BK virus (BKV) infection can cause graft loss in kidney transplant recipients. Several factors increase the risk of infection, including high level of immunosuppression, older age, and human leukocyte antigen (HLA) mismatch. The primary function of the major histocompatibility complex (HLA in human) is the presentation of peptides that originated from foreign or self-antigens to T cells to trigger an immune response, such as during infections. Identifying HLA genotypes that can influence the course of BKV infection could allow for stratifying patients according to their risk of developing the infection, thus personalizing the use of immunosuppressants. We conducted a retrospective study in a cohort of 1302 kidney transplant recipients, of whom 243 (19 %) developed BKV viremia. Clinical data and HLA genotype were evaluated for associations with BKV viremia. Among the 51 HLA genotypes analyzed, exploratory analysis revealed that patients expressing the HLA-C*08 genotype had a high risk of developing BKV viremia (p = 0.04). Using multivariate analyses adjusted for clinical variables that differed between patients with and without BK viremia (age and number of HLA-B mismatches), we confirmed that the HLA-C*08 genotype was associated with BK viremia. HLA-C*08, expressed by a sizeable proportion of the patients (82 individuals, or 6.3 % of the cohort), increased the risk of BKV viremia by 1.61 fold (p = 0.03). The HLA genotype may be useful in managing screening strategies for BKV in transplant recipients.

The aim of this study was to examine the prevalence and influencing factors of comorbid frailty and sarcopenia in hospitalized patients with hepatic echinococcosis undergoing liver transplantation, thereby providing evidence for targeted clinical interventions.

Allogeneic hematopoietic stem cell transplantation (allo-HSCT) and emerging allogeneic T cell-based immunotherapies offer curative potential for hematologic malignancies, solid tumors, and selected non-malignant disorders through graft-versus-tumor (GvT) and immune reconstitution effects mediated by donor immune cells. However, their clinical success is constrained by graft-versus-host disease (GvHD) and other immune-mediated toxicities resulting from donor-host alloreactivity. Therefore, a central challenge is to develop personalized, safer allogeneic cellular therapies that preserve potent anti-tumor and immune-restorative functions while minimizing tissue injury. This review integrates the current understanding of acute and chronic GvHD immunopathogenesis, covering cytokine and chemokine networks, growth-factor signaling, and co-stimulatory/co-inhibitory pathways, and links these mechanisms to therapeutic strategies for selective immune modulation. Drawing on translational insights, we propose a framework for next-generation allogeneic cell-based therapies that are precision-tuned to donor/recipient biology, advancing individualized anticancer and immune-reconstitution outcomes with improved safety.

Organ transplantation is a life-saving medical intervention to reverse end-stage organ failure. Despite its life-saving potential, organ transplantation faces inefficiencies like organ shortages, long wait times, and rejection risks due to manual, clinically limited donor-recipient matching. The rapid growth of AI and cloud computing offers new opportunities to enhance organ transplantation. This study proposes Smart Transplant+, a HyCARE system enabling intelligent matching, decision-making, and process automation. The architecture leverages a huge Organ Transplant Dataset and the most advanced methods such as Feedforward Neural Networks and Genetic Algorithms to maximize donor-recipient matching. Gated Recurrent Units are utilized in pre-transplant risk prediction, and post-transplant care is augmented with real-time tracking by IoT-based wearable sensors. The system has been programmed using Python, along with software tools like TensorFlow for machine learning and AES encryption for secure data storage and transmission. The Smart Transplant+ system provides 95-98 % accuracy which is higher than existing methods in identifying suitable donors and recipients and the potential for successful transplantation, and greatly enhances organ transplant efficiency and success rate. This book illustrates the revolutionary potential of synergizing IoT, cloud technology, and AI to optimize transplant care and improve outcomes.

The end-stage liver diseases require liver transplantation as the life-saving solution. It is known that monocytes/macrophages and high-density lipoprotein cholesterol (HDLC) have important contributions to the development of hepatic inflammation and oxidative stress before liver transplantation. However, the effect of monocyte/HDL-C ratio (MHR) on clinical progression and outcome in the post-transplant period are not fully understood. Our hypothesis is that the MHR value may be associated with poor vs. good outcomes after liver transplantation.

Chronic kidney disease is a major public health concern for which kidney transplantation offers the best survival benefit. Patients with high calculated panel-reactive antibody (cPRA) levels often face extended waiting times owing to donor compatibility challenges.

Calcineurin inhibitor (CNI) related kidney dysfunction is common and associated with worse outcomes after lung transplantation (LTx). To mitigate that risk, belatacept use in a CNI-sparing regimen is an alternative in LTx. We aim to describe our experience using belatacept as a CNI-sparing regimen in LTx.

Lung transplantation offers a life-saving procedure to patients with end-stage lung diseases with 85-89 % one year and 60 % five-year survival rates. Lung transplants are complicated by early ischemia/reperfusion injury (IRI) and late chronic lung allograft dysfunction (CLAD). However, the cellular and molecular links between IRI and CLAD remain unclear.

