Antibodies directed against myeloperoxidase (anti-MPO) are used in the diagnostic and follow-up of ANCA-associated vasculitis (AAV), along anti-PR3.

Diagnosis of AIG is supported by the detection of gastric autoantibodies. Antiparietal cell antibodies (APCAs) are antibodies against gastric proton pump and are detected in approximately 90% of patients with PA. Anti-intrinsic factor antibodies (AIFAs) target proteins necessary for vitamin B12 absorption and are present in approximately 80% of patients with PA.

Anti-neutrophil cytoplasmic antibodies (ANCA) directed to proteinase 3 (PR3) represent highly established markers for patients with ANCA-associated vasculitis (AAV). PR3-ANCA have also demonstrated utility in the management of inflammatory bowel disease (IBD). More specifically, PR3-ANCA discriminate individuals with ulcerative colitis (UC) from Crohn's disease (CD) patients and are associated with disease severity, activity, and treatment non-response.

Nucleosome-specific T cells induce antinucleosome antibodies, anti-double-stranded deoxyribonucleic acid (dsDNA) and antihistone antibodies due to epitope spreading. Complexes of nucleosomes and antinuclear antibodies are nephritogenic because these complexes can bind via their positively charged histones to the negatively charged heparin sulfate in the glomerular basement membrane. Antinucleosome antibodies comprise autoantibodies that can bind to all accessible components of the nucleosome (i.e., dsDNA, histones, and conformational epitopes created by DNA and histones). These latter antibodies are called nucleosome-specific antibodies.

The M-type phospholipase A2 receptor (PLA2R) was identified as the major target podocyte antigen involved in adult autoimmune idiopathic membranous nephropathy

Anti-Saccharomyces cerevisiae antibodies (ASCA) had been known to be specific for Crohn's disease but it has been found in many other autoimmune diseases like systemic lupus erythematosus (SLE).

The cytoplasmic protein glutamic acid decarboxylase (GAD) is the rate-limiting enzyme in the synthesis of the major inhibitory neurotransmitter γ-aminobutyric acid (GABA). High serum levels of antibodies (Abs) against the isoform GAD65 have been associated with neurologic syndromes like stiff-person syndrome (SPS), cerebellar ataxia (CA), limbic encephalitis (LE), and temporal lobe epilepsy (TLE) together referred to as GAD65 antibody spectrum disorders (GAD65-Ab SDs) and circulating GAD-reactive B cells in peripheral blood are abundant in these patients

LKM antibodies are rare. They contribute to establish a diagnosis of autoimmune hepatitis, although they are also found in other liver diseases. The cytochrome P450 2D6 is one of the antigens recognized by LKM antibodies, but other antigens are likely targeted considering that 2D6 is minimally expressed in the kidney and yet LKM antibodies bind to kidney tubuli.

The soluble membrane attack complex (sMAC, a.k.a., sC5b-9 or TCC) is generated on activation of complement and contains the complement proteins C5b, C6, C7, C8, C9 together with the regulatory proteins clusterin and/or vitronectin. sMAC is a unique complement activation macromolecule as it is comprised of several different subunits. To date no complement-mediated function has been identified for sMAC.