Confrontation between Intracellular Bacteria and the Immune System

Schaible, Ulrich E.; Collins, Helen; Kaufmann, Stefan H. E.

doi:10.1016/s0065-2776(08)60405-8

Cited by 171 publications

(157 citation statements)

References 675 publications

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“…cdT cells produce IFN-c [38] and anti-inflammatory cytokines such as IL-10 [6,15] that inhibit the production of pro-inflammatory mediators including IL-1, TNF-a, and IL-8 produced by inflammatory cells within affected tissues. Through such indirect mechanisms, cdT cells may prevent the recruitment of PMN to inflammatory sites, suppress oxidative burst and degranulation, and reduce PMN-mediated tissue injury [7,8].…”

Section: Discussionmentioning

confidence: 99%

“…The regulatory function of cdT cells is mediated through the production of cytokines such as IFN-c, IL-10, and TNF-a as well as through direct cytotoxicity towards target cells, resulting in the resolution of inflammatory processes [6][7][8]. Accumulation of cdT cells is seen in sites of inflammation that are associated with intracellular bacterial, viral, and parasitic infections.…”

Section: Introductionmentioning

confidence: 99%

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Surface expression of HSP72 by LPS‐stimulated neutrophils facilitates γδT cell‐mediated killing

Hirsh¹,

Hashiguchi²,

Chen³

et al. 2006

Eur J Immunol

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During inflammation and sepsis, accumulation of activated neutrophils causes lung tissue damage and organ failure. Effective clearance of neutrophils reduces the risk of organ failure; however, its mechanisms are poorly understood. Because lungs are rich in cdT cells, we investigated the physiological role of these cells in the protection of lung tissue from infiltrating neutrophils. In a mouse model of sepsis, we found that the lungs of survivors contained significantly higher numbers of cdT cells than those of mice that died from sepsis. The number of cdT cells correlated inversely with the number of neutrophils in the lungs and with the degree of lung tissue damage. LPS rapidly elicited the expression of heat shock protein (HSP) 72 on the surface of human neutrophils. Inhibitors of transcription, protein synthesis, and intracellular protein transport blocked HSP72 expression, indicating that de novo synthesis is required. cdT cells targeted and rapidly killed LPS-treated neutrophils through direct cell-to-cell contact. Pre-treatment with neutralizing antibodies to HSP72 diminished neutrophil killing. Our data indicate that HSP72 expression on the cell surface predisposes inflamed neutrophils to killing by cdT cells. This intercellular exchange may allow cdT cells to resolve inflammation and limit host tissue damage during sepsis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Surface expression of HSP72 by LPS‐stimulated neutrophils facilitates γδT cell‐mediated killing

Hirsh¹,

Hashiguchi²,

Chen³

et al. 2006

Eur J Immunol

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“…In this study, addition of B. pseudomallei to naive spleen cells resulted in the rapid activation of DX5 ϩ / NK1.1 ϩ cells for IFN-␥ production. Recent evidence suggests that several distinct T cell populations also have the potential to make IFN-␥ with an intermediate kinetics between the rapid NK cell response and the acquisition of acquired immunity (24,25). These include NK T cells (26,27), ␥␦ T cells (11,28), CD4 Ϫ CD8 Ϫ (29), or CD8 ϩ T cells responding to microbial products presented via the CD1 system (30,31) and other CD8 ϩ T cells triggered via recognition of N-formylated bacterial peptides via the H2-M3 Ag presentation system (32).…”

Section: Discussionmentioning

confidence: 99%

Bystander Activation of CD8+ T Cells Contributes to the Rapid Production of IFN-γ in Response to Bacterial Pathogens

Lertmemongkolchai

Cai

Hunter

et al. 2001

The Journal of Immunology

265

235

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The bacterium Burkholderia pseudomallei causes a life-threatening disease called melioidosis. In vivo experiments in mice have identified that a rapid IFN-γ response is essential for host survival. To identify the cellular sources of IFN-γ, spleen cells from uninfected mice were stimulated with B. pseudomallei in vitro and assayed by ELISA and flow cytometry. Costaining for intracellular IFN-γ vs cell surface markers demonstrated that NK cells and, more surprisingly, CD8+ T cells were the dominant sources of IFN-γ. IFN-γ+ NK cells were detectable after 5 h and IFN-γ+ CD8+ T cells within 15 h after addition of bacteria. IFN-γ production by both cell populations was inhibited by coincubation with neutralizing mAb to IL-12 or IL-18, while a mAb to TNF had much less effect. Three-color flow cytometry showed that IFN-γ-producing CD8+ T cells were of the CD44high phenotype. The preferential activation of NK cells and CD8+ T cells, rather than CD4+ T cells, was also observed in response to Listeria monocytogenes or a combination of IL-12 and IL-18 both in vitro and in vivo. This rapid mechanism of CD8+ T cell activation may be an important component of innate immunity to intracellular pathogens.

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“…Most immunocompetent individuals infected with tubercle bacilli do not develop disease, which indicates the important role of the specific immune response in restricting mycobacterial growth (26). The protective immune response comprises both CD4 and CD8 T cells and perhaps unconventional T cell populations such as ␥/␦ T cells (27).…”

Section: Discussionmentioning

confidence: 99%

Intersection of Group I CD1 Molecules and Mycobacteria in Different Intracellular Compartments of Dendritic Cells

Schaible

Hagens

Fischer

et al. 2000

The Journal of Immunology

Self Cite

109

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Human CD1a, CD1b, and CD1c molecules can present mycobacterial glycolipids to T cells. Because phagosomes containing viable mycobacteria represent early endosomal compartments, we studied where mycobacterial glycolipids intersect with CD1 molecules in infected APC. CD1b and CD1c, but not CD1a, localized to late endosomes/lysosomes. CD1a and CD1c were predominantly expressed on the cell surface and in mycobacterial phagosomes of the early endosomal stage. In contrast, CD1b was present in a subset of mycobacterial phagosomes representing mature phagolysosomes. Released mycobacterial glycolipids including lipoarabinomannan and phosphatidylinositol mannosides were transported from the phagosome into late endosomes/lysosomes and to uninfected bystander cells. The macrophage mannose receptor, which has been implicated in glycolipid uptake by APC for CD1b-mediated presentation, was absent from mycobacterial phagosomes and may therefore not be involved in trafficking of glycolipids between phagosomes and late endosomes/lysosomes. In conclusion, all three CD1 molecules have access to mycobacteria and glycolipids thereof, but at different intracellular sites. This allows sampling by CD1a, CD1b, and CD1c of mycobacterial glycolipids from different intracellular sites of the infected cell, which has important implications for processing and presentation of such Ags during mycobacterial infections.

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Confrontation between Intracellular Bacteria and the Immune System

Cited by 171 publications

References 675 publications

Surface expression of HSP72 by LPS‐stimulated neutrophils facilitates γδT cell‐mediated killing

Surface expression of HSP72 by LPS‐stimulated neutrophils facilitates γδT cell‐mediated killing

Bystander Activation of CD8+ T Cells Contributes to the Rapid Production of IFN-γ in Response to Bacterial Pathogens

Intersection of Group I CD1 Molecules and Mycobacteria in Different Intracellular Compartments of Dendritic Cells

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