Our latest paper, together with Emily Gwyer Findlay’s group, by Katie Smith, is now published in PLoS Biology. This has been a long-standing project and we are delighted to see the research published and freely available to read.
This research shows that cathelicidin plays a key role in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), a mouse model of Multiple Sclerosis (MS) – driving severe EAE disease by potentiating Th17 differentiation in lymph nodes and Th17 to exTh17 plasticity and IFN-gamma production in the spinal cord. As a consequence, mice lacking cathelicidin are protected from severe EAE. In addition, we show that cathelicidin is produced by the same cell types in the active brain lesions in human MS disease. We propose that cathelicidin exposure results in highly activated, cytokine-producing T cells, which drive autoimmunity; a potential mechanism by which neutrophils may amplify inflammation in the central nervous system.
The antimicrobial peptide cathelicidin drives development of experimental autoimmune encephalomyelitis in mice by affecting Th17 differentiation.
Katie J Smith, Danielle Minns, Brian J McHugh, Rebecca K Holloway, Richard O’Connor, Anna Williams, Lauren Melrose, Rhoanne McPherson, Veronique E Miron, Donald J Davidson, Emily Gwyer Findlay
PLoS Biol 20(8):e3001554.
Full paper available open access at PLoS Biology