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Abstract Number: 1665

B Cells Revisited In Giant Cell Arteritis

Kornelis S.M. van der Geest1, Wayel H. Abdulahad2, Gerda Horst2, Caroline Roozendaal3, Abraham Rutgers2, Annemieke M.H. Boots2 and Elisabeth Brouwer2, 1Dept. of Rheumatology and Clinical Immunology, University Medical Center Groningen, Groningen, Netherlands, 2Rheumatology and Clinical Immunology, University Medical Center Groningen, Groningen, Netherlands, 3Laboratory Medicine, University Medical Center Groningen, Groningen, Netherlands

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: B cells, BAFF, giant cell arteritis, polymyalgia rheumatica and vasculitis

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Session Information

Title: Vasculitis II

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Giant cell arteritis (GCA) is a primary vasculitis affecting large to medium-sized arteries. Ample evidence suggests that dendritic cells, T cells and monocytes/macrophages contribute to the immunopathology of GCA. Previous reports showed that B cells are not predominant cells in temporal arteries of GCA patients (Cid et al. AR 1989). However, a high prevalence of various auto-antibodies in serum of GCA patients is suggestive of B cell activation in GCA (Baerlecken et al. ARD 2012; Regent et al. ART 2011; Schmits et al. Clin Exp Immunol 2002). Furthermore, emerging data indicate that B cells can modulate immune responses of T cells and monocytes by producing IL-10 and TNF-α (Lund et al. Nat Rev Immunol 2010). In the current study, we assessed the distribution of defined B cell subsets, including IL-10+ regulatory B cells and TNF-α+ effector B cells, in GCA patients before and after glucocorticoid (GC) treatment.

Methods:

B cells were analyzed in peripheral blood of 15 newly-diagnosed GCA patients. In addition, we studied 40 age-matched, healthy controls (HCs) and 28 disease controls, including 17 polymyalgia rheumatica (PMR) patients and 11 rheumatoid arthritis (RA) patients. In a prospective, longitudinal study design, 39 samples were obtained from GCA and PMR patients who were in remission after 2 and 12 weeks of treatment with GCs. Serum levels of BAFF were determined. Flow cytometric staining of B cells for intracellular TNF-α and IL-10 was performed after 4 hours of stimulation with PMA and calcium ionophore in the presence of brefeldin A.

Results:

Circulating B cells were decreased in newly-diagnosed GCA and PMR patients, but not in RA patients, compared to HCs. Following 2 and 12 weeks of GC treatment, B cell numbers normalized in GCA and PMR patients. This normalization was neither attributable to repopulation by immature-transitional B cells from the bone marrow, nor to compensatory hyperproliferation in the blood. Instead, already existing mature B cell subsets seemed to be mobilised towards the circulation of treated GCA and PMR patients. In particular the circulating pool of unswitched and switched memory B cells was expanded after GC treatment.  B cell numbers inversely correlated with ESR, CRP and serum levels of the B cell growth factor BAFF. In newly-diagnosed GCA patients, TNF-α+ effector B cells but not IL-10+ regulatory B cells were decreased. Following treatment, numbers of TNF-α+ effector B cells and IL-10+ regulatory B cells were normal in GCA patients.

Conclusion:

Our data indicate that B cells, including TNF-α+ effector B cells, are redistributed during active GCA and PMR. Following treatment, mature B cells subsets, in particular memory B cells, are mobilized to the circulation. In accordance with the high prevalence of various auto-antibodies reported in GCA and PMR, our data further suggest that activation of B cells occurs during the active stages of both diseases. Additional studies on the pro-inflammatory and regulatory role of B cells in GCA and PMR are ongoing.


Disclosure:

K. S. M. van der Geest,
None;

W. H. Abdulahad,
None;

G. Horst,
None;

C. Roozendaal,
None;

A. Rutgers,
None;

A. M. H. Boots,
None;

E. Brouwer,
None.

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