Innate Immune Genetic Profile to Predict Infection Risk and Outcome After Liver Transplant†,‡

Mannose-binding lectin and Ficolin-2 gene polymorphisms predispose to cytomegalovirus (re)infection after orthotopic liver transplantation

“…These observations may have potential clinical implications, as recently discussed regarding this component of the innate immune system and infections after liver transplantation in general [30]. Therefore, further studies on these genetic risk factors in liver transplantation, including longer follow-up, more patient cohorts, and patients with invasive CMV disease, could contribute to novel CMV infection prevention strategies in these patients.…”

Impact of MBL2 gene polymorphisms on the risk of infection in solid organ transplant recipients: A systematic review and meta-analysis

“…Four further articles were manually identified from reference lists. After removing of duplicate studies and detailed evaluation of titles and abstracts, 45 articles were fully assessed for eligibility . Eleven studies (Table ) fulfilled the inclusion and exclusion criteria and were finally included in the present study (PRISMA flow chart shown in Figure ).…”

“…Long‐term immunosuppression administered to solid organ transplant (SOT) recipients is associated with an increased risk of infectious complications. Current immunosuppressive drugs are mostly aimed at suppressing T cell–mediated adaptive immunity, potentially giving innate immunity a crucial role in protecting against pathogens in the transplant setting …”

Second-trimester plasma mannose-binding lectin levels and risk of preterm birth

“…For example, high MBL levels are related to higher risk of nephropathy in Type 1 diabetes due to the enhancing complement activation or increased opsonophagocytosis of autoantigens [26]. Low MBL levels are associated with increased susceptibility to a infectious illnesses, such as severe infections after liver transplantation [27]. Polymorphisms in immunoregulatory genes such as MBL2 may affect susceptibility to chorioamnionitis due to alteration of the host response to infection [21].…”