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Abstract Number: 125

Elevated Proliferative Capacity of CD8+ T Cells in Giant Cell Arteritis

Rosanne Reitsema1, Rebeca Hid Cadena 2, Wayel Abdulahad 3, Annemieke Boots 3, Peter Heeringa 4 and Elisabeth Brouwer 1, 1Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands, 2Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands, 3Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, 4Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Groningen

Meeting: 2019 ACR/ARP Annual Meeting

Keywords: CD8 cells and giant cell arteritis

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Session Information

Date: Sunday, November 10, 2019

Session Title: T Cell Biology & Targets in Autoimmune & Inflammatory Disease Poster

Session Type: Poster Session (Sunday)

Session Time: 9:00AM-11:00AM

Background/Purpose: Giant cell arteritis (GCA) is the most frequent form of systemic vasculitis affecting the large- and medium-sized vessels. The involvement of innate immune cells and CD4+ T cells in the pathogenesis of GCA has been intensively studied. Interestingly, recent findings suggest a role of CD8+ T cells in disease development. However, CD8+ subsets and their functional capacities have not yet been studied in detail. Therefore, this study aims to investigate the phenotype and function of circulating CD8+ T cells in newly diagnosed GCA patients compared to healthy age- and sex- matched controls.

Methods: Newly diagnosed, untreated GCA patients (n=9), diagnosed according to international GCA consensus criteria, and  age- and sex-matched healthy controls (HCs, n= 12) were enrolled. Firstly, peripheral blood mononuclear cells (PBMCs) were stained with fluorochrome-conjugated antibodies directed against CD3, CD4, CD8, CCR7, CD45RO, Ki-67, CD69 and CD25 and analyzed by flow cytometry. The following differentiation subsets were defined: CD8+ T naive (CD45RO-CCR7+), central memory (TCM, CD45RO+CCR7+), effector memory (TEM, CD45RO+CCR7-) and effector memory re-expressing CD45RA (TEMRA, CD45RO-CCR7-) cells. Secondly, the proliferative capacity of CD8+ T cells was determined in isolated CD3+ T cells by measuring the intensity of cell proliferation dye (CPD) upon 5 days of stimulation with plate-bound anti-CD3 or anti-CD3 plus soluble anti-CD28. Lastly, the proliferative capacity of whole blood sorted CD8+ T naive, T­­EM and T­EMRA cells from two GCA patients in remission and two HCs was determined.

Results: No differences in the proportions of differentiation subsets were present between GCA patients and HCs. A proportional increase of Ki-67 within CD8+ TEM cells was found in GCA patients compared to HCs (p < 0.01) suggesting increased homeostatic proliferation in these cells. After stimulation with anti-CD3, the percentage of divided CD8+ T cells was higher in patients than in HCs (p< 0.05). After stimulation with both anti-CD3 and anti-CD28, no differences in proliferative capacity were found. Furthermore, a strong positive correlation between the proportion of CD8+ TEMRA cells and the percentage of divided cells upon CD3 stimulation was found in newly diagnosed GCA patients (R=0.8), and not in HCs. Preliminary data from sorted CD8+ differentiation subsets suggest that CD8+ TEMRA cells from GCA patients indeed have a higher proliferative capacity than those from HCs.

Conclusion: This study demonstrated that CD8+ TEM cells show increased homeostatic proliferation in GCA patients compared to HCs. Functional data on proliferative capacity suggest that CD8+ TEMRA cells from GCA patients are more rapidly activated by crosslinking CD3, suggesting either reduced regulation in these patients or more intrinsic threshold changes. This higher proliferative capacity of CD8+ TEMRA cells is contrary to existing literature, since it is well appreciated that the expansion potential of CD8+ T cells decreases from naive T cells to TCM to TEM and TEMRA. The lower activation thresholds for CD8+ TEMRA cells in GCA imply that these cells are not innocent bystanders but contribute to disease progression in GCA.


Disclosure: R. Reitsema, None; R. Hid Cadena, None; W. Abdulahad, None; A. Boots, Gruenenthal, 5; P. Heeringa, None; E. Brouwer, Roche, 5, 8.

To cite this abstract in AMA style:

Reitsema R, Hid Cadena R, Abdulahad W, Boots A, Heeringa P, Brouwer E. Elevated Proliferative Capacity of CD8+ T Cells in Giant Cell Arteritis [abstract]. Arthritis Rheumatol. 2019; 71 (suppl 10). https://acrabstracts.org/abstract/elevated-proliferative-capacity-of-cd8-t-cells-in-giant-cell-arteritis/. Accessed January 16, 2021.
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