Co-stimulation: novel methods for preventing viral-induced lung inflammation.
Respiratory infections cause significant morbidity and mortality worldwide. Although an immune response is required to eliminate respiratory pathogens, if unchecked, it can damage surrounding tissues and block primary lung function. Based on our knowledge of immune T-cell activation, there are several pathways to which immune intervention could be applied. However, relatively few interventions target only those immune cells that are responding to antigens. OX40 and 4-1BB are members of the tumour necrosis factor receptor family and are expressed on the surface of T cells in several inflammatory conditions. Recently, the inhibition of OX40 has proved beneficial during influenza virus infection. This review highlights the recent advances in the manipulation of such molecules and how they have been applied to inflammatory conditions that are caused by viruses in the lung.
Centre for Molecular Microbiology and Infection, Lord Flowers Building, Imperial College of Science, Technology and Medicine, Exhibition Road, London SW7 2AZ, UK. t.hussell@iperial.ac.uk
Tracy
T
Hussell
Robert
R
Snelgrove
Ian R
IR
Humphreys
Andrew E
AE
Williams
D019013:CD40 Antigens / Q000378:metabolism; D006801:Humans; D017730:Ki-1 Antigen / Q000378:metabolism; D008213:Lymphocyte Activation; D008562:Membrane Glycoproteins; D053278:OX40 Ligand; D011024:Pneumonia, Viral / Q000517:prevention & control*; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D013601:T-Lymphocytes / Q000276:immunology*; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7 / Q000378:metabolism
D019013:CD40 Antigens; D017730:Ki-1 Antigen; D008562:Membrane Glycoproteins; D053278:OX40 Ligand; D018124:Receptors, Tumor Necrosis Factor; C089251:TNFSF4 protein, human; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7