Mice deficient in IL-1beta manifest impaired contact hypersensitivity to trinitrochlorobenzone.

Shornick, Laurie P.; Togni, P De; Mariathasan, Sanjeev; Goellner, Joseph J.; Strauss-Schoenberger, Jena; Karr, Robert W.; Ferguson, T.; Chaplin, David

doi:10.1084/jem.183.4.1427

Cited by 227 publications

(147 citation statements)

References 47 publications

(43 reference statements)

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“…This is an important point because genetargeted mice, such as the ones utilized in this study, often have lymphatic organs with disturbed architecture or they even lack peripheral lymph nodes [22]. This may help explain some discrepancies that become evident between the data reported by us (unimpaired migration in TNF receptor knock-out mice) and by others (impaired contact hypersensitivity in TNF receptor knock-out mice [20] and in IL-1␤ knock-out mice [21]). …”

Section: Methodical Considerationscontrasting

confidence: 48%

“…It would therefore be interesting to study skin explant cultures in mice deficient for IL-1␤ [21,41,48] or IL-1 receptors [49,50].…”

Section: Methodical Considerationsmentioning

confidence: 99%

“…This has been shown for Langerhans cells [15,16] as well as for DCs from other organs such as spleen or heart [17,18]. Studies employing contact hypersensitivity as a model in knock-out mice also suggest critical roles for TNF-␣ [19,20] and IL-1␤ [21]. The relative contributions of these cytokines as well as their mutual interactions are only poorly understood, however.…”

Section: Introductionmentioning

confidence: 99%

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Migration of Langerhans cells and dermal dendritic cells in skin organ cultures: augmentation by TNF-α and IL-1 β

Stoitzner

Zanella

Ortner

et al. 1999

Journal of Leukocyte Biology

114

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Migration from sites of antigen encounter to lymphoid organs is essential to the strong immunogenic function of dendritic cells (DC). In the skin, migration proceeds through dermal lymphatic vessels and is regulated in an incompletely understood way by inflammatory mediators. We studied the effects of tumor necrosis factor ␣ (TNF-␣) and interleukin-1␤ (IL-1␤) in mouse skin organ cultures by direct enumeration of migrating DC and by immunohistochemistry.

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Section: Methodical Considerationscontrasting

confidence: 48%

“…It would therefore be interesting to study skin explant cultures in mice deficient for IL-1␤ [21,41,48] or IL-1 receptors [49,50].…”

Section: Methodical Considerationsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Migration of Langerhans cells and dermal dendritic cells in skin organ cultures: augmentation by TNF-α and IL-1 β

Stoitzner

Zanella

Ortner

et al. 1999

Journal of Leukocyte Biology

114

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“…Caspase-1 and IL-1b have been previously implicated in the sensitization phase. 91,92 Similarly, NALP3-deficient mice that receive cells from wild-type sensitized animals develop the T-cell dependent elicitor phase, suggesting that NALP3 is involved in the sensitization phase and may bridge the TNP-Cl stress signal with the activation of the adaptive immunity. A related agent 2,4-dinitrofluorobenzene that is able to induce contact hypersensitivity promotes the release of IL-1b via caspase-1 in a skin dendritic cell line suggesting that the inflammasome may directly detect such compounds.…”

Section: Nalp3 and Activation Of The Adaptive Immune Systemmentioning

confidence: 99%

Inflammatory caspases and inflammasomes: master switches of inflammation

2006

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Fifteen years have passed since the cloning and characterization of the interleukin-1b-converting enzyme (ICE/caspase-1), the first identified member of a family of proteases currently known as caspases. Caspase-1 is the prototypical member of a subclass of caspases involved in cytokine maturation termed inflammatory caspases that also include caspase-4 caspase -5, caspase -11 and caspase -12. Efforts to elucidate the molecular mechanisms involved in the activation of these proteases have uncovered an important role for the NLR family members, NALPs, NAIP and IPAF. These proteins promote the assembly of multiprotein complexes termed inflammasomes, which are required for activation of inflammatory caspases. This article will review some evolutionary aspects, biochemical evidences and genetic studies, underlining the role of inflammasomes and inflammatory caspases in innate immunity against pathogens, autoinflammatory syndromes and in the biology of reproduction. Inflammatory CaspasesThe history of caspases began with the identification of an aspartate-specific protease activity involved in the conversion of the 31 kDa proIL-1b precursor to its active 17 kDa biologically active form, 1,2 and the identification of caspase-1 as the protease responsible for proIL-1b maturation. 3,4 The subsequent discovery of ced-3, that shares similarities with caspase-1 and which is involved in programmed cell death (PCD) in Caenorhabditis elegans, suggested that caspases might play fundamental roles in apoptosis. 5 As reviewed in the papers accompanying this issue of Cell Death and Differentiation, the role of apoptotic caspases in C. elegans and in vertebrates is crucial and deal with many facets of cell biology, development and diseases. In this review, we will focus on a subset of caspases present only in vertebrates and known as inflammatory caspases.Inflammatory caspases (also known as group I caspases) are encoded by three main genes in humans caspase-1, caspase-4 and caspase-5 and three main genes in mouse, caspase-1, caspase-11 and caspase-12. 6,7 In mammals, these caspases are characterized by the presence of a CARD domain at the N-terminus (Figure 1a). Human, chimp and mouse inflammatory caspases share significant similarity and are organized in a single locus (Figure 1c). Phylogenetic analysis of the conserved CARD domain suggests that the inflammatory caspases can be separated in evolutionaryrelated clusters (Figure 1b). The caspase-1 cluster contains caspase-1 and four other genes encoding decoy caspases: cop, inca1, inca2 and iceberg. These decoy caspase-1-like genes are absent in the mouse genome, suggesting that they have arisen recently by duplication of caspase-1. Although human and mouse caspase-1 are likely orthologues, sequence analysis suggests that human caspase-4 and caspase-5 have originated from a duplication of caspase-11. 7 However, the human caspase-12 gene, which in the chimp genome contains an SHG box important for it enzymatic activity, 8 evolved towards an enzymatically inactive form at some stage...

