Via complement-mediated lysis

When bacteria, such together Neisseria meningitidis, invade the body, castle are attacked by immune proteins dubbed complement proteins. Complement proteins assist in bacterial killing via 3 pathways, the classical complement pathway, the alternate complement pathway or the lectin pathway.

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The first steps the the classical complement pathway require the binding of antitoxin to the surface of the target bacterium. The antibodies then end up being targets because that one specific complement protein complex, recognized as C1 – C1 binding to the tail (known together Fc region) of the antibody. Once bound, C1 initiates a cascade the cleavage and reforming of complement complexes the ends in the binding that several enhance proteins to the surface of the bacter in the form of a membrane attack complex (MAC) (Figure 1), or deserve to generate opsonins that label a bacterium for destruction. MAC deserve to insert into the cell membrane the Gram-negative, but not Gram-positive, bacteria. There, the produces pores that permit the entrance of membrane damaging molecules, such together lysozyme, and also makes the bacterium susceptible to osmotic lysis.


The alternative complement pathway go not call for antibody to initiate the lysis that bacteria. In this pathway, complement proteins indigenous a complex known together C3 straight bind to bacteria and also activate downstream contents in the match cascade, once again finishing in development of MAC that causes lysis that the bacterium.

During the lectin pathway, mannan-binding lectin (MBL) binds to proteins containing mannose residues that are found in some species of bacteria (such as Salmonella spp.). As soon as bound, MBL develops a facility with an enzyme called MBL-activated serine protease (MASP). In this form, this enzyme activates C3 convertase (by cleaving C2 and also C4 enhance components) that participates in forming MAC.

Via phagocytosis

Bacteria may additionally be eliminated by phagocytes. Immune proteins favor acute step proteins (like complement) and also antibodies tie to the surface of bacteria by a procedure called opsonisation. Opsonised bacteria are, therefore, coated with molecules the phagocytic cells recognise and respond to. Triggered phagocytes engulf and destroy opsonised bacteria through a process called phagocytosis. Complement C3b is a an especially important opsonisation protein for regulating bacterial infections by this mechanism. Opsonisation enables killing the Gram-positive bacteria (e.g. Staphylococcus spp.) that are resistant to death by MAC.

After bacteria space ingested through phagocytosis (Figure 2), lock are killed by various processes that take place inside the cell, and broken into tiny fragments through enzymes. Phagocytes existing the pieces on their surface via class II major histocompatibility (MHC course II) molecules.


Circulating helper T cells recognise this bacterial fragments and also begin to produce proteins called cytokines. Two significant groups the helper T cells are recognized as Th1 and also Th2 cells. These cell species differ in the species of cytokine castle secrete. Th1 cells predominantly produce interferon-g (IFN-g), which promotes cell-mediated immune instrument (see below). Th2 cells create mostly interleukin-4 (IL-4), which disclosure humoral immunity by activating B cells. B cells make antibodies the stick come extracellular bacteria and prevent your growth and also survival.

Via cell-mediated immunity

Some bacteria engulfed during phagocytosis protect against the death mechanisms the the phagocyte to make it through inside cells. Macrophages space a typical targets because that intracellular bacteria (e.g. Salmonella spp.) that live inside cell compartments. This bacteria can not be detected by enhance or antibody but, instead, are removed using a cell-mediated response. Infected macrophages existing bacterial peptides on your cell surface ar using MHC class II molecules. This mechanism is dubbed antigen presentation.

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A helper T cabinet surveys MHC course II molecules through its T-cell receptor (TCR) to watch the peptides castle hold. If a bacter peptide is presented, the Th1 cabinet releases IFN-g. This cytokine stimulates death mechanisms, (such as manufacturing of lysozyme) inside the infected macrophage to digest and destroy the invading bacterium. IFN-g additionally increases antigen presentation through cells, making the bacterium more visible to the immune system and much more prone to assault (Figure 3).