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Abstract Number: 2256

A Population of IL-21 Producing CD4+ T Cells Correlates with Disease Damage in Systemic Lupus Erythematosus (SLE) Patients

Babak Noamani1, Stacey Morrison2, Dafna D. Gladman3, Jorge Sanchez-Guerrero4, Murray B. Urowitz5, Joan E. Wither6 and Carolina Landolt-Marticorena7, 1Genetics and developmental biology, Toronto Western Research Institute, Toronto, ON, Canada, 2Div Rheumatology Rm MP-10-304, The Toronto Western Hospital, Toronto, ON, Canada, 3Division of Rheumatology, Toronto Western Hospital and University of Toronto, Toronto, ON, Canada, 4UHN Toronto Western Hospital, Toronto, ON, Canada, 5Division of Rheumatology, University of Toronto, Toronto Western Hospital, Toronto, ON, Canada, 61E420/Div of Rheumatology, Toronto Western Research Institute, Toronto Western Hospital, University of Toronto, Toronto, ON, Canada, 7Rheumatology, Toronto Western Hospital, University of Toronto, Toronto, ON, Canada

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Biomarkers and systemic lupus erythematosus (SLE)

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Session Information

Title: Systemic Lupus Erythematosus: Clinical Aspects

Session Type: Abstract Submissions (ACR)

Background/Purpose: SLE mice models implicate IL-21, a T cell-derived cytokine, in disease pathogenesis with cytokine over-expression promoting the development of auto-antibodies and lupus-like clinical syndromes.  IL-21 dysregulation has also been noted in human SLE with a subset of patients having an increased proportion of IL-21-producing CD4+ T cells. This study aims to examine the relationship between IL-21 synthesis and distinct clinical phenotypes in human SLE.

Methods: SLE patients (n = 42) fulfilling ≥ 4 ACR criteria were recruited from an established longitudinal lupus cohort. Clinical and biochemical assessment at the time of recruitment permitted calculation of disease activity (SLEDAI-2K) and SLICC damage index.  Healthy age matched controls (n = 19) were also recruited. Peripheral blood mononuclear cells were isolated over a Ficoll gradient and stimulated for 4 hours with PMA/ionomycin in the presence of GolgiStop.  Cells were analyzed by flow cytometry following cell surface (anti-CD3, -CD4) and intracellular staining (anti-IL-21, -IL-17). A Mann Whitney non-parametric test was used for comparisons between groups.  Elevated IL-21 expression for selected CD4+ populations was defined as values ≥ 2 standard deviations above the mean for controls.

Results: A significant proportion (26.4%) of SLE patients was found to have increased levels of CD4+ IL-21 producing T cells when compared to controls.  To refine this cellular population the proportion of IL-21+, IL-17+ and double positive CD4 T cells was examined.  The proportion of IL-21+IL-17negCD4+ cells was significantly elevated in SLE patients when compared to controls (p = 0.03). The IL-17+IL-21negCD4+ SLE compartment was also increased but did not reach statistical significance.  No differences were noted in the double positive (IL-21+IL-17+) CD4+ T cell populations.  To examine the relationship between the IL-21+IL17negCD4+ population and specific clinical phenotypes patients were segregated on the basis of the proportion of IL-21+IL17negCD4+ cells into IL-21 high patients (n = 10) with an equal number of patients with the lowest IL-21 expression selected as a comparator group. No statistically significant differences between these two groups (high vs low, mean ± SD) with regards to disease activity (5.8 ± 3.5 vs 5.7 ± 6.4), anti-dsDNA antibodies (35.6 ± 39.8 vs 44.0 ± 41.9) or complement levels (0.89 ± 0.18 vs 0.98 ± 0.38) was noted. IL-21 high patients had significantly higher disease damage index (SDI, p < 0.0001) than IL-21 low individuals.  As a corollary patients were stratified into quartiles based on their SDI score.  Patients with the highest SDI score had statistically significant higher proportion of IL-21+ IL17neg CD4+ T cells (p = 0.02) than patients in the lowest quartile.

Conclusion: These results suggest that T cell population(s) contributing to IL-21 dysregulation in SLE reside within the IL-21+ IL-17neg CD4+ T cell subset.  Further, as disease damage can be viewed as a surrogate marker of disease severity, this data implies that increased IL-21 synthesis may be linked to more aggressive forms of SLE.


Disclosure:

B. Noamani,
None;

S. Morrison,
None;

D. D. Gladman,
None;

J. Sanchez-Guerrero,
None;

M. B. Urowitz,
None;

J. E. Wither,
None;

C. Landolt-Marticorena,
None.

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