glucosaminylmuramyl-2-alanine-d-isoglutamine and Spondylitis--Ankylosing

Earlier studies have shown that high doses of TNF-alpha increase apoptosis in human autoimmune T-cell clones. Based on these studies, a treatment approach was proposed to reduce or eliminate autoimmune T cells in patients with type 1 diabetes using drugs that temporarily elevate TNF levels. Here, we report the treatment of ankylosing spondylitis patient with a single high oral dose of Likopid (glucosaminyl-muramyl dipeptide), which aimed at increasing the levels of TNF-alpha in order to induce apoptosis of autoreactive T cells. The flow cytometric analysis of blood samples collected before and after treatment demonstrated massive elimination of CD8(+) T cells. However, the treatment did not result in any notable therapeutic effect, and real-time PCR analysis demonstrated that stably expanded T-cell clones that were earlier tracked in this patient were unaffected. This report suggests that the controversial approach to eliminate autoimmune T-cell clones through overstimulation is not effective in treating ankylosing spondylitis.

Topics: Acetylmuramyl-Alanyl-Isoglutamine; Adalimumab; Adjuvants, Immunologic; Antibodies, Monoclonal, Humanized; Antirheumatic Agents; CD8-Positive T-Lymphocytes; Cell Death; Dose-Response Relationship, Drug; Flow Cytometry; Humans; Leukocyte Count; Male; Middle Aged; Spondylitis, Ankylosing; T-Lymphocyte Subsets; Treatment Failure