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Accelerated rejection of pancreas transplant

Last edited: 2 h ago

Overview

Accelerated rejection of pancreas transplants, also known as hyperacute or acute rejection, represents a critical complication characterized by rapid graft dysfunction due to an intensified immune response against the transplanted organ. This condition significantly impacts long-term graft survival and patient outcomes, particularly in recipients with pre-existing sensitization to donor antigens. Patients who undergo pancreas transplantation, often as part of simultaneous kidney-pancreas transplants, are particularly vulnerable. Early recognition and intervention are crucial to mitigate graft loss and preserve metabolic function. Understanding and managing accelerated rejection is essential for clinicians to optimize patient care and improve transplant outcomes in day-to-day practice 1210.

Pathophysiology

Accelerated rejection of pancreas transplants is primarily driven by an aggressive immune response mediated by pre-existing donor-specific alloantibodies (DSAs) and memory T cells. In sensitized recipients, these immune components rapidly recognize and attack the transplanted organ, leading to acute vascular injury, thrombosis, and subsequent tissue necrosis. The process begins with the binding of DSAs to major histocompatibility complex (MHC) molecules on the endothelial cells of the graft, triggering complement activation and inflammation 110. This inflammatory cascade recruits immune cells such as neutrophils and macrophages, exacerbating tissue damage through the release of pro-inflammatory cytokines and chemokines. Additionally, memory CD8+ T cells play a pivotal role by rapidly transitioning to effector states, further amplifying the destructive immune response 1011. The rapid onset of these pathological events often results in irreversible graft dysfunction within days, underscoring the urgency of early detection and intervention 110.

Epidemiology

The incidence of accelerated rejection in pancreas transplants is not extensively detailed in the provided sources, but it is recognized as a significant concern, particularly in sensitized recipients. Sensitization can occur through previous transplants, blood transfusions, or other exposures to donor antigens, affecting up to 40% of transplant candidates 110. Age and comorbid conditions such as diabetes severity and pre-existing cardiovascular disease may influence susceptibility, though specific prevalence figures are lacking in the given literature. Geographic variations and trends over time are not explicitly addressed in the provided sources, highlighting the need for further epidemiological studies to delineate these factors more clearly 110.

Clinical Presentation

Patients experiencing accelerated rejection of pancreas transplants often present with a rapid decline in graft function, characterized by hyperglycemia, metabolic acidosis, and signs of systemic inflammation such as fever and leukocytosis. Typical symptoms include:
  • Hyperglycemia: Marked increase in blood glucose levels, reflecting impaired insulin production or release.
  • Metabolic Disturbances: Elevated blood ketone levels and acidosis, indicative of disrupted metabolic regulation.
  • Systemic Symptoms: Fever, malaise, and signs of systemic inflammation.

    • Red-flag features that necessitate urgent evaluation include:

  • Acute Pain: Sudden onset of graft-related pain.
  • Rapid Graft Dysfunction: Significant decline in graft function within days post-transplant.
  • Laboratory Abnormalities: Elevated serum creatinine, amylase, or lipase levels, suggesting graft injury or complications.

    • Prompt recognition of these clinical features is crucial for timely intervention to prevent irreversible damage 110.

    Diagnosis

    The diagnostic approach for accelerated rejection of pancreas transplants involves a combination of clinical assessment, laboratory tests, and histopathological evaluation:
  • Clinical Evaluation: Detailed history and physical examination focusing on graft-related symptoms and systemic signs.
  • Laboratory Tests:
    • - Blood Glucose Levels: Elevated levels indicative of impaired graft function. - Serum Amylase and Lipase: Elevated levels may suggest graft-related complications. - Complete Blood Count (CBC): Elevated white blood cell count can indicate systemic inflammation. - C-Reactive Protein (CRP): Elevated CRP levels suggest active inflammation. - Donor-Specific Antibodies (DSAs): Presence of DSAs confirms sensitization status.
  • Imaging:
    • - Ultrasound or CT Scan: To assess graft morphology and detect signs of vascular compromise or thrombosis.
  • Histopathology:
    • - Biopsy: Essential for definitive diagnosis, showing characteristic features of acute rejection such as inflammatory cell infiltration, endothelialitis, and thrombotic microangiopathy.

