Table 1.
Demographic and clinical features of AAV patients.
BVAS, Birmingham vasculitis activity score; EGPA, eosinophilic granulomatosis with polyangiitis; ENT, Ear nose throat; ELISA, Enzyme-linked immunosorbent assay; GPA, granulomatosis with polyangiitis; MPA, Micropolyangiitis.
Fig 1.
Prevalence of anti-PTX3 aAbs in AAV patients.
A, Anti-PTX3 aAbs were analysed by ELISA in 150 AAV patients with MPA, GPA, or EGPA, 40 patients with SSc, 25 patients with GCA and of 227 sera from healthy subjects (HS). B, Prevalence of anti-PTX3 aAbs in AAV, SSc, GCA patients and HS. C, Anti-PTX3 aAbs according to AAV subtypes (MPA, GPA or EGPA). D, Prevalence of anti-PTX3 aAbs according to the AAV subtypes. E, Anti-PTX3 aAbs in AAV patients according to disease status (active or non active disease). F, Prevalence of anti-PTX3 aAbs according to AAV status. A, C, E, Results are expressed in OD values. Dotted line corresponds to mean + 2 SD titres of anti-PTX3 aAbs in HS sera; full line corresponds to the mean OD in each group of patients. B, D, F, Results are expressed in percentage. ***p<0,001; *p<0.05; ns, not significant.
Fig 2.
Longitudinal analysis of anti-PTX3 aAbs.
Anti-PTX3 aAbs were analysed by ELISA in 14 patients with active disease (onset or relapse) and at remission. Results are expressed in OD values. Dotted line corresponds to mean + 2 SD titres of anti-PTX3 aAbs in HS sera; full line corresponds to the mean OD in each group of patients. Each line represents one patient. *p<0.05.
Fig 3.
Anti-pentraxin aAbs in AAV patients and specificity of anti-PTX3 aAbs.
The presence of anti-CRP (A), anti-SAP (B) aAbs were investigated by ELISA in 120 AAV sera (randomly selected; anti-PTX3 aAbs were detected in 53 sera out of 120 [44.2%]) and in healthy subjects (HS). A&B, Dotted lines correspond to mean + 2 SD titers of anti-CRP and -SAP aAbs in HS sera. Full lines correspond to the mean reactivity + SEM of sera in each group. ***p<0.001. C, The titers of anti-PTX3 (x-axis) and anti-PTX3 N-terminal domain (y-axis) were both determined in 24 AAV sera (randomly selected). Association was analysed using Spearman’s rank correlation.
Table 2.
Presence of anti-CRP, -SAP, and -PTX3 aAbs in 120 sera of AAV patients.
Fig 4.
Immunofluorescence staining of neutrophils by anti-PTX3 Abs.
Slides containing 4 biochips as substrate ethanol-fixed (upper left), formol-aceton fixed neutrophils (upper right) methanol-fixed neutrophils (lower left) and HEp2 cells (lower right) were incubated with A, a serum from a patient with anti-PTX3 aAbs and neither MPO, PR3, BPI, lactoferrine, elastase nor cathepsin G ANCA, B, an anti-PTX3 polyclonal antibody or C-E, control sera for p-ANCA (C), a-ANCA (D), c-ANCA (E). A, C-E, results are representative of the results obtained with one out of four sera. B, Results are representative of one out of three experiments.