Apc Hladr

Peptide X

TCR specific for peptide X/ HLA-DR

Peptide X/HLA-DR specific T cell -.000001% of all T cells)

Superantigen binding to Class II MHC and TCR Vß3

HLA-DR a chain SEB TCR VP3

Any HLA-DR binding peptide

Activation of peptide X specific T cell clones only: protective immunity I

Polyclonal activation of Vp3+ T cells: cytokine storm and deletion of T cells

FIGURE 15-2 Polyclonal activation of T cells by bacterial superantigens. A, Conventional microbial T cell antigens, composed of a peptide bound to the peptide-binding groove of an MHC molecule, are recognized by a very small fraction of T cells in any one individual, and only these T cells are activated to become effector T cells that protect against the microbe. B, In contrast, a superantigen binds to class II MHC molecules outside the peptide-binding groove and simultaneously binds to the variable region of any TCR p chain, as long as it belongs to a particular Vp family, regardless of the peptide-MHC specificity of the TCR. In this way, superantigens activate T cells to secrete cytokines and also induce apoptosis of T cells. Different superantigens bind to TCRs of different Vp families. Because thousands of clones of T cells will express a TCR p chain from a particular Vp family, superantigens can induce massive cytokine release (cytokine storm) and cause deletion of many T cells. In the example shown, staphylococcal enterotoxin B (SEB) is the superantigen, which binds mainly to HLA-DR and the Vp segments of TCRs belonging to the Vp3 family. APC, antigen-presenting cell.

TABLE 15-2 Mechanisms of Immune Evasion by Bacteria

Mechanism of Immune Evasion

Examples

Extracellular bacteria

Antigenic variation

Neisseria gonorrhoeae, Escherichia coli, Salmonella typhimurium

Inhibition of complement activation

Many bacteria

Resistance to phagocytosis

Pneumococcus

Scavenging of reactive oxygen species

Catalase-positive staphylococci

Intracellular bacteria

Inhibition of phagolysosome formation

Mycobacterium tuberculosis, Legionella pneumophila

Inactivation of reactive oxygen and nitrogen species

Mycobacterium leprae (phenolic glycolipid)

Disruption of phagosome membrane, escape into cytoplasm

Listeria monocytogenes (hemolysin protein)

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