The cytokine stew and innate resistance to <i>L. monocytogenes</i>

Mocci, Simonetta; Dalrymple, Stacie A.; Nishinakamura, Ryuichi; Murray, Richard M.

doi:10.1111/j.1600-065x.1997.tb00996.x

Cited by 46 publications

(50 citation statements)

References 62 publications

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“…While reconstitution with IFN-+ -/-NK cells was unable to increase resistance of + c -/-(y) -Rag-2 -/-mice to L. monocytogenes infection, adoptive transfer of IFN-+ R -/-NK cells increased resistance to infection. These results together with previous results using beige mice or perforin-knockout mice [37,45] establish that cytotoxic activity of NK cell has little role, if any, in the innate resistance to foreign pathogens in vivo.…”

Section: Discussionsupporting

confidence: 78%

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In vivo role of IFN‐γ produced by antigen‐presenting cells in early host defense against intracellular pathogens

et al. 2003

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Antigen-presenting cells (APC), including dendritic cells and macrophages, produce a large amount of interferon (IFN)-+ , a crucial cytokine for the control of infectious diseases. To elucidate the role of IFN-+ from APC in vivo, we employed cytokine receptor common + subunit ( + c) and recombination-activating gene (Rag)-2 double-knockout ( + c -/-(y) -Rag-2 -/-) mice, which are severely impaired in IFN-+ production and are extremely susceptible to infection of intracellular pathogens including Listeria monocytogenes and Toxoplasma gondii. Adoptive transfer of IFN-+ -producing APC increased levels of serum IFN-+ and the resistance to Listeria. Although depletion of NK cells from Rag-2 -/-mice slightly increased the susceptibility to bacterial infection, they are substantially more resistant than + c -/-(y) -Rag-2 -/-mice, which are also devoid of all lymphoid cells. These results demonstrate that the APC-derived IFN-+ contributes to the control of infectious agents in vivo.

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Section: Discussionsupporting

confidence: 78%

“…Previous studies have suggested that NK cells contribute to controlling early infection with intracellular pathogen [32,36,37]. To assess the role of NK cells, Rag-2 -/- (Fig.…”

Section: Contribution Of Nk Cells In Protection Against L Monocytogementioning

confidence: 99%

In vivo role of IFN‐γ produced by antigen‐presenting cells in early host defense against intracellular pathogens

et al. 2003

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“…Indeed, protection against primary LM infection in immunocompetent hosts is mediated mainly by the innate immune system. 29 It is known that innate immune cells upregulate expression of cIAPs during differentiation and activation, 4,20,30 however, their function during an immune Our results show that the degradation of cIAPs through application of SMAC mimetic (SM) results in macrophage cell death. This result appears to contradict a recent report showing that human monocytes are susceptible to SMinduced cell death whereas macrophages are resistant.…”

Section: Discussionmentioning

confidence: 66%

“…We infected mice with the intracellular bacterium, Listeria monocytogenes (LM), as it causes illness in immune compromised hosts, with the innate immune system having a key role in control of infection. 29 At 3 days post infection we found that SM-treated mice showed an approximately 10-fold (Figure 8a). This correlated to decreased numbers and increased cell death of macrophages in SM-treated mice, while T-cell pools were largely unaffected (Figures 8b and c).…”

Section: Resultsmentioning

confidence: 96%

cIAP1 and cIAP2 limit macrophage necroptosis by inhibiting Rip1 and Rip3 activation

et al. 2012

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Cellular inhibitor of apoptosis proteins (cIAPs) have emerged as important anti-cell death mediators, particularly in cancer. Although they are known to be expressed in immune tissue, their specific immune function remains unclear. We observed that degradation of cIAPs with SMAC mimetic (SM) results in death of primary bone-marrow-derived macrophages. SM-induced death of macrophages occurred by programmed necrosis (necroptosis), which was dependent on TNF receptor expression. Consistent with necroptosis, SM-induced death of macrophages was abrogated by inhibition of receptor interacting protein 1 (Rip1) kinase signaling or by receptor interacting protein 3 (Rip3) knockdown. SM-induced necroptosis was also dependent on inhibition of SM-induced apoptosis due to the expression of the endogenous caspase inhibitor, xIAP. We found that cIAPs limit Rip3, and to a lesser extent Rip1, expression via post-transcriptional mechanisms, leading to inhibition of the Rip1-Rip3 death complex (necrosome). Reduced cIAP activity in vivo, via SM treatment or specific knockout of either cIAP, resulted in elevated macrophage cell death and compromised control of an intracellular bacterium, Listeria monocytogenes. These results show that cIAPs have an important role in limiting programmed necrosis of macrophages, which facilitates effective control of a pathogen.

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“…Infected cells can express a variety of cytokines, including ␤-IFN, which alert the host immune system to the presence of an infectious agent. Macrophages play an especially important role in promoting the differentiation of immune effector cells; in general, the response of the first infected cells in a host organism shapes subsequent innate and adaptive immunity to L. monocytogenes (11).…”

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confidence: 99%