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Wrong Resemblance? Role of the Immune System in the Biocompatibility of Nanostructured Materials
Published in Dan Peer, Handbook of Harnessing Biomaterials in Nanomedicine, 2021
While the above-mentioned activation pathway with antibody as the initiating event is referred to as the “classical” pathway, other antibody independent pathways of complement activation also exist. These include the “alternative pathway” where a spontaneous deposition of autoactivated C3 on surfaces catalyzes further deposition of C3b through formation of the C3bBb convertase. On host cell, such deposition is avoided by cell surface-expressed molecules that catalyzes the proteolytic degradation of C3. During the past 20 years of research, it has become evident that certain lectins, i.e., carbohydrate-binding proteins that are not antibodies, also may contribute to the activation of the complement system through the “lectin pathway” in plasma [22]. Mannan-binding lectin (MBL) binds glycans with terminal mannose, N-acetylglucose, or glucose residues. These are typically exposed on the surfaces of viruses, bacteria, and fungi and the opsonization of these microorganisms via complement deposition is clearly important to avoid infections. MBL mediates complement deposition through the associated MBL-associated serine proteases (MASP), notably through the activation of C4 and C2 by MASP-2. More recently, the group of ficolins has also attracted attention [23]. While ficolins also associate with MASP-2, their ligands are not primarily carbohydrates but acetylated compounds, including acetylated sugars, e.g., N-acetylglucosamine.
A human whole-blood model to study the activation of innate immunity system triggered by nanoparticles as a demonstrator for toxicity
Published in Science and Technology of Advanced Materials, 2019
Kristina N Ekdahl, Karin Fromell, Camilla Mohlin, Yuji Teramura, Bo Nilsson
The adsorbed proteins also include specific recognition molecules from the different cascade system of the blood (Figure 1): C1q, mannan-binding lectin (MBL) and properdin within the complement system, belonging to the classical pathway, the lectin pathway, respectively, the alternative pathway, FXII (as already mentioned) and HMWK of the contact activation system, and TF and FVII within the coagulation system. These recognition molecules then trigger activation of the respective cascade systems, which leads to the generation of soluble mediators (signal substances) capable of binding to receptors on different types of leukocytes (primarily PMNs and monocytes), platelets, and ECs. This induces activation of these cells and causes inflammation and/or thrombosis (= thromboinflammation) since there is a substantial amount of cross-talk between these systems as discussed in [36].