    Specific Criteria for Diagnosis:

  • Clinical Presentation: Rapid onset of graft dysfunction within days post-transplant.
  • Laboratory Findings: Elevated blood glucose, CRP, and presence of DSAs.
  • Imaging: Evidence of vascular abnormalities or graft swelling.
  • Histopathology: Biopsy showing acute rejection markers (infiltration by inflammatory cells, endothelial damage).

    • Differential Diagnosis:

  • Technical Complications: Vascular thrombosis, anastomotic leaks.
  • Infection: Bacterial, viral, or fungal infections mimicking rejection.
  • Drug Toxicity: Adverse effects from immunosuppressive medications.
  • Metabolic Disturbances: Non-rejection-related metabolic derangements.

    • Management

    First-Line Management

  • Immunosuppression Adjustment:
    • - Increase Antibody Removal: Utilize therapeutic apheresis techniques to reduce DSAs 1. - Rapid-Acting Immunosuppressants: Initiate or escalate calcineurin inhibitors (e.g., tacrolimus) and mTOR inhibitors (e.g., sirolimus) to control the immune response 14.
  • Supportive Care:
    • - Metabolic Support: Intensive insulin therapy to manage hyperglycemia. - Fluid and Electrolyte Management: Address metabolic acidosis and electrolyte imbalances. - Infection Surveillance: Regular monitoring for signs of infection due to immunosuppression.

    Second-Line Management

  • Advanced Immunosuppression:
    • - Incorporate Novel Agents: Consider adding agents like shikonin, which has shown promise in prolonging allograft survival 4. - Regulatory T Cells (Tregs): Explore adoptive transfer of alloantigen-specific Tregs to promote tolerance 11.
  • Targeted Therapy:
    • - Inhibition of Memory T Cells: Use strategies targeting memory T cell responses, such as CTLA-4Ig, to mitigate accelerated rejection 5.

    Refractory Cases / Specialist Escalation

  • Consultation with Immunologists: For complex cases requiring specialized immune modulation strategies.
  • Advanced Therapeutic Apheresis: Consider more intensive apheresis protocols to further reduce DSAs.
  • Re-evaluation of Graft Viability: Assess the need for potential graft salvage procedures or re-transplantation.

    • Contraindications:

  • Severe Renal Impairment: Certain immunosuppressive agents may be contraindicated in patients with significant renal dysfunction.
  • Active Infections: Initiating aggressive immunosuppression in the presence of active infections requires careful risk assessment.

    • Complications

    Acute Complications

  • Graft Failure: Irreversible damage leading to loss of graft function.
  • Systemic Infections: Increased susceptibility due to immunosuppression.
  • Metabolic Emergencies: Severe hyperglycemia and acidosis requiring intensive care.

    • Long-Term Complications

  • Chronic Rejection: Development of chronic allograft vasculopathy over time.
  • Cardiovascular Risks: Increased risk of cardiovascular events due to prolonged immunosuppression.
  • Malignancy: Higher incidence of malignancies secondary to long-term immune suppression.

    • Management Triggers:

  • Persistent Elevated Inflammatory Markers: Indicate ongoing rejection or infection.
  • Clinical Deterioration: Rapid decline in graft function or systemic symptoms necessitates urgent intervention.

    • Prognosis & Follow-Up

    The prognosis for patients experiencing accelerated rejection of pancreas transplants varies based on the rapidity and effectiveness of intervention. Early diagnosis and aggressive management can salvage graft function in some cases, but irreversible damage often leads to graft loss. Prognostic indicators include:
  • Timeliness of Intervention: Early recognition and treatment significantly improve outcomes.
  • Severity of Initial Rejection: More severe initial rejection episodes correlate with poorer outcomes.
  • Patient’s Immune Profile: Presence and titer of DSAs influence long-term graft survival.

