Annexin A5 and anti-annexin antibodies in patients with systemic lupus erythematosus

Abstract

Plasma levels of annexin A5 (ANX A5) and anti-annexin A5 (aANX A5) antibodies were evaluated in 51 women with systemic lupus erythematosus (SLE). The results were compared between the total SLE group, subgroups on/without immunosuppressive therapy and the control (28 women). The relationships between ANX A5/aANX A5 antibodies levels and laboratory variables (anti-cardiolipin antibodies-aCL, total cholesterol, thrombocyte count, activated partial thromboplastin time-APTT, prothrombin time, international normalized ratio-INR) were performed in the total SLE group and in the patient subgroups identified as the arithmetic mean of ANX A5 concentration in the control plus 1-4 standard deviations (SD). The whole SLE group and the subgroup on immunosuppression showed significantly higher ANX A5 and IgG aANX A5 antibodies concentrations. A weak positive correlation was found between ANX A5 and thrombocyte count, a moderate one between IgG and IgM aANX A5 antibodies, a weak negative correlation between IgG aANX A5 and APTT in the whole SLE group. SLE subgroups with ANX A5 concentrations higher than the control mean plus 3 or 4 SD showed a weak/moderate negative correlation of this parameter with aANX A5 antibodies, moderate one with IgG aCL antibodies levels, a moderate positive correlation with cholesterol concentration, moderate/high positive correlations with thrombocyte count. The association between plasma ANX A5/IgG aANX A5 levels and severity of disease was noticed. The role of aANX A5 and IgG aCL antibodies as causative factors of increased ANX A5 levels was suggested, and the relationship between ANX A5 and thrombocyte count was revealed.

Annexin A5 in treated hypertensive patients and its association with target organ damage

“…In our hypothesis AnxA5 is secreted early into the bloodstream of hypertension patients by endothelial cell (both coronary and systemic) as a mechanism of defense that try to palliate a potential proinflammatory and hypercoagulable state that will finally lead to cardiac and vascular TOD. According to our data, higher plasma levels of AnxA5 have also been detected in other conditions associated with inflammation and increased coagulation states such as sickle cell disease [25] and systemic lupus erythematosus (SLE) [26,27].…”

Annexin A2 and A5 Serve as New Ligands for C1q on Apoptotic Cells

“…It is therefore possible that there are other factors preventing interaction of C1q with apoptotic cells in SLE patients, such as autoantibodies to C1q ligands. Interestingly, autoantibodies to both annexin A2 and annexin A5 (21,22), as well as to other C1q ligands and C1q itself (43,44), have been found in patients suffering from autoimmune diseases such as SLE. These antibodies could either decrease direct binding of C1q to apoptotic cells or recruit additional C1q.…”

Complement in removal of the dead – balancing inflammation

“…Remarkably, autoantibodies against the FH ligands dsDNA and histones are abundant in SLE patients, and autoantibodies against FH itself as well as its ligand annexin A2 are observed. [150][151][152][153][154] Thus, it is possible that the binding and subsequent internalization of FH by apoptotic cells is sterically hindered by these autoantibodies, which could cause impaired or delayed clearance.…”