Switching between humoral and cellular immune responses in Drosophila is guided by the cytokine GBP

Seiji Tsuzuki, Hitoshi Matsumoto, Shunsuke Furihata, Masasuke Ryuda, Hirotoshi Tanaka, Eui Jae Sung, Gary S. Bird, Yixing Zhou, Stephen B. Shears and Yoichi Hayakawa ()
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Seiji Tsuzuki: Saga University
Hitoshi Matsumoto: Saga University
Shunsuke Furihata: Saga University
Masasuke Ryuda: Saga University
Hirotoshi Tanaka: Saga University
Eui Jae Sung: Inositol Signaling Section, NIEHS, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA
Gary S. Bird: Inositol Signaling Section, NIEHS, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA
Yixing Zhou: Inositol Signaling Section, NIEHS, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA
Stephen B. Shears: Inositol Signaling Section, NIEHS, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA
Yoichi Hayakawa: Saga University

Nature Communications, 2014, vol. 5, issue 1, 1-11

Abstract: Abstract Insects combat infection through carefully measured cellular (for example, phagocytosis) and humoral (for example, secretion of antimicrobial peptides (AMPs)) innate immune responses. Little is known concerning how these different defense mechanisms are coordinated. Here, we use insect plasmatocytes and hemocyte-like Drosophila S2 cells to characterize mechanisms of immunity that operate in the haemocoel. We demonstrate that a Drosophila cytokine, growth-blocking peptides (GBP), acts through the phospholipase C (PLC)/Ca2+ signalling cascade to mediate the secretion of Pvf, a ligand for platelet-derived growth factor- and vascular endothelial growth factor-receptor (Pvr) homologue. Activated Pvr recruits extracellular signal-regulated protein kinase to inhibit humoral immune responses, while stimulating cell ‘spreading’, an initiating event in cellular immunity. The double-stranded RNA (dsRNA)-targeted knockdown of either Pvf2 or Pvr inhibits GBP-mediated cell spreading and activates AMP expression. Conversely, Pvf2 overexpression enhances cell spreading but inhibits AMP expression. Thus, we describe mechanisms to initiate immune programs that are either humoral or cellular in nature, but not both; such immunophysiological polarization may minimize homeostatic imbalance during infection.

Date: 2014
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DOI: 10.1038/ncomms5628

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