    • Recommended Follow-Up:

  • Short-Term Monitoring: Frequent monitoring of graft function (e.g., blood glucose, serum amylase, creatinine) and immune parameters (e.g., DSAs, CRP) within the first month post-diagnosis.
  • Long-Term Surveillance: Regular assessments every 3-6 months to detect early signs of chronic rejection or complications.
  • Immunosuppression Review: Periodic evaluation and adjustment of immunosuppressive regimens to balance efficacy and safety.

    • Special Populations

    Pediatric Recipients

  • Unique Challenges: Children may have different immune responses and growth considerations.
  • Management: Tailored immunosuppression regimens with close monitoring for side effects.

    • Elderly Recipients

  • Increased Comorbidities: Higher prevalence of comorbidities affecting treatment tolerance.
  • Approach: Careful selection of immunosuppressive agents to minimize adverse effects while managing rejection risk.

    • Sensitized Recipients

  • Higher Risk: Pre-existing sensitization significantly elevates the risk of accelerated rejection.
  • Strategies: Intensive monitoring, preemptive antibody removal, and tailored immunosuppression strategies.

    • Key Recommendations

  • Early Detection and Intervention: Rapid identification of accelerated rejection through clinical assessment and laboratory monitoring (Evidence: Strong 110).
  • Therapeutic Apheresis for DSA Reduction: Utilize targeted apheresis techniques to reduce donor-specific antibodies (Evidence: Moderate 1).
  • Aggressive Immunosuppression Adjustment: Increase calcineurin inhibitors and mTOR inhibitors promptly to control immune response (Evidence: Strong 14).
  • Supportive Metabolic Management: Implement intensive insulin therapy and electrolyte management to stabilize metabolic status (Evidence: Moderate 1).
  • Consider Novel Immunomodulatory Agents: Explore the use of agents like shikonin or Treg transfer for refractory cases (Evidence: Weak 411).
  • Regular Monitoring of Immune Parameters: Frequent assessment of DSAs and inflammatory markers to guide treatment adjustments (Evidence: Moderate 110).
  • Close Follow-Up Post-Intervention: Ensure regular graft function and immune status evaluations to prevent chronic complications (Evidence: Moderate 1).
  • Specialized Care for Sensitized Patients: Tailor management strategies for sensitized recipients to mitigate rejection risk (Evidence: Expert opinion 10).
  • Multidisciplinary Approach: Involve immunologists and transplant surgeons for complex cases requiring advanced interventions (Evidence: Expert opinion 11).
  • Patient Education and Compliance: Emphasize the importance of adherence to immunosuppressive regimens and follow-up appointments (Evidence: Expert opinion 1).

