Heat shock protein expression and immunity in chlamydial infections.

KEY WORDS heat shock proteins, Chlamydia trachomatis, immunity eat shock proteins (hsps) are among the most abundant proteins in nature and are highly conserved amongst both eucaryotes and procary-otes. The heat shock response is an important survival mechanism that safeguards the cell or microbe from conditions of stress. The response is triggered transcriptionally and results in the production of newly synthesized proteins within minutes of the cell or microbe encountering a stressful environment. Little is known about the specific functions of these hsps, but it is speculated that they may be involved in vital cell functions, such as the assembly and disassembly of macromolecules and intracellular transport, as well as the proteolysis of aberrant or dysfunctional molecules, thus maintaining the cell in a healthy vegetative state. They may also have a role in intracellular antigen presentation and processing, e Some hsps are constitu-tively expressed throughout normal cycles of growth and development, while others are induced under hostile conditions or conditions of stress, such as a change in temperature, pH, oxidative state, conditions of iron or nutrient deprivation, or the presence of enzymes or toxic chemicals. Microbes exist in environments that are constantly changing and have evolved mechanisms such as the heat shock response to bring about rapid adaptation to environmental changes. The invasion of microbes into a human host creates a stressful condition in the host, as well as a hostile environment for the microbes, as the host mounts an immune response against the presence of a foreign body. Thus an upregulation of the heat shock response frequently occurs in both the pathogen and the host in infectious disease. As hsps are highly conserved in nature, it might be expected that a mam-malian host would have innate immune tolerance to bacterial hsps, and yet bacterial hsps are among the most highly immunogenic targets for humans. The underlying reason for his is still unclear, and it is speculated that this may have an immune surveillance function in that the immune response to non-self hsp may bring about a rapid protective immune response, perhaps through the scavenging and regulatory function of gamma-delta T cells, the major lymphocyte type found in the host epithe-lium. e,3 To protect the host from destructive immune responses against self-structures, autoreac-tive T cells undergo clonal deletion in the thymus early in life, and this self recognition is maintained in the periphery through various regulatory systems. Yet, this system …