Programmed death ligand 1 is over‐expressed by neutrophils in the blood of patients with active tuberculosis

European Journal of Immunology - Tập 41 Số 7 - Trang 1941-1947 - 2011
Finlay W. McNab1, Matthew Berry2,1, Christine M. Graham1, Susannah Bloch2, Tolu Oni3,4, Katalin A. Wilkinson5,4, Robert J. Wilkinson3,5,4, Onn Min Kon2, Jacques Banchereau6, Damien Chaussabel7,8, Anne O’Garra1
1Division of Immunoregulation, MRC National Institute for Medical Research, London, UK
2Department of Respiratory Medicine, St Mary's Hospital, Imperial College Healthcare NHS Trust, London, UK
3Division of Medicine, Imperial College London, London, UK
4Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa
5Division of Mycobacterial Research, MRC National Institute for Medical Research, London, UK
6Roche, Inflammation Discovery, Nutley, NJ, USA
7Benaroya Research Institute, Seattle, WA, USA
8INSERM U899, Baylor Institute for Immunology Research-ANRS Center for Human Vaccines, Dallas, TX, USA

Tóm tắt

AbstractTuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains one of the world's largest infectious disease problems. Despite decades of intensive study, the immune response to Mtb is incompletely characterised, reflecting the extremely complex interaction between pathogen and host. Pathways that may alter the balance between host protection and pathogenesis are therefore of great interest. One pathway shown to play a role in the pathogenesis of chronic infections, including TB, is the programmed death‐1 (PD‐1) pathway. We show here that the expression of the programmed death ligand 1 (PD‐L1), which interacts with PD‐1, is increased in whole blood from active TB patients compared with whole blood from healthy controls or Mtb‐exposed individuals, and that expression by neutrophils is largely responsible for this increase.

Từ khóa


Tài liệu tham khảo

10.1001/jama.282.7.677

10.1146/annurev.immunol.19.1.93

10.1146/annurev.immunol.021908.132703

10.1146/annurev.immunol.26.021607.090331

10.1038/nature04444

10.1084/jem.20061496

10.1038/nm1482

10.1038/nature05115

10.1128/JVI.01177-06

10.1128/IAI.00553-07

10.4049/jimmunol.176.5.3000

10.4049/jimmunol.181.1.116

10.1086/654932

10.1038/nature09247

10.1128/JVI.80.7.3532-3540.2006

10.1128/JVI.02844-06

10.1038/nbt1385

10.1016/j.imlet.2010.01.006

10.1152/ajplung.00094.2002

10.1016/j.clim.2008.05.009

10.1016/j.jneuroim.2004.06.013

10.1073/pnas.1007394107

10.4049/jimmunol.180.11.7553

10.1111/j.1365-2567.2007.02708.x

10.4049/jimmunol.1003304

10.1073/pnas.1006298107