Pathogenesis of bacterial infections and immunity

@article{georgel_drosophila_2001,

title = {Drosophila immune deficiency (IMD) is a death domain protein that activates antibacterial defense and can promote apoptosis},

author = {Philippe Georgel and S Naitza and Christine Kappler and Dominique Ferrandon and Daniel Zachary and C Swimmer and C Kopczynski and G Duyk and Jean-Marc Reichhart and Jules A Hoffmann},

issn = {1534-5807},

year  = {2001},

date = {2001-10-01},

journal = {Dev. Cell},

volume = {1},

number = {4},

pages = {503--514},

abstract = {We report the molecular characterization of the immune deficiency (imd) gene, which controls antibacterial defense in Drosophila. imd encodes a protein with a death domain similar to that of mammalian RIP (receptor interacting protein), a protein that plays a role in both NF-kappaB activation and apoptosis. We show that imd functions upstream of the DmIKK signalosome and the caspase DREDD in the control of antibacterial peptide genes. Strikingly, overexpression of imd leads to constitutive transcription of these genes and to apoptosis, and both effects are blocked by coexpression of the caspase inhibitor P35. We also show that imd is involved in the apoptotic response to UV irradiation. These data raise the possibility that antibacterial response and apoptosis share common control elements in Drosophila.},

keywords = {Animals, Anti-Infective Agents, Apoptosis, Bacterial Infections, Caspases, Chromosome Mapping, Cysteine Proteinase Inhibitors, DNA Damage, Female, ferrandon, Gene Expression, hoffmann, I-kappa B Kinase, Immunocompromised Host, In Situ Nick-End Labeling, Insect Proteins, M3i, Male, Mutation, Phenotype, Protein Structure, Protein-Serine-Threonine Kinases, reichhart, Tertiary},

pubstate = {published},

tppubtype = {article}

}

@article{rutschmann_role_2000,

title = {Role of Drosophila IKK gamma in a toll-independent antibacterial immune response},

author = {Sophie Rutschmann and Alain C Jung and R Zhou and N Silverman and Jules A Hoffmann and Dominique Ferrandon},

doi = {10.1038/79801},

issn = {1529-2908},

year  = {2000},

date = {2000-10-01},

journal = {Nat. Immunol.},

volume = {1},

number = {4},

pages = {342--347},

abstract = {We have generated, by ethylmethane sulfonate mutagenesis, loss-of-function mutants in the Drosophila homolog of the mammalian I-kappa B kinase (IKK) complex component IKK gamma (also called NEMO). Our data show that Drosophila IKK gamma is required for the Relish-dependent immune induction of the genes encoding antibacterial peptides and for resistance to infections by Escherichia coli. However, it is not required for the Toll-DIF-dependent antifungal host defense. The results indicate distinct control mechanisms of the Rel-like transactivators DIF and Relish in the Drosophila innate immune response and show that Drosophila Toll does not signal through a IKK gamma-dependent signaling complex. Thus, in contrast to the vertebrate inflammatory response, IKK gamma is required for the activation of only one immune signaling pathway in Drosophila.},

keywords = {Animals, Antigens, Bacterial, Cell Surface, ferrandon, Gene Expression Regulation, hoffmann, I-kappa B Kinase, Immunity, Innate, Insect Proteins, M3i, Membrane Glycoproteins, Protein-Serine-Threonine Kinases, Receptors, Signal Transduction, Toll-Like Receptors, Transcription Factors},

pubstate = {published},

tppubtype = {article}

}