Differential B- and T-cell activation in Wegener’s granulomatosis

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Volume 59, Issue 1, Pages (January 2001)

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Volume 55, Issue 5, Pages (May 1999)

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Differential B- and T-cell activation in Wegener’s granulomatosis Eliane R. Popa, MSc, Coen A. Stegeman, MD, PhD, Nicolaas A. Bos, PhD, Cees G.M. Kallenberg, MD, PhD, Jan Willem Cohen Tervaert, MD, PhD Journal of Allergy and Clinical Immunology Volume 103, Issue 5, Pages 885-894 (May 1999) DOI: 10.1016/S0091-6749(99)70434-3 Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 1 Plasma levels of anti-PR3 ANCA in relation to disease activity and extent. P values for each patient group were determined relative to healthy control subjects (*) or relative to another patient group (* above line ). Indicated are the 10th, 25th, 50th, 75th, and 90th percentiles (horizontal lines ) and outliers (circles ). Gen , Generalized disease; lim , limited disease. *P < .05; **P < .005; ***P < .0005. Open bars , Active patients (n = 12; generalized, 7 patients; limited, 5 patients); light hatched bars , patients experiencing remission of disease (n = 21; generalized, 16 patients; limited, 5 patients). Journal of Allergy and Clinical Immunology 1999 103, 885-894DOI: (10.1016/S0091-6749(99)70434-3) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 2 Lymphocyte activation profiles. Whole peripheral blood was incubated with combinations of mAbs against lymphocyte lineage and activation markers. After lysis of erythrocytes and washing, the expression of activation markers on the surface of B and T cells was measured by FACS. For the detection of CD38-expressing B cells, a live gate was set on the CD19+ population. A , B-cell activation profile; B , activation profile of CD4+ T cells; C , activation profile of CD8+ T cells. Journal of Allergy and Clinical Immunology 1999 103, 885-894DOI: (10.1016/S0091-6749(99)70434-3) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 3 Frequency of activated B and T cells in the peripheral blood of patients with WG and healthy control subjects in relation to disease activity and extent. A , Frequency of CD38-expressing cells within the CD19+ population; B , frequency of CD25-expressing cells within the CD4+ T-cell population; C , frequency of HLA-DR–expressing cells within the CD8+ T-cell population. Indicated are the 10th, 25th, 50th, 75th, and 90th percentiles (horizontal lines ) and outliers (circles ). P values for each patient group were determined relative to healthy control subjects (*) or relative to another patient group (* above line ). *P < .05; **P < .005; ***P < .0005; ****P < .0001. Open bars , Active patients (n = 12); light hatched bars , patients experiencing remission of disease (n = 21). Journal of Allergy and Clinical Immunology 1999 103, 885-894DOI: (10.1016/S0091-6749(99)70434-3) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 4 Plasma levels of sIL-2R in relation to disease activity and extent. Indicated are the 10th, 25th, 75th, and 90th percentiles (horizontal lines ) and outliers (circles ). P values were calculated with respect to healthy control subjects. *P < .05; **P < .005. Open bars , Active patients (n = 12); light hatched bars , quiescent patients (n = 21). Journal of Allergy and Clinical Immunology 1999 103, 885-894DOI: (10.1016/S0091-6749(99)70434-3) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 5 Postulated cause for and effects of lymphocyte activation in WG. Chronic carriage of S aureus in patients with WG is associated with the release and persistent presence of superantigens (SAgs ). These potent stimulators of the immune system can lead to chronic activation of T cells (phase 1, persistent T-cell activation). In the event of a staphylococcal infection, PMN phagocytose S aureus , a process leading to neutrophil activation and release of proteinase 3 (PR3 ), the major antigen in WG. In the presence of the released autoantigen and costimulatory help from persistently activated T cells, PR3-specific B cells can be activated (phase 2, intermittent B-cell activation) to produce autoantibody (ANCA; phase 3, ANCA production). ANCA have a pathogenic potential by activating neutrophils. In this process reactive oxygen species (ROS ) and PR3 are released, contributing to endothelial damage and vasculitis (phase 4, vasculitis). Components of this scenario from the present study are depicted in color. Journal of Allergy and Clinical Immunology 1999 103, 885-894DOI: (10.1016/S0091-6749(99)70434-3) Copyright © 1999 Mosby, Inc. Terms and Conditions