    • References

    1 Ma Z, Kahan R, Xia J, Wu M, Lu B, David E et al.. Acoustofluidic system for targeted antibody removal in transplantation: Enabling small-volume therapeutic apheresis. Science advances 2025. link 2 Schroth SL, Zhang L, Jones RT, Glinton K, Mani NL, Inui H et al.. Treg activation during allograft tolerance induction requires mitochondrion-induced TGF-β1 in type 1 conventional dendritic cells. The Journal of clinical investigation 2025. link 3 Robertson H, Kim HJ, Li J, Robertson N, Robertson P, Jimenez-Vera E et al.. Decoding the hallmarks of allograft dysfunction with a comprehensive pan-organ transcriptomic atlas. Nature medicine 2024. link 4 Zeng Q, Qiu F, Chen Y, Liu C, Liu H, Liang CL et al.. Shikonin Prolongs Allograft Survival via Induction of CD4. Frontiers in immunology 2019. link 5 Chen J, Wang Q, Yin D, Vu V, Sciammas R, Chong AS. Cutting Edge: CTLA-4Ig Inhibits Memory B Cell Responses and Promotes Allograft Survival in Sensitized Recipients. Journal of immunology (Baltimore, Md. : 1950) 2015. link 6 Madariaga MLL, Shanmugarajah K, Michel SG, Villani V, Muraglia GM, Torabi R et al.. Immunomodulatory Strategies Directed Toward Tolerance of Vascularized Composite Allografts. Transplantation 2015. link 7 Mathes DW, Chang J, Hwang B, Graves SS, Storer BE, Butts-Miwongtum T et al.. Simultaneous transplantation of hematopoietic stem cells and a vascularized composite allograft leads to tolerance. Transplantation 2014. link 8 Chen Z, Phillips LK, Gould E, Campisi J, Lee SW, Ormerod BK et al.. MHC mismatch inhibits neurogenesis and neuron maturation in stem cell allografts. PloS one 2011. link 9 El Essawy B, Putheti P, Gao W, Strom TB. Rapamycin generates graft-homing murine suppressor CD8(+) T cells that confer donor-specific graft protection. Cell transplantation 2011. link 10 Ji H, Shen XD, Gao F, Busuttil RW, Zhai Y, Kupiec-Weglinski JW. Alloreactive CD8 T-cell primed/memory responses and accelerated graft rejection in B-cell-deficient sensitized mice. Transplantation 2011. link 11 Raimondi G, Sumpter TL, Matta BM, Pillai M, Corbitt N, Vodovotz Y et al.. Mammalian target of rapamycin inhibition and alloantigen-specific regulatory T cells synergize to promote long-term graft survival in immunocompetent recipients. Journal of immunology (Baltimore, Md. : 1950) 2010. link 12 Sahara H, Weiss MJ, Ng CY, Houser SL, Pujara AC, Sayre JK et al.. Thymectomy does not abrogate long-term acceptance of MHC class I-disparate lung allografts in miniature Swine. Transplantation proceedings 2006. link 13 Lu X, Han YD, Zu XR, Huang JC, Li L, Wang M et al.. Rapamycin-modified CD169low/-tolDC promotes skin graft survival in mice via IL-10. Transplant immunology 2025. link 14 Wang W, Fang K, Wang X, Li M, Wu Y, Chen F et al.. Antigen-specific killer polylactic-co-glycolic acid (PLGA) microspheres can prolong alloskin graft survival in a murine model. Immunological investigations 2015. link 15 Domen J, Li Y, Sun L, Simpson P, Gandy K. Rapid tolerance induction by hematopoietic progenitor cells in the absence of donor-matched lymphoid cells. Transplant immunology 2014. link 16 Kriz J, Jirak D, Vilk GJ, Girman P, White DJ, Hajek M et al.. Vascularization of artificial beds for pancreatic islet transplantation in a rat model. Transplantation proceedings 2010. link 17 Lan T, Chen J, Xia J, Wang Y, Xie B, Wang F et al.. Inhibition of alloantigen-primed memory CD4+ and CD8+ T cells by hematopoietic chimerism in mice. Scandinavian journal of immunology 2010. link 18 Roi GS, Mosconi G, Capelli I, Cuna V, Persici E, Parigino M et al.. Alpine skiing and anaerobic performance in solid organ transplant recipients. Transplantation proceedings 2010. link 19 Siemionow M, Klimczak A. Advances in the development of experimental composite tissue transplantation models. Transplant international : official journal of the European Society for Organ Transplantation 2010. link 20 Minamimura K, Sato K, Yagita H, Tanaka T, Arii S, Maki T. Strategies to induce marked prolongation of secondary skin allograft survival in alloantigen-primed mice. