Vδ2 T cell deficiency in granulomatosis with polyangiitis (Wegener's granulomatosis)

Juliane Fazio; Elgar Susanne Quabius; Antje Müller; Sabine Adam-Klages; Daniela Wesch; Susanne Sebens; Shirin Kalyan; Peter Lamprecht; Dieter Kabelitz

doi:10.1016/j.clim.2013.06.003

Vδ2 T cell deficiency in granulomatosis with polyangiitis (Wegener's granulomatosis)

Juliane Fazio, Elgar Susanne Quabius, Antje Müller, Sabine Adam-Klages, Daniela Wesch, Susanne Sebens, Shirin Kalyan, Peter Lamprecht, Dieter Kabelitz^*

^*Corresponding author for this work

Clinic of Rheumatology

University of Kiel

7 Citations (Scopus)

Abstract

Previous studies have characterized phenotypic and functional alterations within T-cell receptor αβ-expressing T cells in patients with granulomatosis with polyangiitis (GPA). We analyzed the frequency, subset composition and in vitro activation of blood γδ T cells in GPA patients. We observed a significant reduction of γδ T cell numbers, due to the selective depletion of the Vδ2 subset which remained consistent over time upon repeated analysis. The loss of Vδ2 T cells was not due to migration into the inflamed lesions as very few γδ T cells were detected in inflammatory infiltrates. The memory subset distribution did not differ among Vδ2 T cells from healthy donors and GPA patients. Importantly, the remaining Vδ2 T cells were capable of responding to phosphoantigen stimulation in vitro. The marked depletion of blood Vδ2 T cells in GPA suggests cellular exhaustion, possibly due to chronic exposure to and continuous overstimulation by microbial phosphoantigens.

Original language	English
Journal	Clinical Immunology
Volume	149
Issue number	1
Pages (from-to)	65-72
Number of pages	8
ISSN	1521-6616
DOIs	https://doi.org/10.1016/j.clim.2013.06.003
Publication status	Published - 01.10.2013

Funding

PL and DK were supported by the Deutsche Forschungsgemeinschaft ( KFO170 , project 3) and the Cluster of Excellence Inflammation-at-Interfaces , and SK by a fellowship from the Alexander-von-Humboldt Foundation . This work forms part of the Ph.D. thesis of JF.

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.clim.2013.06.003

Cite this

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title = "Vδ2 T cell deficiency in granulomatosis with polyangiitis (Wegener's granulomatosis)",

abstract = "Previous studies have characterized phenotypic and functional alterations within T-cell receptor αβ-expressing T cells in patients with granulomatosis with polyangiitis (GPA). We analyzed the frequency, subset composition and in vitro activation of blood γδ T cells in GPA patients. We observed a significant reduction of γδ T cell numbers, due to the selective depletion of the Vδ2 subset which remained consistent over time upon repeated analysis. The loss of Vδ2 T cells was not due to migration into the inflamed lesions as very few γδ T cells were detected in inflammatory infiltrates. The memory subset distribution did not differ among Vδ2 T cells from healthy donors and GPA patients. Importantly, the remaining Vδ2 T cells were capable of responding to phosphoantigen stimulation in vitro. The marked depletion of blood Vδ2 T cells in GPA suggests cellular exhaustion, possibly due to chronic exposure to and continuous overstimulation by microbial phosphoantigens.",

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T1 - Vδ2 T cell deficiency in granulomatosis with polyangiitis (Wegener's granulomatosis)

AU - Fazio, Juliane

AU - Quabius, Elgar Susanne

AU - Müller, Antje

AU - Adam-Klages, Sabine

AU - Wesch, Daniela

AU - Sebens, Susanne

AU - Kalyan, Shirin

AU - Lamprecht, Peter

AU - Kabelitz, Dieter

PY - 2013/10/1

Y1 - 2013/10/1

N2 - Previous studies have characterized phenotypic and functional alterations within T-cell receptor αβ-expressing T cells in patients with granulomatosis with polyangiitis (GPA). We analyzed the frequency, subset composition and in vitro activation of blood γδ T cells in GPA patients. We observed a significant reduction of γδ T cell numbers, due to the selective depletion of the Vδ2 subset which remained consistent over time upon repeated analysis. The loss of Vδ2 T cells was not due to migration into the inflamed lesions as very few γδ T cells were detected in inflammatory infiltrates. The memory subset distribution did not differ among Vδ2 T cells from healthy donors and GPA patients. Importantly, the remaining Vδ2 T cells were capable of responding to phosphoantigen stimulation in vitro. The marked depletion of blood Vδ2 T cells in GPA suggests cellular exhaustion, possibly due to chronic exposure to and continuous overstimulation by microbial phosphoantigens.

AB - Previous studies have characterized phenotypic and functional alterations within T-cell receptor αβ-expressing T cells in patients with granulomatosis with polyangiitis (GPA). We analyzed the frequency, subset composition and in vitro activation of blood γδ T cells in GPA patients. We observed a significant reduction of γδ T cell numbers, due to the selective depletion of the Vδ2 subset which remained consistent over time upon repeated analysis. The loss of Vδ2 T cells was not due to migration into the inflamed lesions as very few γδ T cells were detected in inflammatory infiltrates. The memory subset distribution did not differ among Vδ2 T cells from healthy donors and GPA patients. Importantly, the remaining Vδ2 T cells were capable of responding to phosphoantigen stimulation in vitro. The marked depletion of blood Vδ2 T cells in GPA suggests cellular exhaustion, possibly due to chronic exposure to and continuous overstimulation by microbial phosphoantigens.

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Vδ2 T cell deficiency in granulomatosis with polyangiitis (Wegener's granulomatosis)

Abstract

Funding

UN SDGs

Access to Document

Other files and links

Fingerprint

CRU 170: Early Pathogenesis of Wegener's Granulomatosis: From Innate Immunity with Granuloma Formation to Autoimmunity.

Cite this

Vδ2 T cell deficiency in granulomatosis with polyangiitis (Wegener's granulomatosis)

Abstract

Funding

UN SDGs

Access to Document

Other files and links

Fingerprint

Projects

CRU 170: Early Pathogenesis of Wegener's Granulomatosis: From Innate Immunity with Granuloma Formation to Autoimmunity.

Cite this