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. 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.