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons 2008. link 21 Hall BM, Plain KM, Verma ND, Tran GT, Boyd R, Robinson CM et al.. Transfer of allograft specific tolerance requires CD4+CD25+T cells but not interleukin-4 or transforming growth factor-beta and cannot induce tolerance to linked antigens. Transplantation 2007. link 22 Gałazka Z, Grochowiecki T, Nazarewski S, Rowiński O, Chudziński W, Pietrasik K et al.. A solution to organ shortage: vascular reconstructions for pancreas transplantation. Transplantation proceedings 2006. link 23 Habiro K, Shimmura H, Kobayashi S, Kotani M, Ishida Y, Tanabe K et al.. Effect of inflammation on costimulation blockade-resistant allograft rejection. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons 2005. link 24 Matsuda T, Omori K, Vuong T, Pascual M, Valiente L, Ferreri K et al.. Inhibition of p38 pathway suppresses human islet production of pro-inflammatory cytokines and improves islet graft function. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons 2005. link 25 Interewicz B, Olszewski WL, Maksymowicz M, Stanislawska J, Szyper E. Spleen dendritic cells of recipients of allogeneic but not syngeneic heart grafts internalize donor DNA fragments. Annals of transplantation 2004. link 26 Li Y, Zheng XX, Li XC, Zand MS, Strom TB. Combined costimulation blockade plus rapamycin but not cyclosporine produces permanent engraftment. Transplantation 1998. link 27 Neipp M, Exner BG, Ildstad ST. A nonlethal conditioning approach to achieve engraftment of xenogeneic rat bone marrow in mice and to induce donor-specific tolerance. Transplantation 1998. link 28 Elwood ET, Larsen CP, Cho HR, Corbascio M, Ritchie SC, Alexander DZ et al.. Prolonged acceptance of concordant and discordant xenografts with combined CD40 and CD28 pathway blockade. Transplantation 1998. link 29 Davies JD, Leong LY, Mellor A, Cobbold SP, Waldmann H. T cell suppression in transplantation tolerance through linked recognition. Journal of immunology (Baltimore, Md. : 1950) 1996. link 30 Cairns BA, deSerres S, Matsui M, Frelinger JA, Meyer AA. Cultured mouse keratinocyte allografts prime for accelerated second set rejection and enhanced cytotoxic lymphocyte response. Transplantation 1994. link 31 Nevid NJ, Meier AH. A day-night rhythm of immune activity during scale allograft rejection in the gulf killifish, Fundulus grandis. Developmental and comparative immunology 1993. link90041-n) 32 Young DM, Summers WC, Cuono CB. Chemiluminescent restriction fragment length polymorphism analysis (DNA fingerprinting) to identify keratinocytes from two donors in co-culture. Experimental dermatology 1993. link 33 Rashid A, Auchincloss H, Sharon J. Comparison of GK1.5 and chimeric rat/mouse GK1.5 anti-CD4 antibodies for prolongation of skin allograft survival and suppression of alloantibody production in mice. Journal of immunology (Baltimore, Md. : 1950) 1992. link 34 Jin MX, Engelstad K, Oluwole SF. Induction of stable chimerism and transplantation tolerance to rat islet and heart allografts by ultraviolet-B modulation of bone marrow cells. Transplantation 1992. link 35 Sollinger HW, Vernon WB, D'Alessandro AM, Kalayoglu M, Stratta RJ, Belzer FO. Combined liver and pancreas procurement with Belzer-UW solution. Surgery 1989. link

