in T cells, we examined transgenic mice that express a transdominant inhibitor of NF-kappaB [IkappaB(DeltaN)] regulated by a T cell-restricted promoter. Allograft survival was prolonged indefinitely in the c-Rel-deficient and IkappaB(DeltaN)-transgenic recipients. To determine the molecular basis of NF-kappaB modulation of rejection, we analyzed a panel of 58 parameters including effector molecules, chemokines, cytokines, receptors, and cellular markers using hierarchical clustering algorithms and self-organizing maps in p50(-/-), c-Rel(-/-), and IkappaB(DeltaN)-transgenic, experimental groups plus allogeneic-, syngeneic-, and lymphocyte-deficient (alymphoid) control groups. Surprisingly, profiles of gene expression in the c-Rel recipients (which have indefinite graft survival) were similar to the p50(-/-) and allogeneic recipients (which rapidly reject grafts). As expected, gene expression in the IkappaB(DeltaN) recipients (which also have indefinite graft survival) was similar to profiles of nonrejecting syngeneic and alymphoid recipients. Importantly, self-organizing maps identified a small subset of genes including several chemokine receptors and cytokines with expression profiles that correlate with graft survival. Thus, our results demonstrate a crucial role for NF-kappaB in acute allograft rejection, identify different molecular mechanisms of rejection by distinct NF-kappaB family members, and identify a small subset of inducible genes whose inhibition is linked to graft acceptance.
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21 MeSH Terms
The immunobiology of inductive anti-CD40L therapy in transplantation: allograft acceptance is not dependent upon the deletion of graft-reactive T cells.
Nathan MJ, Yin D, Eichwald EJ, Bishop DK
(2002) Am J Transplant 2: 323-32
MeSH Terms: Animals, CD40 Ligand, Female, Graft Rejection, Heart Transplantation, Immunotherapy, Interferon-gamma, Interleukin-2, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, T-Lymphocytes, Time Factors, Transplantation Immunology, Transplantation Tolerance, Transplantation, Homologous
Show Abstract · Added December 10, 2013
CD40-CD40L costimulatory interactions are crucial for allograft rejection, in that treatment with anti-CD40L mAb markedly prolongs allograft survival in several systems. Recent reports indicate that costimulatory blockade results in deletion of graft-reactive cells, which leads to allograft tolerance. To assess immunologic parameters that were influenced by inductive CD40-CD40L blockade, cardiac allograft recipients were treated with multiple doses of the anti-CD40L mAb MR1, which was remarkably effective at prolonging allograft survival. Acute allograft rejection responses such as IL-2 producing helper cell priming, Th1 priming, and alloantibody production were abrogated by anti-CD40L treatment. Interestingly, the spleens of mice bearing long-term cardiac allografts following inductive anti-CD40L treatment retained precursor donor alloantigen-reactive CTL, IL-2 producing helper cells, and Th1 in numbers comparable to those observed in naïve mice. These mice retained the ability to reject donor-strain skin allografts, but were incapable of rejecting the original cardiac allograft, or a second donor-strain cardiac allograft. Further, differentiated effector cells were incapable of mediating rejection following adoptive transfer into mice bearing long-term allografts, suggesting that regulatory cell function, rather than effector cell deletion was responsible for long-term graft acceptance. Collectively, these data demonstrate that inductive CD40-CD40L blockade does not result in the deletion of graft-reactive T cells, but induces the maintenance of these cells in a quiescent precursor state. They further point to a tissue specificity of this hyporesponsiveness, suggesting that not all donor alloantigen-reactive cells are subject to this regulation.
0 Communities
1 Members
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16 MeSH Terms
Immunology at Vanderbilt University.
Oltz EM, Hawiger J
(2001) Immunol Res 23: 97-8
MeSH Terms: Allergy and Immunology, Research, Tennessee, Universities
Added December 10, 2013
0 Communities
1 Members
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4 MeSH Terms