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Lupus
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LJP 1082: a toleragen for Hughes syndrome

J T Merrill

Clinical Pharmacology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, USA, joan-merrill{at}omrf.ouhsc.edu

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 distinguishesself 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 ß2-glycoprotein I. Issues of antigenic selection and multiplex forces influencing tolerance and immunity may have impact on its optimal development and use in patients.

Key Words: autoantibody • beta-2 glycoprotein I • toleragen • tolerance

Lupus, Vol. 13, No. 5, 335-338 (2004)
DOI: 10.1191/0961203304lu1022oa
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This article has been cited by other articles:


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S Vasoo and G R. Hughes
Theory, targets and therapy in systemic lupus erythematosus
Lupus, March 1, 2005; 14(3): 181 - 188.
[Abstract] [PDF]


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