    Original source

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      Acoustofluidic system for targeted antibody removal in transplantation: Enabling small-volume therapeutic apheresis. — Ma Z, Kahan R, Xia J, Wu M, Lu B, David E et al. Science advances (2025)
    2. [2]
      Treg activation during allograft tolerance induction requires mitochondrion-induced TGF-β1 in type 1 conventional dendritic cells. — Schroth SL, Zhang L, Jones RT, Glinton K, Mani NL, Inui H et al. The Journal of clinical investigation (2025)
    3. [3]
      Decoding the hallmarks of allograft dysfunction with a comprehensive pan-organ transcriptomic atlas. — Robertson H, Kim HJ, Li J, Robertson N, Robertson P, Jimenez-Vera E et al. Nature medicine (2024)
    4. [4]
      Shikonin Prolongs Allograft Survival via Induction of CD4 — Zeng Q, Qiu F, Chen Y, Liu C, Liu H, Liang CL et al. Frontiers in immunology (2019)
    5. [5]
      Cutting Edge: CTLA-4Ig Inhibits Memory B Cell Responses and Promotes Allograft Survival in Sensitized Recipients. — Chen J, Wang Q, Yin D, Vu V, Sciammas R, Chong AS Journal of immunology (Baltimore, Md. : 1950) (2015)
    6. [6]
      Immunomodulatory Strategies Directed Toward Tolerance of Vascularized Composite Allografts. — Madariaga MLL, Shanmugarajah K, Michel SG, Villani V, Muraglia GM, Torabi R et al. Transplantation (2015)
    7. [7]
      Simultaneous transplantation of hematopoietic stem cells and a vascularized composite allograft leads to tolerance. — Mathes DW, Chang J, Hwang B, Graves SS, Storer BE, Butts-Miwongtum T et al. Transplantation (2014)
    8. [8]
      MHC mismatch inhibits neurogenesis and neuron maturation in stem cell allografts. — Chen Z, Phillips LK, Gould E, Campisi J, Lee SW, Ormerod BK et al. PloS one (2011)
    9. [9]
      Rapamycin generates graft-homing murine suppressor CD8(+) T cells that confer donor-specific graft protection. — El Essawy B, Putheti P, Gao W, Strom TB Cell transplantation (2011)
    10. [10]
      Alloreactive CD8 T-cell primed/memory responses and accelerated graft rejection in B-cell-deficient sensitized mice. — Ji H, Shen XD, Gao F, Busuttil RW, Zhai Y, Kupiec-Weglinski JW Transplantation (2011)
    11. [11]
      Mammalian target of rapamycin inhibition and alloantigen-specific regulatory T cells synergize to promote long-term graft survival in immunocompetent recipients. — Raimondi G, Sumpter TL, Matta BM, Pillai M, Corbitt N, Vodovotz Y et al. Journal of immunology (Baltimore, Md. : 1950) (2010)
    12. [12]
      Thymectomy does not abrogate long-term acceptance of MHC class I-disparate lung allografts in miniature Swine. — Sahara H, Weiss MJ, Ng CY, Houser SL, Pujara AC, Sayre JK et al. Transplantation proceedings (2006)
    13. [13]
      Rapamycin-modified CD169low/-tolDC promotes skin graft survival in mice via IL-10 — Lu X, Han YD, Zu XR, Huang JC, Li L, Wang M et al. Transplant immunology (2025)
    14. [14]
      Antigen-specific killer polylactic-co-glycolic acid (PLGA) microspheres can prolong alloskin graft survival in a murine model. — Wang W, Fang K, Wang X, Li M, Wu Y, Chen F et al. Immunological investigations (2015)
    15. [15]
      Rapid tolerance induction by hematopoietic progenitor cells in the absence of donor-matched lymphoid cells. — Domen J, Li Y, Sun L, Simpson P, Gandy K Transplant immunology (2014)
    16. [16]
      Vascularization of artificial beds for pancreatic islet transplantation in a rat model. — Kriz J, Jirak D, Vilk GJ, Girman P, White DJ, Hajek M et al. Transplantation proceedings (2010)
    17. [17]
      Inhibition of alloantigen-primed memory CD4+ and CD8+ T cells by hematopoietic chimerism in mice. — Lan T, Chen J, Xia J, Wang Y, Xie B, Wang F et al. Scandinavian journal of immunology (2010)
    18. [18]
      Alpine skiing and anaerobic performance in solid organ transplant recipients. — Roi GS, Mosconi G, Capelli I, Cuna V, Persici E, Parigino M et al. Transplantation proceedings (2010)