Spouse kidney transplantation represents a significant source of kidney donations. However, gender dynamics often result in husbands being recipients and wives being donors. Research on the immunological rejection and prognosis in wife recipients-who may develop immune memory due to pregnancy or sexual contact but lack preformed antibodies before transplantation-remains limited.

A previous small study (2007) of patients who received short-course, low-dose total lymphoid irradiation (sTLI) as treatment for recalcitrant cardiac rejection post-heart transplantation (HTx) reported good treatment compliance without significant toxicities and improvement in rejection frequency. We conducted a retrospective analysis, evaluating longer-term outcomes in this patient cohort.

Dexmedetomidine, an α2-adrenoceptor agonist, is known for its sedative effects and unique pharmacological mechanism. Research increasingly emphasizes its potential to modulate immune responses. Further investigation is needed to fully understand how dexmedetomidine influences T cell differentiation and its potential synergy with tolerance-promoting agents. This study aims to explore a new approach to enhance allograft acceptance by combining dexmedetomidine with the mTOR inhibitor rapamycin.

Organ transplantation improves survival and quality of life in end-stage organ failure, but rejection remains a key barrier to long-term graft success. While current immunosuppression primarily targets adaptive immunity, its limitations and side effects necessitate alternative therapeutic strategies. Macrophages infiltrate grafts extensively, which are involved in antigen presentation function, ischemia-reperfusion injury, and both acute and chronic rejection processes. Notably, their polarization toward an anti-inflammatory phenotype may alleviate rejection and potentially contribute to graft immune tolerance. In this review, we will give an overview on macrophage phenotypes and their functional diversity in allograft rejection. Also, we will discuss emerging strategies to modulate macrophage polarization, including therapies exploiting their dual regulatory capacity, nanoparticle-based targeting systems, gene therapies, and microRNA-mediated regulation. A deeper understanding of macrophage biology in transplantation could enable more sophisticated anti-rejection approaches, whose integration with conventional immunosuppression may ultimately enhance long-term graft outcomes.

Liver transplantation (LT) requires immunosuppression to prevent rejection while minimizing adverse effects. Tacrolimus (TAC) is standard but linked to nephrotoxicity and leukopenia. Everolimus (EVR) with reduced-dose TAC (rTAC) offers a potential alternative, potentially improving safety while preserving efficacy.

Hematopoietic stem cell transplantation (HSCT) is a crucial treatment for leukemia. Allogeneic Hematopoietic cell transplantation (HCT), in which stem cells from a healthy donor are used, carries significant risks, including graft versus host disease (GVHD), a severe complication that leads to high morbidity and mortality. This study aimed to identify significant predictors of acute GVHD (aGVHD) in pediatric patients with acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).

Post-transplant lymphoproliferative disorder (PTLD) represents a major cause of mortality in pediatric liver transplant recipients. However, data on clinicopathological risk factors across its subtypes remain limited. An analysis of 33 pediatric liver transplant recipients revealed significant differences in the time to onset among PTLD subtypes: monomorphic PTLD developed significantly later than non-destructive/polymorphic PTLD, with higher tacrolimus blood concentration at diagnosis in the latter, consistent with the immunosuppressive tapering protocols. Among monomorphic PTLD cases, patients with Burkitt lymphoma (BL-PTLD) had a younger transplant age and higher early tacrolimus blood concentration than those with diffuse large B-cell lymphoma (DLBCL-PTLD), indicating that younger transplant age and more intense immunosuppression may promote Burkitt lymphomagenesis. Notably, among monomorphic PTLD, patients transplanted at <1 year showed a significantly prolonged interval from transplantation to diagnosis than those transplanted at 1-18 years. Universal EBV-encoded RNA (EBER) positivity confirmed Epstein-Barr virus (EBV) as a key pathogenic factor, while the blood EBV DNA load at diagnosis showed no significant differences across subtypes, suggesting it does not influence PTLD subclassification. These findings suggest that the time interval from transplantation to PTLD, immunosuppression intensity, and age at liver transplantation play a more determinant role in PTLD subtype progression.

Desensitization protocols are employed in patients with antibody-mediated organ rejection or hematopoietic stem cell (HSC) transplant recipients from ´HLA-mismatched´ donors with donor-specific antibodies (DSA). However, these protocols sometimes have limitations in effectively reducing anti-HLA antibody levels and maintaining this reduction over time. As a result, there is an ongoing search for new, effective therapies to implement current protocols, involving anti-CD20, bortezomib, and plasma exchange. This case report explores the impact of daratumumab, a well-known anti-CD38 antibody used in the treatment of multiple myeloma, on a patient enrolled in a prospective observational study MyTH ("(My)eloma (T)herapy vs. Anti-(H)LA antibodies"). The patient has been treated since 2021 and follow-up data are presented here, showing a correlation between the kinetics of daratumumab administration and the MFI levels of an anti-HLA antibody against DR12 (baseline MFI of 3,890). These data support the role of anti-CD38 in reducing anti-HLA antibody synthesis.

