Anti-ATIC antibodies target the enzyme Aminoimidazole Carboxamide Ribonucleotide Transformylase/IMP Cyclohydrolase (ATIC), a bifunctional protein critical in the *de novo* purine biosynthesis pathway. ATIC catalyzes the final two steps of this pathway, converting 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) to inosine monophosphate (IMP), which is essential for DNA/RNA synthesis and cellular proliferation. Dysregulation of ATIC has been implicated in cancer, autoimmune disorders, and inflammatory diseases.
In autoimmune contexts, anti-ATIC antibodies are primarily associated with dermatomyositis (DM), particularly in patients with anti-synthetase syndrome. These autoantibodies are detected in ~1–4% of DM cases and often correlate with specific clinical features like interstitial lung disease and Raynaud’s phenomenon. Their presence aids in disease subtyping and prognosis.
Research suggests ATIC may act as an autoantigen due to its overexpression or aberrant exposure during cellular stress, triggering immune recognition. Anti-ATIC antibodies are detected via immunoprecipitation, ELISA, or line immunoassays. Beyond diagnostics, studying these antibodies provides insights into disease mechanisms, such as interferon pathway activation in myositis.
Therapeutic strategies targeting ATIC (e.g., methotrexate analogs) are explored in cancer, while in autoimmunity, understanding antibody-antigen interactions may inform biomarker development or immune-modulating therapies. However, the exact pathogenic role of anti-ATIC antibodies remains under investigation, highlighting their dual significance in cellular metabolism and immune dysregulation.