NF-kappaB/Rel Proteins and the Humoral Immune Responses of Drosophila melanogaster

UMMS Affiliation

Department of Medicine, Division of Infectious Diseases and Immunology

Publication Date


Document Type

Book Chapter


NF-kappa B; Drosophila melanogaster; Drosophila Proteins; Immunity, Humoral; Signal Transduction; Toll-Like Receptors


Immunology and Infectious Disease


Nuclear Factor-kappaB (NF-kappaB)/Rel transcription factors form an integral part of innate immune defenses and are conserved throughout the animal kingdom. Studying the function, mechanism of activation and regulation of these factors is crucial for understanding host responses to microbial infections. The fruit fly Drosophila melanogaster has proved to be a valuable model system to study these evolutionarily conserved NF-kappaB mediated immune responses. Drosophila combats pathogens through humoral and cellular immune responses. These humoral responses are well characterized and are marked by the robust production of a battery of anti-microbial peptides. Two NF-kappaB signaling pathways, the Toll and the IMD pathways, are responsible for the induction of these antimicrobial peptides. Signal transduction in these pathways is strikingly similar to that in mammalian TLR pathways. In this chapter, we discuss in detail the molecular mechanisms of microbial recognition, signal transduction and NF-kappaB regulation, in both the Toll and the IMD pathways. Similarities and differences relative to their mammalian counterparts are discussed, and recent advances in our understanding of the intricate regulatory networks in these NF-kappaB signaling pathways are also highlighted.

DOI of Published Version



Curr Top Microbiol Immunol. 2011;349:25-60. doi: 10.1007/82_2010_107. Link to article on publisher's site

Journal/Book/Conference Title

Current topics in microbiology and immunology


Will be published in 2011 as a chapter in Current Topics in Microbiology and Immunology, Vol. 349, Karin, Michael (Ed.) ISBN: 9783642160165.

Related Resources

Link to Article in PubMed

PubMed ID