Opsonisation and phagocytosis of bacteria

Phagocytes (cells such as neutrophils and macrophages that engulf and digest microbes) can sense microbes directly through pattern recognition receptors, which detect molecular patterns shared by many microbes and include the Toll-like receptors. Encapsulated bacteria are harder to grip. They are wrapped in a slimy outer capsule, and they are poorly immunogenic, which means they provoke little immune response by themselves.

The solution is opsonisation, which literally means "to make tasty". Host molecules called opsonins stick to the bacterial surface and give phagocyte receptors something to bind. The two to learn are IgG (an antibody, gripped through its tail, the Fc end) and C3b (a fragment of complement, a set of blood proteins that works with antibodies and cells). Phagocytes carry receptors for both, so the coat acts as a bridge between the bacterium and the phagocyte. Opsonins also make microbes clump together, which lets phagocytes deal with them in one go.

In the blood, the main innate opsonin comes from complement. The innate immune system is present from birth and needs no earlier exposure to the microbe, so this coating can begin at once. IgG is also an opsonin, but it belongs to the adaptive system (the slower, antigen-specific work of T and B cells) and needs an antibody response first. C-reactive protein and mannose-binding lectin are further opsonins, acute phase proteins made by the liver during inflammation.

After the coating comes engulfment into a membrane-enclosed bubble called a phagosome. The phagosome then fuses with lysosomes (small sacs of digestive enzymes), so the bacterium is destroyed inside the cell. Because encapsulated bacteria depend on opsonins to be cleared, recurrent infections with them suggest a defect in opsonisation, such as deficiency of the complement protein C3, or reduced spleen function.