PMID- 36688843 OWN - NLM STAT- Publisher LR - 20240216 IS - 1538-4683 (Electronic) IS - 1061-5377 (Print) IS - 1061-5377 (Linking) DP - 2023 Jan 23 TI - Immunogenicity of Homologous Heart Valves: Mechanisms and Future Considerations. LID - 10.1097/CRD.0000000000000519 [doi] AB - Pediatric valvar heart disease continues to be a topic of interest due to the common and severe clinical manifestations. Problems with heart valve replacement, including lack of adaptive valve growth and accelerated structural valve degeneration, mandate morbid reoperations to serially replace valve implants. Homologous or homograft heart valves are a compelling option for valve replacement in the pediatric population but are susceptible to structural valve degeneration. The immunogenicity of homologous heart valves is not fully understood, and mechanisms explaining how implanted heart valves are attacked are unclear. It has been demonstrated that preservation methods determine homograft cell viability and there may be a direct correlation between increased cellular viability and a higher immune response. This consists of an early increase in human leukocyte antigen (HLA)-class I and II antibodies over days to months posthomograft implantation, followed by the sustained increase in HLA-class II antibodies for years after implantation. Cytotoxic T lymphocytes and T-helper lymphocytes specific to both HLA classes can infiltrate tissue almost immediately after implantation. Furthermore, increased HLA-class II mismatches result in an increased cell-mediated response and an accelerated rate of structural valve degeneration especially in younger patients. Further long-term clinical studies should be completed investigating the immunological mechanisms of heart valve rejection and their relation to structural valve degeneration as well as testing of immunosuppressant therapies to determine the needed immunosuppression for homologous heart valve implantation. CI - Copyright (c) 2023 Wolters Kluwer Health, Inc. All rights reserved. FAU - Vogel, Andrew D AU - Vogel AD AD - From the Department of Surgery, Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, SC. AD - Department of Surgery, Alabama College of Osteopathic Medicine, Dothan, AL. FAU - Kwon, Jennie H AU - Kwon JH AD - From the Department of Surgery, Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, SC. FAU - Mitta, Alekhya AU - Mitta A AD - From the Department of Surgery, Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, SC. AD - Department of Surgery, School of Medicine, University of South Carolina, Columbia, SC. FAU - Sherard, Curry AU - Sherard C AD - From the Department of Surgery, Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, SC. AD - Department of Surgery, College of Medicine, Medical University of South Carolina, Charleston, SC. FAU - Brockbank, Kelvin G M AU - Brockbank KGM AD - Department of Surgery, Tissue Testing Technologies LLC, North Charleston, SC. AD - Department of Bioengineering, Clemson University, Charleston, SC. FAU - Rajab, Taufiek Konrad AU - Rajab TK AD - From the Department of Surgery, Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, SC. LA - eng GR - UL1 TR001450/TR/NCATS NIH HHS/United States PT - Journal Article DEP - 20230123 PL - United States TA - Cardiol Rev JT - Cardiology in review JID - 9304686 SB - IM PMC - PMC10363244 MID - NIHMS1856658 COIS- Disclosure: The authors declare no conflict of interest. EDAT- 2023/01/24 06:00 MHDA- 2023/01/24 06:00 PMCR- 2024/07/23 CRDT- 2023/01/23 10:12 PHST- 2024/07/23 00:00 [pmc-release] PHST- 2023/01/23 10:12 [entrez] PHST- 2023/01/24 06:00 [pubmed] PHST- 2023/01/24 06:00 [medline] AID - 00045415-990000000-00071 [pii] AID - 10.1097/CRD.0000000000000519 [doi] PST - aheadofprint SO - Cardiol Rev. 2023 Jan 23:10.1097/CRD.0000000000000519. doi: 10.1097/CRD.0000000000000519.