The inhibitory receptor LILRB4 (ILT3) modulates antigen presenting cell phenotype and, along with LILRB2 (ILT4), is upregulated in response to Salmonella infection

doi:10.1186/1471-2172-10-56

BMC Immunology
Volume 10

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Anderson KJ
Lapaque N
Buerki RA
Trowsdale J
Allen RL

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Allen RL
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Research article

The inhibitory receptor LILRB4 (ILT3) modulates antigen presenting cell phenotype and, along with LILRB2 (ILT4), is upregulated in response to Salmonella infection

Damien P Brown^*² , Des C Jones^*² , Katie J Anderson^*¹ , Nicolas Lapaque² , Robin A Buerki²^,3 , John Trowsdale² and Rachel L Allen¹

¹Centre for Infection, Division of Cellular and Molecular Medicine, St Georges, University of London, London, UK

²Department of Pathology, Cambridge University, Cambridge, UK

³NorthWestern University, Evanston, USA

author email corresponding author email* Contributed equally

BMC Immunology 2009, 10:56doi:10.1186/1471-2172-10-56


Published:	27 October 2009

Abstract

Background

Leukocyte Ig-like receptors (LILR) are a family of innate immune receptors with immunomodulatory functions. High-level expression of the receptors LILRB2 (ILT4) and LILRB4 (ILT3) is a feature of tolerogenic antigen presenting cells and has been observed in cancer and transplant situations. There are relatively few studies regarding these receptors in the context of infection and it is not yet clear how LILRB4 exerts its inhibitory effects.

Results

We studied the effects of LILRB4 ligation on antigen presenting cell phenotype, and the expression of LILRB2 and LILRB4 on Salmonella-infected antigen presenting cells. Ligation of LILRB4 throughout in vitro culture of dendritic cells led to an upregulation of the co-stimulatory protein CD86. Alterations in the production of IL-8 and IL-10 by LILRB4-ligated macrophages were also observed. Infection with Salmonella typhimurium or TLR stimulation with Salmonella components led to an upregulation of LILRB2 and LILRB4.

Conclusion

Our results indicate that the inhibitory effects of LILRB4 do not result from a failure to upregulate co-stimulatory proteins. In addition to the high level expression that can render antigen presenting cells tolerogenic, there may be a role for lower level expression and activity of LILRB2 and LILRB4 in response to TLR signalling during an immune response to bacterial infection.