Complement-mediated muscle cell lysis: A possible mechanism of myonecrosis in anti-SRP associated necrotizing myopathy (ASANM)

Four dermatomyositis-specific autoantibodies—anti-TIF1γ, anti-NXP2, anti-SAE and anti-MDA5—in adult and juvenile patients with idiopathic inflammatory myopathies in a Hungarian cohort

“…According to recent research anti-ARS autoantibodies include anti-Jo1, anti-PL-7, anti-PL-12, anti-OJ, anti-EJ, anti-KS, anti-SC, anti-JS, anti-Ha and anti-Zo autoantibodies [27]. Autoantibodies found in patients with NAM are anti-SRP and the recently recognised anti-HMGCR and anti-200/100 [28][29][30]. The statin-induced form of NAM is associated with the presence of anti-HMGCR autoantibodies [31].…”

Immunotherapies for Immune-Mediated Myopathies: A Current Perspective

“…There can be upregulation of MHC-I antigens in myofibers, particularly in cases associated with statin drug therapy [31,32]. In anti-SRPassociated cases a complement-dependent antibody-mediated mechanism has been implicated [33].…”

Molecular and functional characterization of CD59 from Nile tilapia (Oreochromis niloticus) involved in the immune response to Streptococcus agalactiae

“…[34]. In brief, 100 mL of 2 mg/ml NHS-LC-biotin was mixed with 1 ml of rOn-CD59 (0.8 mg/ml) or histidine-tagged TRX (0.8 mg/ml) solution, incubated at 25 C for 2 h, and then 20 mL of 0.5 M NH 4 Cl was added to the mixtures to inactivate the uncombined biotin. The uncombined biotin was removed by ultrafiltration.…”

“…There exist three major pathways to activate the complement system: the classical, the alternative and the lectin pathways [3]. Activation through either pathway eventually initiates the terminal pathway involving the formation of membrane attack complex (MAC, C5b-9), which leads to complement-mediated lysis [4,5]. Given the potency of the complement system, its activation has the potential to cause unwanted inflammation on host tissue [6].…”