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2017 ; 56
(7
): 1206-1216
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Altered expression of signalling lymphocyte activation molecule receptors in
T-cells from lupus nephritis patients-a potential biomarker of disease activity
#MMPMID28387859
Stratigou V
; Doyle AF
; Carlucci F
; Stephens L
; Foschi V
; Castelli M
; McKenna N
; Cook HT
; Lightstone L
; Cairns TD
; Pickering MC
; Botto M
Rheumatology (Oxford)
2017[Jul]; 56
(7
): 1206-1216
PMID28387859
show ga
OBJECTIVES: 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. METHODS: 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.
RESULTS: 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. CONCLUSION: 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.