title: LJP 1082: a toleragen for Hughes syndrome.
abstract: A hallmark of systemic lupus erythematosus (SLE) and related autoimmune diseases such as the antiphospholipid syndrome (APL or Hughes syndrome) is an apparent breakdown in tolerance, the process by which the body distinguishes self from nonself in order to maintain a versatile immune defense while protecting itself from self-annihilation. To some extent, loss of tolerance is a desirable feature of host immunity, and is known to occur in healthy individuals. Optimal tolerance then is probably not an all or nothing phenomenon. Autoimmunity should be seen as a breakdown in homeostasis rather than a completely aberrant kind of immunity. This leads to special considerations in the assessment of potentially toleragenic therapies, in which an attempt is made to re-educate the immune system. LJP 1082 is designed as a polyvalent antigenic structure aimed at crosslinking specific surface immunoglobulin and tolerizing B cells to beta2-glycoprotein I. Issues of antigenic selection and multiplex forces influencing tolerance and immunity may have impact on its optimal development and use in patients.
authors.affiliation: Clinical Pharmacology Research Program, Oklahoma Medical Research Foundation, Oklahoma City 73104, USA. joan-merrill@omrf.ouhsc.edu
authors.forename: J T
authors.initials: JT
authors.lastname: Merrill
mesh_terms: D016736:Antiphospholipid Syndrome / Q000188:drug therapy* / Q000276:immunology; D006023:Glycoproteins / Q000737:chemistry*; D006801:Humans; D007108:Immune Tolerance; D009841:Oligonucleotides / Q000627:therapeutic use*; D053482:beta 2-Glycoprotein I
chemical_list: D006023:Glycoproteins; D009841:Oligonucleotides; D053482:beta 2-Glycoprotein I; C094104:abetimus