Donor‐derived alloantibodies and passenger lymphocyte syndrome in two of four patients who received different organs from the same donor

Seltsam, Axel; Hell, Anette; Heymann, Guido A.; Salama, Abdulgabar

doi:10.1046/j.1537-2995.2001.41030365.x

Cited by 43 publications

(45 citation statements)

References 20 publications

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“…Studies have shown the importance of humoral immune reaction to these donor-specific HLA-related antigens (14). Specifically, the presence of pretransplantation PRA is associated with an adverse post-transplantation outcome compared with those patients in whom the PRA test is low or negative (15,16). Among the adverse post transplant events are acute cellular rejection, decreased longterm graft survival, increased mortality and accelerated coronary heart disease (17)(18)(19).…”

Section: Discussionmentioning

confidence: 99%

Evidence That Humoral Allograft Rejection in Lung Transplant Patients Is Not Histocompatibility Antigen-Related

Magro¹,

Klinger²,

Adams³

et al. 2003

American Journal of Transplantation

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We have recently recognized humoral rejection (HR) in lung allograft recipients and its association with acute and chronic graft dysfunction. We have shown that C4d, a stable marker of classic complement activation, is deposited in lung allografts, correlating with clinical rejection and parenchymal injury. The antigenic target may be endothelium in the setting of recurrent acute rejection while varying components of the bronchial wall may be important in chronic graft dysfunction. We sought to establish whether there is a role for antibodies with histocompatibility antigen specificity in the lung humoral allograft phenomenon. Flow cytometric and ELISA assays to assess donor-specific antigens were conducted on sera from 25 lung transplant recipients who had experienced one or more episodes of clinical rejection; in addition, the serum samples were tested for evidence of antiendothelial cell antibody activity. Morphologically, each case had biopsies showing septal capillary injury with significant deposits of immunoreactants with microvascular localization and positive indirect immunofluorescent antiendothelial cell antibody assay. Panel-reactive antibody testing showed absence of MHC Class I/II alloantibodies; ELISA based crossmatch detecting donor-specific MHC Class I/II specific antibodies was negative. HR can occur in the absence of antibodies with HLA specificity; antigenic targets may be of endothelial cell origin.

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Section: Discussionmentioning

confidence: 99%

Evidence That Humoral Allograft Rejection in Lung Transplant Patients Is Not Histocompatibility Antigen-Related

Magro¹,

Klinger²,

Adams³

et al. 2003

American Journal of Transplantation

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“…In patients with graftversus-host disease after liver, lung, or intestinal transplantation donor T cell chimerism is well described (12), but is very rare after kidney or heart transplantation. Donor B cell microchimerism has, however, been detected in patients who developed red blood cell alloantibodies following liver and kidney-pancreas transplantation (16). In the two recipients described here, the novel suggestion that the development of posttransplant de novo HLA-specific alloantibodies was caused by the adoptive transfer of donor alloreactive passenger B cells/plasma cells within the kidney was not initially apparent and we did not therefore test for peripheral blood donor B cell chimerism.…”

mentioning

confidence: 75%

Transfer of HLA-Specific Allosensitization From a Highly Sensitized Deceased Organ Donor to the Recipients of Each Kidney

Maxfield

Taylor

Kosmoliaptsis

et al. 2015

American Journal of Transplantation

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We report for the first time the adoptive transfer of donor HLA‐specific allosensitization in two recipients following kidney transplantation from a highly sensitized donor. Kidneys from a donation after circulatory death donor were transplanted into two nontransfused, HLA‐specific antibody negative males receiving their first transplant. Antibody screening 7 days after transplant showed high level de novo IgG HLA class I‐ and class II‐specific antibodies in both recipients, with largely overlapping antibody profiles but no antibodies to donor HLA. The unusually rapid appearance of de novo alloantibodies in immunosuppressed nonsensitized recipients and absence of donor HLA‐specific antibody prompted testing of stored donor serum that revealed high antibody levels with specificities very similar to those seen in both recipients, but in addition the presence of strong antibodies to each recipient HLA. Alloantibody levels gradually declined but were still detectable at 3 months. These findings suggest that alloreactive passenger B cells/plasma cells within the kidneys of highly sensitized donors may give rise to rapid development of posttransplant de novo HLA‐specific alloantibodies. While the clinical significance of this phenomenon is uncertain it provides one explanation for the appearance of de novo HLA‐specific antibodies directed against third party but not donor HLA.

