Innate Immunity in Solid Organ Transplantation

Dear Colleagues, 

Solid organ transplantation (SOT) represents the treatment of choice for patients with advanced/terminal organ failure. To be fully effective, the transplanted organ must be protected against the attack of the recipient’s immune system that rejects it because it is seen as “non-self and dangerous”. While transplant rejection was first identified as the result of the host adaptive immune response to donor MHC antigens, recent studies have shown that innate immune response is a condition necessary to activate the rejection machinary. The principal components of innate immune system are represented by cellular members such as monocytes, phagocytic cells (neutrophils and macrophages), dendritic cells, natural killers and other innate lymphoid cells, as well as blood proteins, including the constituents of the complement system and other inflammatory mediators. The main role of innate immunity is to provide the host a rapid defense against the invading pathogens through recognition of pathogen-associated molecular patterns by germline-encoded pattern recognition receptors (PRRs). However, as postulated by Dr. Polly Matzinger, the PRRs can also recognize “danger signals” (damage/danger-associated molecular patterns, DAMPs), i.e., endogenous molecules generated following cell stress and tissue injury, despite the absence of infection. In SOT, every injury of the graft, including the unavoidable ischemia reperfusion injury and drug toxicity, generates DAMPs able to activate the recipient innate immune responses. The activated innate immunity rapidly leads to activation of adaptive immunity whose consequences are both acute rejection and long term chronic graft dysfunction.

Furthermore, it must be kept in mind that organs harbor various classes of resident cells of the innate immune system (such as innate lymphoid cells and resident macrophages) and these cells are inevitably transplanted together with the organ. Such cells are potentially deleterious, as carriers of donor derived allogeneic MHC, but they may also have active roles in mitigating inflammation and promoting tissue repair.

The aim of this Special Issue is offering an Open Access forum, bringing together a collection of original research and review articles addressing the role of innate immunity in solid organ transplantation. We hope to provide a stimulating resource for this fascinating subject. Suggested potential topics include: ischemia-reperfusion injury in SOT, including kidney, liver, heart and lung transplantation; the role of DAMPs and alarmins in SOT; ex vivo perfusion in transplantation to prevent detrimental effects of IRI-associated DAMP release; the role of complement system in SOT; the role of resident macrophages and innate lymphoid cells in IRI and SOT; or the innovative concept of innate allorecognition and trained immunity.    

Dr. Federica Casiraghi
Dr. Sistiana Aiello
Guest Editors

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• Solid-organ transplantation
• Innate immunity
• Ischemia-reperfusion injury
• Ex vivo perfusion
• Resident innate cells – macrophages and innate lymphoid cells
• Complement system
• DAMPs and alarmins – IL-33 and IL-1α
• Monocytes
• Innate allorecognition
• Trained immunity