Antivimentin Antibodies Are an Independent Predictor of Transplant-Associated Coronary Artery Disease After Cardiac Transplantation1

Jurčević, Stipo; Ainsworth, Mark E.; Pomerance, Ariala; Smith, John D.; Robinson, Derek; Dünn, Michael J.; Yacoub, Magdi H.; Rose, Marlene L.

doi:10.1097/00007890-200104150-00011

Cited by 229 publications

(147 citation statements)

References 26 publications

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“…An intriguing recent study demonstrated an association between an autoantibody specific for angiotensin II type 1 receptor and hypertension, fibrinoid necrosis, and acute renal allograft dysfunction (8). Antivimentin and antimyosin antibodies have been shown in cardiac transplantation to relate to long-term allograft survival (9,10), and antibodies against collagen and percalan are associated with chronic renal rejection in animal studies (11).…”

Section: Antigen Targetsmentioning

confidence: 99%

“…Correlations between anti-endothelial antibodies and chronic allograft rejection have been documented (96,97). Antivimentin (a cytosolic protein derived from endothelial cells and expressed in the intima and media of arteries) antibodies are associated with early transplantation coronary artery disease (chronic rejection) in cardiac allografts (9). It has been shown that posttransplantation development of alloantibody specific to MICA is correlated with chronic rejection and poor allograft survival (6,98).…”

Section: Role Of Non-hla Antibodiesmentioning

confidence: 99%

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Mechanisms and Role of HLA and non-HLA Alloantibodies

Tinckam

Chandraker²

2006

Clinical Journal of the American Society of Nephrology

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The role of alloantibodies against HLA and non-HLA targets is becoming increasingly recognized as critical in the pathogenesis of acute and chronic renal allograft outcomes. This review discusses the antigenic targets, the mechanisms of T and B cell activation that result in the production of antibody, the complement cascade, methods of antibody detection, and the evidence that alloantibody-mediated mechanisms are active in acute and chronic rejection.

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Section: Antigen Targetsmentioning

confidence: 99%

Section: Role Of Non-hla Antibodiesmentioning

confidence: 99%

Mechanisms and Role of HLA and non-HLA Alloantibodies

Tinckam

Chandraker²

2006

Clinical Journal of the American Society of Nephrology

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“…Among alloantigen-dependent pathways, host immunity to processed fragments of donor MHC molecules (indirect alloresponse) plays a major role in the pathogenesis of chronic graft rejection (8)(9)(10)(11)(12)(13). In addition, immune response to non-MHC antigens has recently been shown to be associated with chronic rejection (14)(15)(16)(17)(18)(19)(20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

Progression of Alloresponse and Tissue-Specific Immunity during Graft Coronary Artery Disease

Tanaka

Zwierzchoniewska

Mokhtari

et al. 2005

American Journal of Transplantation

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Chronic rejection remains the major obstacle for long-term transplant survival. Both indirect alloresponse and tissue-specific autoimmunity have been implicated in its pathogenesis. The interrelationship between these two types of host anti-graft response remains poorly understood. We have developed an immunosuppression-free mouse model of graft coronary artery disease (GCAD), in which all FVB (H-2 q ) cardiac allografts placed into minor Ag (mHC)-mismatched DBA/1 (H-2 q ) hosts survived more than 112 days, and developed GCAD. We then examined the kinetics of both anti-mHC alloresponse and host autoimmunity against heart-specific antigen, cardiac myosin (CM). At 8 days post-transplantation, recipient mice showed minimal intragraft inflammation and apoptosis, and limited expansion of allo-specific T cells. In addition, we observed early production of anti-myosin IgG1 autoantibodies, which occurred in the absence of activated CM-specific T lymphocytes. By day 56, GCAD indices, the numbers of mHC-and CM-reactive T cells, and the levels of circulating alloand CM-specific antibodies were all significantly increased. While host alloresponse was exhausted at 112 days post-transplant, T-cell reactivity against CM persisted. Our data suggest that both allo-and tissuespecific immunity might contribute to the induction of GCAD. They indicate that continual autoimmune response against graft tissue antigens may provide for GCAD sustenance.

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“…In addition, nonpolymorphic tissue-specific proteins may play an important role in antigraft immunity. Indeed, several studies showed the presence of T and B cell responses to these Ags in transplanted individuals (7)(8)(9)(10)(11). However, little is known regarding the exact contribution of these responses to the allograft rejection process.…”

mentioning

confidence: 99%

Modulation of Tissue-Specific Immune Response to Cardiac Myosin Can Prolong Survival of Allogeneic Heart Transplants

Fedoseyeva

Kishimoto

Rolls

et al. 2002

The Journal of Immunology

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The role of immune response to tissue-specific Ags in transplant rejection is poorly defined. We have previously reported that transplantation of cardiac allografts triggers a CD4+ Th1 cell response to cardiac myosin (CM), a major contractile protein of the heart, and that pretransplant activation of proinflammatory CM-specific T cells accelerates rejection. In this study, we show that administration of CM together with IFA (CM/IFA) can prevent acute rejection of an allogeneic heart transplant. Prolongation of cardiac graft survival is associated with activation of CM- and allo-specific T cells secreting type 2 cytokines (IL-4, IL-5) and reduction of the frequency of proinflammatory IFN-γ-secreting (type 1) alloreactive T cells. Blocking of IL-4 cytokine with Abs abrogates the prolongation. CM/IFA treatment prevents acute rejection of MHC class I-mismatched, but not fully mismatched grafts. However, if donor heart is devoid of MHC class II expression, CM-IFA administration delays rejection of fully allogeneic cardiac transplants. This finding suggests that the effect of CM modulation depends on the type (direct vs indirect) and strength of recipient’s CD4+ T cell alloresponse. Our results underscore the important role of host immunity to tissue-specific Ags in the rejection of an allograft. This study demonstrates that modulation of the immune response to a tissue-specific Ag can significantly prolong cardiac allograft survival, an observation that may have important implications for the development of novel selective immune therapies in transplantation.

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Antivimentin Antibodies Are an Independent Predictor of Transplant-Associated Coronary Artery Disease After Cardiac Transplantation1

Abstract: Antivimentin antibodies are an independent predictor of TxCAD and can be used to identify some of the patients who are at high risk of developing this complication.

Cited by 229 publications

References 26 publications

Mechanisms and Role of HLA and non-HLA Alloantibodies

Mechanisms and Role of HLA and non-HLA Alloantibodies

Progression of Alloresponse and Tissue-Specific Immunity during Graft Coronary Artery Disease

Modulation of Tissue-Specific Immune Response to Cardiac Myosin Can Prolong Survival of Allogeneic Heart Transplants

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