Purpose Of Review: To summarize recent findings linking donor-specific antibodies with innate immunity resulting in chronic allograft rejection.
Recent Findings: Studies in recent years highlight the significance of donor-specific antibodies (DSA) in both acute and chronic allograft rejection. Since chronic rejection is the leading cause of graft failure, this review centers on the contribution of three areas of innate immunity of particular recent focus: complement, NK cells, and macrophages. Recent advances indicate the diverse roles that complement components play both in directly initiating allograft injury and indirectly by contributing to enhanced alloreactivity. NK cells also have emerged as an additional innate response that directly links DSA with chronic graft injury. Finally, recent studies identify alternatively activated macrophages as an additional arm of innate immunity contributing to chronic allograft rejection.
Summary: Chronic allograft rejection involves a significant contribution of DSA and differing pathways of the innate immune system. However, key issues remain unresolved. First, it is not always clear which of these varied sources of innate immunity contributing to chronic rejection may be antibody dependent. Moreover, it is not yet clear if these innate pathways represent independent routes that contribute to chronic rejection or rather act in concert to mediate allograft injury.
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http://dx.doi.org/10.1097/MOT.0000000000000708 | DOI Listing |
Emerg Microbes Infect
January 2025
HIV/AIDS Unit, National Institute for Infectious Diseases "Lazzaro Spallanzani" IRCCS, Rome, Italy.
The first evidence that Orthopoxvirus induced the expansion and the recall of effector innate Vδ2T-cells was described in a macaque model. Although, an engagement of αβ T-cells specific response in patients infected with human monkeypox (Mpox) was demonstrated, little is known about the role of γδ T-cells during Mpox infection. IFN-γ-producing γδ T-cells in the resistance to poxviruses may a key role in inducing a protective type 1 memory immunity.
View Article and Find Full Text PDFCurr Neuropharmacol
January 2025
Department of Pharmacy, DIFAR, Pharmacology and Toxicology Section, University of Genoa, Viale Cembrano 4, 16148, Genoa, Italy.
The central nervous system (CNS) is not an immune-privileged compartment, but it is intimately intertwined with the immune system. Among the components shared by the two compartments is the complement, a main constituent of innate immunity, which is also produced centrally and controls the development and organization of synaptic connections. Complement is considered a doubled-faced system that, besides controlling the physiological development of the central network, also subserves synaptic engulfment pivotal to the progression of neurodegenerative diseases.
View Article and Find Full Text PDFACS Nano
January 2025
Medical Research Center, The First Affiliated Hospital of Zhengzhou University, The Center of Infection and Immunity, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan 450001, China.
Tumor-specific T cells play a vital role in potent antitumor immunity. However, their efficacy is severely affected by the spatiotemporal orchestration of antigen-presentation as well as the innate immune response in dendritic cells (DCs). Herein, we develop a minimalist nanovaccine that exploits a dual immunofunctional polymeric nanoplatform (DIPNP) to encapsulate ovalbumin (OVA) via electrostatic interaction when the nanocarrier serves as both STING agonist and immune adjuvant in DCs.
View Article and Find Full Text PDFArthritis Rheumatol
January 2025
Department of Immunology and inflammation, Imperial College London, UK.
Background: Takayasu arteritis (TAK) and giant cell arteritis (GCA), the most common forms of large-vessel vasculitis (LVV), can result in serious morbidity. Understanding the molecular basis of LVV should aid in developing better biomarkers and treatments.
Methods: Plasma proteomic profiling of 184 proteins was performed in two cohorts.
Front Parasitol
March 2023
Medical Parasitology and Infection Biology, Swiss Tropical and Public Health Institute, Allschwil, Switzerland.
Parasitic helminths have evolved a plethora of elegant stratagems to regulate and evade the host immune system, contributing to their considerable persistence and longevity in their vertebrate hosts. Various mechanisms to achieve this state have been described, ranging from interfering with or actively modulating host immune responses to hiding from immune recognition. Because they damage surrounding vessels and disturb blood flow, blood-borne and blood-feeding parasites in particular must deal with much more than immune effector cells.
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