Kubes auto mora12/28/2023 This is illustrated by the increased phagocytic activity in neutrophils in for example rheumatoid arthritis ( 10, 11). Neutrophil phagocytosis capacity is known to be influenced by conditions such as age and disease. Several intra- and extracellular neutrophil markers have been proposed to define subsets in humans, yet none could be linked to functional heterogeneity in homeostasis ( 9). Recently, specific T cell suppressive neutrophil subsets have been described in acute inflammation and G-CSF-treated donors ( 7, 8). Several studies have identified such functional compartmentalization ( 6). These different functionalities are likely mediated by a functional heterogeneity in the neutrophil compartment. In addition, neutrophils play an immunomodulatory role in the control in inflammation and cancer immunology ( 5). NET formation has been proposed as an additional mechanism for extracellular killing of microorganisms by neutrophils ( 4). Apart from phagocytosis, a range of other mechanisms associated with bacterial killing have been identified. Phagocytosis of microorganisms is known to be particularly executed by two cells from the innate immune system: macrophages and neutrophils ( 3). This prevents bacterial spreading within the host and provides protection against clinical manifest infections. Engulfing the pathogen and providing a highly cytotoxic milieu inside the phagolysosome are the hallmarks in the killing mechanism ( 2). Phagocytosis is an essential cellular mechanism involved in the killing of bacteria by the innate immune system ( 1).
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