Recognition of heat shock proteins and γΔ cell function

Born, Willi K.; Happ, Mary Pat; Dallas, Angela; Reardon, Christopher; Kubo, Ralph T.; Shinnick, Thomas M.; Brennan, Patrick J.; O’Brien, Rebecca L.

doi:10.1016/0167-5699(90)90015-2

Cited by 233 publications

(67 citation statements)

References 47 publications

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“…There is a strong correlation between intracellular infection and the accumulation of certain -yb T cells at the sites of infection (such as the skin, reproductive tract, and lung epithelium). The relationship between such -yB T cells and invading microorganisms is central to an immune surveillance hypothesis (3,12,27,40) which suggests that a primitive subset of cells provides initial defense by recognizing molecules produced during environmental change.…”

Section: 'Y T Cells and Microbial Immunitymentioning

confidence: 99%

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Stress and immunological recognition in host-pathogen interactions

Murray

Young

1992

J Bacteriol

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Section: 'Y T Cells and Microbial Immunitymentioning

confidence: 99%

“…on May 10, 2018 by guest http://jb.asm.org/ Downloaded from specificity (3,12,25,27). -yb T cells have been found to expand during infection by Leishmania spp., Mycobacterium leprae, and M. tuberculosis (14,20,33,34 …”

Section: 'Y T Cells and Microbial Immunitymentioning

confidence: 99%

Stress and immunological recognition in host-pathogen interactions

Murray

Young

1992

J Bacteriol

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“…Recent evidence indicates that at least some parasitic and bacterial stress proteins can also induce a relatively strong T cell response. Moreover, roughly 10-20% of gamma/delta T cells, a poorly understood population of T cells, have been shown to be specific for stress proteins of various pathogens (42). A particularly attractive hypothesis is that this class of T cells, which by lining the airway, gut, and epidermal epithelium, are well positioned to provide an early line of immune defense at major body-environment interfaces where pathogen entry into the host is likely to occur.…”

Section: Infectious Diseasesmentioning

confidence: 99%

Clinical implications of the stress response.

Minowada¹,

Welch²

1995

J. Clin. Invest.

268

184

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The heat shock response, first observed in Drosophila melanogaster over thirty years ago, provided investigators a relatively simple way to study rapid changes in gene expression. Simply raising the temperature of Drosophila above its physiologic norm resulted in the decreased expression of those genes which were active before the temperature shock and the increased expression of genes encoding a group of proteins referred to as the heat shock proteins (hsp's).' Over the last 30 years similar changes in gene expression following relevant temperature shocks have been observed in cells from all organisms, be they derived from bacteria, plants, yeast, or mammals. Moreover, the heat shock proteins from various organisms appear highly conserved with respect to their primary structure, mode of regulation, and biochemical function. In addition to heat shock treatment, many other types of metabolic insults including exposure to heavy metals, amino acid analogs, different metabolic poisons as well as a variety of relevant insults in vivo (e.g., ischemia/reperfusion) also elicit increased expression of the hsp's. Accordingly, many investigators now refer to the response more generally as the stress response, and the proteins whose expression increases, the stress proteins.As one might predict, the stress response represents a universally conserved cellular defense program. Perhaps the best example of how the stress response provides for increased cellular protection is illustrated by the phenomenon of "acquired thermotolerance." Cells subjected to a sublethal heat shock treatment, if provided a subsequent recovery period at their normal growth temperature, now are able to survive a second and what would otherwise be a lethal heat shock challenge. Acquired thermotolerance is usually transient, lasting about 24 h in cells grown in culture, and appears dependent upon a number of changes induced by the initial or "priming" heat shock treatment, including the increased expression and accumulation of the stress proteins. Moreover, we now know that any particular agent or treatment which results in an induction of the stress

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“…These cells line mucosal surfaces, including intestine, and are the first line of defense in bacterial infections. 14,39 These cells recognize antigens, including mycobacterial heat-shock proteins, 14,76 although it is uncertain whether these cells recognize antigen in context with major histocompatibility determinants. Although defective cell-mediated immune mechanisms have been identified in paratuberculosis, no way of reversing the defects has been discovered, and no precise interpretation with correlates relating to disease syndrome has been made.…”

Section: Pathogenesis and Pathologymentioning

confidence: 99%

Ruminant Paratuberculosis—a Century of Progress and Frustration

Kreeger

1991

J VET Diagn Invest

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Recognition of heat shock proteins and γΔ cell function

Cited by 233 publications

References 47 publications

Stress and immunological recognition in host-pathogen interactions

Stress and immunological recognition in host-pathogen interactions

Clinical implications of the stress response.

Ruminant Paratuberculosis—a Century of Progress and Frustration

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