Hemophagocytic lymphohistiocytosis (HLH) is a rare but highly fatal complication following allogeneic hematopoietic stem cell transplantation (allo-HSCT), with central nervous system involvement (CNS-HLH) being exceptionally uncommon in adults and posing significant diagnostic challenges. This report details a 24-year-old male with acute myeloid leukemia (AML-M5) who developed CNS-HLH on +50 day after haploidentical allo-HSCT. The patient achieved complete donor chimerism post-transplant with no active infections but subsequently presented with acute neuropsychiatric symptoms, including short-term memory impairment, hypersomnia, reduced verbal output, and psychomotor retardation, rapidly progressing to coma. Laboratory findings revealed pancytopenia, hyperferritinemia (4301 μg/L), hypertriglyceridemia, and elevated CD8 T lymphocytes (58 %). Cerebrospinal fluid analysis showed increased pressure (220 mmH₂O) and markedly elevated protein (1350.3 mg/L), while cranial MRI demonstrated bilateral hippocampal and amygdaloid hyperintensities. Bone marrow examination confirmed hemophagocytosis, fulfilling the HLH-2004 criteria and modified post-HSCT HLH diagnostic criteria for secondary HLH. Despite aggressive interventions-high-dose methylprednisolone, intravenous immunoglobulin, plasma exchange, and ruxolitinib combined with intrathecal therapy-the patient remained comatose and succumbed to multi-organ failure. This case underscores the unique clinical trajectory of post-HSCT CNS-HLH, where neuropsychiatric manifestations precede classical hematologic abnormalities and conventional immunosuppressive therapies exhibit limited efficacy. The findings emphasize the imperative for heightened clinical suspicion of HLH in transplant recipients with unexplained neurological deterioration accompanied by progressive cytopenias and biomarker derangements. Furthermore, this report highlights the urgent need for optimized early diagnostic strategies and targeted therapeutic approaches for CNS-HLH. The case provides critical insights into the clinical management and mechanistic understanding of post-transplant HLH.

Solid organ transplantation (SOT) in diabetic patients presents unique challenges in balancing immunosuppression, glycemic control, and the risk of infection. Post-transplant diabetes mellitus (PTDM) affects 10 %-40 % of transplant recipients, with immunosuppressive therapies such as corticosteroids and calcineurin inhibitors (CNIs) contributing to insulin resistance and impaired beta-cell function. This review critically examines immunomodulation strategies in diabetic SOT recipients, focusing on optimizing immunosuppressive therapy while mitigating hyperglycemia-related complications. Early glycemic control through insulin therapy, followed by a transition to oral hypoglycemic agents such as metformin, GLP-1 receptor agonists, and DPP-4 inhibitors, has proven effective in reducing PTDM and enhancing long-term transplant outcomes. Alternative immunosuppressive strategies, including belatacept-based regimens and switching from tacrolimus to cyclosporine, offer promising methods to lower PTDM incidence while preserving graft survival. Personalized immunosuppressive regimens tailored to an individual's metabolic risks further improve patient outcomes. Emerging strategies, such as monoclonal antibodies, mesenchymal stem cell therapy, and localized immunomodulation, hold promise for enhancing immune balance while mitigating metabolic complications. A multidisciplinary team involving endocrinologists, transplant surgeons, and diabetes specialists is essential for comprehensive management. Additionally, routine screening for new-onset diabetes after transplantation (NODAT) and early interventions are vital to prevent long-term complications. Despite advancements, gaps remain regarding the long-term metabolic effects of immunosuppressive agents, the optimal timing for transitioning from insulin to oral therapy, and the role of new immunomodulatory treatments. Future research should focus on personalized therapeutic approaches that combine immunosuppressive and metabolic management to improve graft function and patient health. This review highlights the importance of a balanced approach to immunosuppression for diabetic transplant recipients, aiming to enhance survival rates and quality of life.

The Flow Cytometry Crossmatch (FCXM) is a vital tool in HLA laboratories for assessing transplantation immunological risk. This study evaluates FCXM results using data from 2018 to 2023, with the aim to assess the efficacy of pronase treatment in FCXM assay by comparing control serum samples in the FCXM assays performed during this time period. Tests followed our standard protocol using the BD FACSLyric™ Flow Cytometry System and BD FACSCalibur™ Flow Cytometry System, employing normal human serum (NHS) as negative control and pooled patient serum samples with strong anti-HLA antibodies as positive control. Pronase and non-pronase tests were performed and compared to rule out any false T cell positive crossmatches that could be attributable to pronase treatment. Results showed no significant difference in delta values for T cell crossmatches between pronase-treated (MCS 256 ± 112) and non-treated (MCS 247 ± 116) groups (p = 0.253). However, B cell crossmatches had significantly higher delta values with pronase treatment (MCS 353 ± 129) versus non-treatment (MCS 300 ± 117), indicating enhanced sensitivity with pronase (p < 0.000001). Pronase-treated B cell negative controls had lower signal (MCS 245 ± 61) compared to non-treated (MCS 300 ± 73), with positive control values consistent across both groups. Anti-CD23 analysis demonstrated a reduction in all the tests performed (MCS 372 ± 64 vs 217 ± 50), confirming efficacy of pronase treatment. These findings highlight the importance of pronase in improving FCXM sensitivity for B cells, enhancing the accuracy and reliability of FCXM protocols for better transplantation outcomes.