7th International Immunoglobulin Conference: Immunomodulation. (December 2014)

• Record Type: Journal Article
• Authors: Danieli, M. G.; Shoenfeld, Y.
• Is Part Of: Clinical and experimental immunology. Volume 178(2014)supplement 1
• Page Start: 112
• Page End: 114
• Publication Date: 2014-12
• Subjects: autoantibodies -- immunobullous skin disease -- intravenous immunoglobulin -- recurrent miscarriage -- rheumatoid arthritis; Immunopathology -- Periodicals; 616.079
• DOI: 10.1111/cei.12533
• Languages: English
• ISSNs: 0009-9104

Abstract

Summary: Immunomodulation uses synthetic, natural and recombinant preparations to modify the immune response to a desired level, typically to treat specific autoimmune diseases, as will be discussed in this section. Rheumatoid arthritis (RA) is a common systemic autoimmune disease, affecting 1% of the population worldwide. Currently, a first‐line disease‐modifying therapy for RA is methotrexate; however, more than 40 monoclonal antibodies are in use or under investigation for the treatment of RA. This panoply of biological disease‐modifying agents means that clinicians can make use of drugs with different mechanisms of action should one type become ineffective. In autoimmune pemphigus conditions, identification of pathogenic autoantibodies against intercellular cadherin desmoglein 1 and/or 3 antigens is one of the criteria for appropriate diagnosis. In pemphigoid conditions, autoantibodies are directed against bullous pemphigoid antigens BP230 and BP180, and in both types of immunobullous disease intravenous immunoglobulin (IVIg), as adjuvant therapy in combination with a cytotoxic drug, is effective in reducing autoantibody levels, disease severity and background steroid use. Further studies are required to establish the role of monoclonal antibodies in the treatment of autoimmune bullous disease. IVIg may also be effective in another at‐risk population with autoimmune disease, namely secondary recurrent miscarriage (RM). However, the mechanism of action of IVIg in secondary RM is largely unknown, although levels of natural killer cell biomarkers, particularly CD56 +, have been shown to decline after IVIg treatment [1‐6]. Data from meta‐analyses of heterogeneous placebo‐controlled trials indicate that IVIg may be effective in secondary RM, but most trials to date have used immunomodulatory doses lower than those considered to be efficient in autoimmune disease. The results of a recently completed study may help to address this question.