Final answer:
Antibodies serve as opsonins that tag pathogens for destruction by phagocytes, enhancing phagocytosis, while complement fixation involves antibodies binding to antigens to further promote phagocytosis. These opsonized pathogens are efficiently recognized by phagocytes. Conversely, factors that block these interactions reduce phagocytosis.
Step-by-step explanation:
The Role of Antibodies and Complement in Phagocytosis
To determine which items promote the attachment of phagocytes to microbes and enhance phagocytosis, or which interfere with the process, thereby reducing phagocytosis, we can refer to the immune mechanisms described. Antibodies act as opsonins by tagging pathogens for destruction, which promotes phagocytosis. These opsonized pathogens are more likely to be recognized and engulfed by phagocytic cells such as macrophages, dendritic cells, and neutrophils.
Furthermore, the process of complement fixation involves antibodies like IgM and IgG binding to antigens on pathogens which then provides docking sites for complement proteins. This initiates a cascade that leads to the pathogen being coated in complement proteins, particularly C3b, marking it for phagocytosis (opsonization). Complement proteins also act as chemotactic agents, attracting phagocytic cells to the site of inflammation and enhancing phagocytosis.
Therefore, elements such as antibodies and complement proteins that bind to the surfaces of pathogens promote phagocytosis. By contrast, factors that prevent the interaction between phagocytes and these opsonizing agents would interfere with the phagocytic process.