Abstract
The complement system is activated cascadically via three distinct major routes: classical pathway (CP), alternative pathway (AP) or lectin pathway (LP). The unique factors associated with the latter are collectins (mannose-binding lectin, collectin-10, collectin-11), ficolins (ficolin-1, ficolin-2, ficolin-3) and proteins of the mannose-binding lectin-associated serine protease (MASP) family (MASP-1, MASP-2, MASP-3, MAp19, MAp44). Collectins and ficolins are both pattern-recognising molecules (PRM), reactive against pathogen-associated molecular patterns (PAMP) or danger-associated molecular patterns (DAMP). The MASP family proteins were first discovered as complexes with mannose-binding lectin (MBL) and therefore named MBL-associated serine proteases, but later, they were found to interact with ficolins, and later still, collectin-10 and collectin-11. As well as proteolytic enzymes (MASP-1, MASP-2, MASP-3), the group includes non-enzymatic factors (MAp19, MAp44). In this review, the association-specific factors of the lectin pathway with haematologic malignancies and related infections are discussed.
Highlights
The complement system is activated cascadically via three distinct major routes: classical pathway (CP), alternative pathway (AP) or lectin pathway (LP)
The mannose-binding lectin-associated serine protease (MASP) family proteins were first described in complexes with mannose-binding lectin (MBL), and named MBL-associated serine proteases but later they were found to interact with ficolins, and later still with collectin-10 and collectin-11
Osthoff et al [114] based on the analysis of data from a longer follow-up, reported a similar association in recipients of allogeneic haematopoietic stem cell transplantation (HSCT). It seems that MBL has no protective role during the period of chemotherapy-induced cytopenia, but it may be much more important when able to act in combination with phagocytes [49]
Summary
Its activation may contribute to both the inhibition and progression of tumour growth, and even to metastasis. Complement is involved in the elimination of apoptotic/necrotic/cancer cells and some carcinogenic pathogens, contributing to the prevention of tumourigenesis [21,22,23,24,25,26]. Anaphylatoxins (C3a, C5a) were demonstrated to induce epithelial-mesenchymal transformation (EMT), activate matrix metalloproteinases and suppress the function of immune cells in the tumour microenvironment [26,30,31,32,34,35,36,37,38,39]. Complements affect the patient response to chemotherapy and contribute to the mobilization of haematopoietic cells from bone marrow to peripheral blood [40,41,42,43]
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