Background Takayasu arteritis and giant cell vasculitis are two forms of large vessel disease mostly affecting women. One of their main differences is the age at onset this being around 20 years for Takayasu’s (TA) and largely above 50 for giant cell vasculitis (GCA). In some patients the affected vessels also differ with a focus on the temporal artery in the aged patients and a stronger focus on the aorta in TA.Until recently T cells were believed to be the major player in those fomrs of large vessel vasculitis. We could show recently that B cell disturbances ca be found in Takayasu arteritis correlating with dsease activity. For giant cell vasculitis data is still lacking about B cell disturbances.
Objectives In this study we compare the frequency and absolute number of B cell subsets in the peripheral blood of patients suffering from TA, GCA and Systemic lupus erythematosus (SLE) as compared to healthy controls.
Methods Peripheral blood mononuclear cells were analysed ex vivo by flow cytometry according to their expression of CD19, CD20, CD27, IgD and MHCII. Samples from 14 with active GCA, 10 with inactive GCA, 8 with active SLE, 5 with active TA and 25 healthy controls were analysed. Plasma cells were characterized by being CD19 pos, CD27 high, CD20 neg. Switched memory B cells were characterized by being CD19pos, CD27pos IgD neg, Naïve B cells were characterized as being CD27 neg IgD pos. Double neg cells were CD19 pos CD27 neg IgD neg. Calculations were done using Graph Pad prism using Mann-Whitney-test and p- values of less than 0.05 were taken as significant.
Results Overall B cell numbers are comparable in GCA, TA and healthy donors whereas they were found to be reduced in SLE as was reported previously. Regarding plasma cells frequency we could detect a significant increase in patients with active GCA, active TA and obviously SLE as compared to healthy controls whereas frequency in patients with inactive disease were only slightly increased. Regarding absolut numbers this change was only detecable for patients with active GCA. For MHCII-high plasma cells a reduction as compared to healthy controls could be observed that did not reach significance. In the other B cell subsets a significant reduction could be found between healthy donors and patients with active GCA regarding the naïve B cells (frequency and absolute numbers p=0,01 and p=0,005). In Takayasu patients a similar change could be observed but not being significant. For the frequency a significant increase could be observed regarding the switched memory B cells (p=0,003) that was nearly as pronounced in inactive GCA but was not observed in TA and SLE.
Conclusions Here we show for the first time that disturbances in B cell subsets in the peripheral blood can be observed not only in TA but also in patients with GCA. The observed changes differ between giant cell vasculitis and TA and are only to some extend comparable to the ones described in SLE. Therefore the flowcytometric analysis of B cell substes in the blood could be a tool to differentiate between thoses diseases and are another hint for a different B-cell-pathomechanism for TA and GCA. In addition B cells might represent an interesting therapeutic target for new drugs.
Disclosure of Interest None Declared