Integrin CD11b positively regulates TLR4-induced signalling pathways in dendritic cells but not in macrophages

Guang Sheng Ling, Jason Bennett, Kevin J. Woollard, Marta Szajna, Liliane Fossati-Jimack, Philip R. Taylor, Diane Scott, Guido Franzoso, H. Terence Cook and Marina Botto ()
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Guang Sheng Ling: Centre for Complement and Inflammation Research, Imperial College, Hammersmith Campus
Jason Bennett: Centre for Cell Signalling and Inflammation, Imperial College, Hammersmith Campus
Kevin J. Woollard: Renal and Vascular Inflammation Section, Imperial College, Hammersmith Campus
Marta Szajna: Centre for Complement and Inflammation Research, Imperial College, Hammersmith Campus
Liliane Fossati-Jimack: Centre for Complement and Inflammation Research, Imperial College, Hammersmith Campus
Philip R. Taylor: Cardiff Institute of Infection and Immunity, Cardiff University School of Medicine
Diane Scott: Centre for Complement and Inflammation Research, Imperial College, Hammersmith Campus
Guido Franzoso: Centre for Cell Signalling and Inflammation, Imperial College, Hammersmith Campus
H. Terence Cook: Centre for Complement and Inflammation Research, Imperial College, Hammersmith Campus
Marina Botto: Centre for Complement and Inflammation Research, Imperial College, Hammersmith Campus

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: Abstract Tuned and distinct responses of macrophages and dendritic cells to Toll-like receptor 4 (TLR4) activation induced by lipopolysaccharide (LPS) underpin the balance between innate and adaptive immunity. However, the molecule(s) that confer these cell-type-specific LPS-induced effects remain poorly understood. Here we report that the integrin αM (CD11b) positively regulates LPS-induced signalling pathways selectively in myeloid dendritic cells but not in macrophages. In dendritic cells, which express lower levels of CD14 and TLR4 than macrophages, CD11b promotes MyD88-dependent and MyD88-independent signalling pathways. In particular, in dendritic cells CD11b facilitates LPS-induced TLR4 endocytosis and is required for the subsequent signalling in the endosomes. Consistent with this, CD11b deficiency dampens dendritic cell-mediated TLR4-triggered responses in vivo leading to impaired T-cell activation. Thus, by modulating the trafficking and signalling functions of TLR4 in a cell-type-specific manner CD11b fine tunes the balance between adaptive and innate immune responses initiated by LPS.

Date: 2014
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DOI: 10.1038/ncomms4039

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