Hancock Group | Systems biology of host-pathogen interactions

Hancock Group | Systems biology of host-pathogen interactions

Hancock Group

Our Research and Approach

Bob Hancock's Associate Faculty group utilises systems biology methods and differentiated mutant embryonic stem (ES) cells to understand the complex inter-relationship between the host and the pathogen and enable the development of new therapies against infections.

We have proposed that manipulation of natural innate immunity will serve as a new therapeutic strategy against antibiotic-resistant infections. However to understand the assets and potential deficits of such a strategy we need to understand the extremely complex process of innate immunity (involving as many as 5000 biomolecules).

To understand the complexity of host immune responses to pathogens, we will utilise targeted genetic modifications of stem cells, to enable the investigation of mouse and human genes that have important functions in pathogen-host interactions and favourable host immune responses. Cellular responses to pathogens and their immune-stimulatory molecules will involve high-throughput analysis of their phenotypes using our new bioinformatic tools for studying the systems biology of innate immunity.

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Professor Bob Hancock
Group Leader

Bob Hancock's research interests include small cationic peptides as novel antimicrobials and modulators of innate immunity, the development of novel treatments for antibiotic resistant infections, the systems biology of innate immunity, inflammatory diseases and Pseudomonas aeruginosa, and antibiotic uptake and resistance. At the Sanger Institute he is involved in the cellular phenotyping programme, converting mutated mouse embryonic stem cells and human induced pluripotent stem cells into macrophages with the aim of understanding functional networks of genes involved in infections and inflammation.

Partners and Funders

Internal Partners

Publications

  • Effective adjunctive therapy by an innate defense regulatory peptide in a preclinical model of severe malaria.

    Achtman AH, Pilat S, Law CW, Lynn DJ, Janot L et al.

    Science translational medicine 2012;4;135;135ra64

  • The critical role of histone H2A-deubiquitinase Mysm1 in hematopoiesis and lymphocyte differentiation.

    Nijnik A, Clare S, Hale C, Raisen C, McIntyre RE et al.

    Blood 2012;119;6;1370-9

  • InnateDB: facilitating systems-level analyses of the mammalian innate immune response.

    Lynn DJ, Winsor GL, Chan C, Richard N, Laird MR et al.

    Molecular systems biology 2008;4;218

  • An anti-infective peptide that selectively modulates the innate immune response.

    Scott MG, Dullaghan E, Mookherjee N, Glavas N, Waldbrook M et al.

    Nature biotechnology 2007;25;4;465-72

  • High-throughput generation of small antibacterial peptides with improved activity.

    Hilpert K, Volkmer-Engert R, Walter T and Hancock RE

    Nature biotechnology 2005;23;8;1008-12

  • Complete genome sequence of Pseudomonas aeruginosa PAO1, an opportunistic pathogen.

    Stover CK, Pham XQ, Erwin AL, Mizoguchi SD, Warrener P et al.

    Nature 2000;406;6799;959-64