title: Altered expression of signalling lymphocyte activation molecule receptors in T-cells from lupus nephritis patients-a potential biomarker of disease activity.
abstract: The aim was to investigate whether the signalling lymphocyte activation molecule (SLAM) signalling pathways contribute to LN and whether SLAM receptors could be valuable biomarkers of disease activity.
  
  
  
  Peripheral blood mononuclear cells from 30National Research Ethics Service SLE patients with biopsy-proven LN were analysed by flow cytometry. Clinical measures of disease activity were assessed. The expression of the SLAM family receptors on T-cell subpopulations [CD4, CD8 and double negative (DN) T cells] was measured and compared between lupus patients with active renal disease and those in remission.
  
  
  
  The frequency of CD8 T cells expressing SLAMF3, SLAMF5 and SLAMF7 was significantly lower in LN patients who were in remission. In contrast, these subsets were similar in patients with active renal disease and in healthy individuals. Patients with active nephritis had an increased percentage of circulating monocytes, consistent with a potential role played by these cells in glomerular inflammation. Changes in the frequency of DN T cells positive for SLAMF2, SLAMF4 and SLAMF7 were observed in lupus patients irrespective of the disease activity. We detected alterations in the cellular expression of the SLAM family receptors, but these changes were less obvious and did not reveal any specific pattern. The percentage of DN T cells expressing SLAMF6 could predict the clinical response to B-cell depletion in patients with LN.
  
  
  
  Our study demonstrates altered expression of the SLAM family receptors in SLE T lymphocytes. This is consistent with the importance of the SLAM-associated pathways in lupus pathogenesis.
authors.affiliation: Department of Medicine, Imperial College London, Centre for Complement and Inflammation Research.
authors.forename: Victoria
authors.initials: V
authors.lastname: Stratigou
authors.affiliation: Department of Medicine, Imperial College London, Centre for Complement and Inflammation Research.
authors.forename: Anne F
authors.initials: AF
authors.lastname: Doyle
authors.affiliation: Department of Medicine, Imperial College London, Centre for Complement and Inflammation Research.
authors.forename: Francesco
authors.initials: F
authors.lastname: Carlucci
authors.affiliation: Department of Medicine, Imperial College London, Centre for Complement and Inflammation Research.
authors.forename: Lauren
authors.initials: L
authors.lastname: Stephens
authors.affiliation: Department of Medicine, Imperial College London, Centre for Complement and Inflammation Research.
authors.forename: Valentina
authors.initials: V
authors.lastname: Foschi
authors.affiliation: Department of Medicine, Imperial College London, Centre for Complement and Inflammation Research.
authors.forename: Marco
authors.initials: M
authors.lastname: Castelli
authors.affiliation: Imperial Lupus Centre, Imperial College NHS Healthcare Trust, London, UK.
authors.forename: Nicola
authors.initials: N
authors.lastname: McKenna
authors.affiliation: Department of Medicine, Imperial College London, Centre for Complement and Inflammation Research.
authors.forename: H Terence
authors.initials: HT
authors.lastname: Cook
authors.affiliation: Imperial Lupus Centre, Imperial College NHS Healthcare Trust, London, UK.
authors.forename: Liz
authors.initials: L
authors.lastname: Lightstone
authors.affiliation: Imperial Lupus Centre, Imperial College NHS Healthcare Trust, London, UK.
authors.forename: Thomas D
authors.initials: TD
authors.lastname: Cairns
authors.affiliation: Department of Medicine, Imperial College London, Centre for Complement and Inflammation Research.|Imperial Lupus Centre, Imperial College NHS Healthcare Trust, London, UK.
authors.forename: Matthew C
authors.initials: MC
authors.lastname: Pickering
authors.affiliation: Department of Medicine, Imperial College London, Centre for Complement and Inflammation Research.|Imperial Lupus Centre, Imperial College NHS Healthcare Trust, London, UK.
authors.forename: Marina
authors.initials: M
authors.lastname: Botto
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology; D015415:Biomarkers / Q000378:metabolism; D001707:Biopsy, Needle; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D015331:Cohort Studies; D018450:Disease Progression; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007262:Infusions, Intravenous; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008181:Lupus Nephritis / Q000188:drug therapy* / Q000276:immunology* / Q000473:pathology; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D018570:Risk Assessment; D000069283:Rituximab / Q000627:therapeutic use*; D012720:Severity of Illness Index; D000071179:Signaling Lymphocytic Activation Molecule Associated Protein / Q000276:immunology / Q000378:metabolism*; D018709:Statistics, Nonparametric; D016896:Treatment Outcome
chemical_list: D015703:Antigens, CD; D015415:Biomarkers; D000071179:Signaling Lymphocytic Activation Molecule Associated Protein; D000069283:Rituximab
keywords: T cell; nephritis; rituximab; systemic lupus erythematosus