Autoimmune diseases (AID) are common chronic inflammatory conditions initiated by the loss of the immunological tolerance to self-antigens. Chronic immune response and uncontrolled inflammation provoke diverse clinical manifestations, causing impairment of various tissues, organs or organ systems. To avoid disability and death, AID must be managed in clinical practice over long periods with complex and closely controlled medication regimens. The anti-tumor necrosis factor biologics (aTNFs) are targeted therapeutic drugs used for AID management. However, in spite of being very successful therapeutics, aTNFs are not able to induce remission in one third of AID phenotypes.
In our research, we investigated genomic variability of AID phenotypes in order to explain unpredictable lack of response to aTNFs. Our hypothesis is that key genetic factors, responsible for the aTNFs unresponsiveness, are positioned at the crossroads between aTNF therapeutic processes that generate remission and pathogenic or disease processes that lead to AID phenotypes expression.