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“…Kiyoshi Takeda and Shizuo Akira, Osaka University, Japan. IL-1b KO mice were provided by D. Chaplin [40]. IL-18/IL-1b DKO and TLR-2/TLR-4 DKO mice were generated from the respective single KO strains as described [41,42].…”

mentioning

confidence: 99%

A role for IL‐18 in protective immunity against Mycobacterium tuberculosis

et al. 2010

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Tuberculosis remains the most hazardous bacterial infection worldwide. The causative agent, Mycobacterium tuberculosis, is a facultative intracellular pathogen of resting MU. IFN-c secreted by natural killer, CD4 Th 1 and CD8 T cells upon instruction by IL-12 and -18 activates MU to restrict mycobacterial growth. Production of both cytokines is induced by TLR signalling in DC and MU. Mice deficient for the TLR adaptor, MyD88, are highly susceptible to M. tuberculosis infection. Shared usage of MyD88 by signalling cascades for TLR and receptors for IL-1 and IL-18 prompted us to revisit the role of IL-18 during experimental infection with M. tuberculosis. We show that mice deficient for IL-18 and MyD88 but not for IL-18 receptor promptly succumbed to M. tuberculosis infection in contrast to WT or TLR-2/-4 double KO mice indicating that lack of IL-18 contributes to the high susceptibility of MyD88 KO mice to M. tuberculosis. Without IL-18, the protective Th1 response was decreased and hence, mycobacterial propagation was favoured. Neutrophildriven lung immunopathology concomitant with unrestrained growth of tubercle bacilli are most likely responsible for the premature death of IL-18 KO mice. Thus, IL-18 plays a decisive role in protective immunity against tuberculosis.Key words: IFN-c . IL-18 . Mouse . Neutrophils . Tuberculosis IntroductionDespite more than 125 years of research and development, tuberculosis (TB) remains the most hazardous bacterial infection worldwide with approximately 2 million people dying of the disease annually [1]. The risk of disease is increased by immunocompromising conditions such as AIDS emphasizing that T-cell immunity protects latently infected individuals against active TB. The innate immune response to Mycobacterium tuberculosis instructs acquired immunity in the initial stage, and executes effector mechanisms in the chronic stage.M. tuberculosis is usually transmitted via aerosols and establishes stable infection in the lung. There, M. tuberculosis is engulfed by MF and DC, which serve as host cells for mycobacterial survival and propagation. Binding of mycobacterial ligands to TLR-2, -4 and -9 promotes release of chemokines and proinflammatory cytokines, expression of adhesion molecules and attraction of MF, DC and PMN. Two crucial MF-and DCderived cytokines, , induce NK-cell activity and bias immunity towards a Th1 cell response characterized by profound 396IFN-g production, which is considered critical for protection against M. tuberculosis [2]. Activated MF express anti-mycobacterial molecules such as nitric oxide synthase (NOS)-2 (also known as inducible NOS) and LRG47 as well as cytokines such as TNF-a, which promotes granuloma formation within the infected tissue to sequester the bacilli from dissemination [2].Despite the prevailing assumption that resistance to M. tuberculosis infection depends on microbe sensing through TLR, their importance for mounting a protective immune response against M. tuberculosis remains controversial. While some groups found that TLR-mediated...

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Mice deficient in IL-1beta manifest impaired contact hypersensitivity to trinitrochlorobenzone.

Cited by 227 publications

References 47 publications

Migration of Langerhans cells and dermal dendritic cells in skin organ cultures: augmentation by TNF-α and IL-1 β

Migration of Langerhans cells and dermal dendritic cells in skin organ cultures: augmentation by TNF-α and IL-1 β

Inflammatory caspases and inflammasomes: master switches of inflammation

A role for IL‐18 in protective immunity against Mycobacterium tuberculosis

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