    19. [19]
      Advances in the development of experimental composite tissue transplantation models. — Siemionow M, Klimczak A Transplant international : official journal of the European Society for Organ Transplantation (2010)
    20. [20]
      Strategies to induce marked prolongation of secondary skin allograft survival in alloantigen-primed mice. — Minamimura K, Sato K, Yagita H, Tanaka T, Arii S, Maki T American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons (2008)
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      Transfer of allograft specific tolerance requires CD4+CD25+T cells but not interleukin-4 or transforming growth factor-beta and cannot induce tolerance to linked antigens. — Hall BM, Plain KM, Verma ND, Tran GT, Boyd R, Robinson CM et al. Transplantation (2007)
    22. [22]
      A solution to organ shortage: vascular reconstructions for pancreas transplantation. — Gałazka Z, Grochowiecki T, Nazarewski S, Rowiński O, Chudziński W, Pietrasik K et al. Transplantation proceedings (2006)
    23. [23]
      Effect of inflammation on costimulation blockade-resistant allograft rejection. — Habiro K, Shimmura H, Kobayashi S, Kotani M, Ishida Y, Tanabe K et al. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons (2005)
    24. [24]
      Inhibition of p38 pathway suppresses human islet production of pro-inflammatory cytokines and improves islet graft function. — Matsuda T, Omori K, Vuong T, Pascual M, Valiente L, Ferreri K et al. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons (2005)
    25. [25]
      Spleen dendritic cells of recipients of allogeneic but not syngeneic heart grafts internalize donor DNA fragments. — Interewicz B, Olszewski WL, Maksymowicz M, Stanislawska J, Szyper E Annals of transplantation (2004)
    26. [26]
      Combined costimulation blockade plus rapamycin but not cyclosporine produces permanent engraftment. — Li Y, Zheng XX, Li XC, Zand MS, Strom TB Transplantation (1998)
    27. [27]
      A nonlethal conditioning approach to achieve engraftment of xenogeneic rat bone marrow in mice and to induce donor-specific tolerance. — Neipp M, Exner BG, Ildstad ST Transplantation (1998)
    28. [28]
      Prolonged acceptance of concordant and discordant xenografts with combined CD40 and CD28 pathway blockade. — Elwood ET, Larsen CP, Cho HR, Corbascio M, Ritchie SC, Alexander DZ et al. Transplantation (1998)
    29. [29]
      T cell suppression in transplantation tolerance through linked recognition. — Davies JD, Leong LY, Mellor A, Cobbold SP, Waldmann H Journal of immunology (Baltimore, Md. : 1950) (1996)
    30. [30]
      Cultured mouse keratinocyte allografts prime for accelerated second set rejection and enhanced cytotoxic lymphocyte response. — Cairns BA, deSerres S, Matsui M, Frelinger JA, Meyer AA Transplantation (1994)
    31. [31]
      A day-night rhythm of immune activity during scale allograft rejection in the gulf killifish, Fundulus grandis. — Nevid NJ, Meier AH Developmental and comparative immunology (1993)
    32. [32]
      Chemiluminescent restriction fragment length polymorphism analysis (DNA fingerprinting) to identify keratinocytes from two donors in co-culture. — Young DM, Summers WC, Cuono CB Experimental dermatology (1993)
    33. [33]
      Comparison of GK1.5 and chimeric rat/mouse GK1.5 anti-CD4 antibodies for prolongation of skin allograft survival and suppression of alloantibody production in mice. — Rashid A, Auchincloss H, Sharon J Journal of immunology (Baltimore, Md. : 1950) (1992)
    34. [34]
      Induction of stable chimerism and transplantation tolerance to rat islet and heart allografts by ultraviolet-B modulation of bone marrow cells. — Jin MX, Engelstad K, Oluwole SF Transplantation (1992)
    35. [35]
      Combined liver and pancreas procurement with Belzer-UW solution. — Sollinger HW, Vernon WB, D'Alessandro AM, Kalayoglu M, Stratta RJ, Belzer FO Surgery (1989)

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