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“…None of the recipients had irregular RBC alloantibodies at the time of transplantation, but anti-K and anti-Fy(a) became detectable in the liver recipient and the pancreas-kidney recipient. As discussed above, the amount of cotransplanted lymphoid tissue may correlate with the extent of peripheral lymphoid microchimerism and alloimmunization in solid-organ transplantation as well as in allogeneic SCT [65,85,87].…”

Section: Minor Abo Incompatibilitymentioning

confidence: 99%

“…Because transfusion of ABO-incompatible blood already below 100 ml can result in acute, severe transfusion reactions, it may be technically impossible to reduce residual circulating recipient RBCs to clinically insignificant levels [7]. Seltsam et al [87] reported of RBC alloimmunization by donor-derived lymphocytes after solid-organ transplantation in 2 of 4 patients who received different organs from an immunized donor. Lymphoid microchimerism in the blood of the recipients was detected by flow cytometry and PCR.…”

Section: Minor Abo Incompatibilitymentioning

confidence: 99%

Relevance of Blood Group Differences and Antibodies in Allogeneic Stem Cell Transplantation

Cassens¹,

Sibrowski²

2002

Transfus Med Hemother

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Improved experimental and clinical experiences resulted in continuously increasing numbers of allogeneic stem cell transplantation (SCT) during the past years. Nevertheless, severe immunologic side effects remain major risk factors. It is well known that disparities in major histocompatibility complex (MHC) genes and antigens play a dominant role in the induction of cellular immune responses, clinically manifested as graft versus host diseases (GVHD) or graft failures. In contrast, blood group differences, e.g. ABO incompatibilities, are often not considered as significant risk factors although severe clinical complications have been described after blood group-discrepant allogeneic SCT. Major ABO-incompatible SCT may lead to delayed cell engraftment and pure red cell aplasia. In contrast, minor ABO blood group incompatibilities are caused by administration of donor antibodies or by donor plasma cells leading to a passenger lymphocyte syndrome. Furthermore, several therapeutic methods such as T-cell depletion of stem cell transplants or treatment with cyclosporine without methotrexate are known as risk factors to develop immune hemolysis. Finally, it was recently demonstrated that other red blood cell antibodies such as anti-Kell inhibit the clonogenicity of erythrocyte and megakaryocyte progenitor cells and may therefore influence the engraftment after allogeneic SCT. Therefore, it is desirable for specialists in transfusion medicine to know the relevance of blood group antibodies in allogeneic SCT in order to perform diagnostic and/or therapeutic procedures. This article reflects the main immunologic and clinical risk factors in allogeneic SCT caused by blood group differences and corresponding antibodies.

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Donor‐derived alloantibodies and passenger lymphocyte syndrome in two of four patients who received different organs from the same donor

Abstract: The amount of cotransplanted lymphoid tissue may correlate with the extent of peripheral lymphoid microchimerism and the antibody-formation capacity in solid organ transplantation.

Cited by 43 publications

References 20 publications

Evidence That Humoral Allograft Rejection in Lung Transplant Patients Is Not Histocompatibility Antigen-Related

Evidence That Humoral Allograft Rejection in Lung Transplant Patients Is Not Histocompatibility Antigen-Related

Transfer of HLA-Specific Allosensitization From a Highly Sensitized Deceased Organ Donor to the Recipients of Each Kidney

Relevance of Blood Group Differences and Antibodies in Allogeneic Stem Cell Transplantation

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