The change in the levels of these key regulators of osteoclast differentiation may play a major role in the bone loss seen in periodontitis.

Objective. Macrophage migration inhibitory factor (MIF) isConclusion. These data represent the first demonstration of the cytokine MIF in human autoimmune disease and suggest MIF as a potential therapeutic target in RA.Macrophage migration inhibitory factor (MIF) is increasingly recognized as an important regulator of immune and inflammatory responses. It is released by activated T lymphocytes and macrophages and upregulates the proinflammatory activity of these cells (1-4). While its original description focused on its ability to prevent the random migration of macrophages in culture, evidence of a broad range of proinflammatory actions continues to emerge. Of note, MIF induces macrophage secretion of tumor necrosis factor ␣ (TNF␣) and promotes interferon-␥ (IFN␥)-induced production of nitric oxide by mouse macrophages (5-7).

Objective. Ankylosing spondylitis (AS) is a common inflammatory arthritis affecting primarily the axial skeleton. IL23R is genetically associated with AS. This study was undertaken to investigate and characterize the role of interleukin-23 (IL-23) signaling in AS pathogenesis.Methods. The study population consisted of patients with active AS (n ‫؍‬ 17), patients with psoriatic arthritis (n ‫؍‬ 8), patients with rheumatoid arthritis, (n ‫؍‬ 9), and healthy subjects (n ‫؍‬ 20). IL-23 receptor (IL-23R) expression in T cells was determined in each subject group, and expression levels were compared. Results. The proportion of IL-23R-expressing T cells in the periphery

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