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Emergence of Chronic Lyme Arthritis: Putting the Breaks on CD28 Costimulation

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[Note: CD28 is a molecule that plays a role in activation of T-cell immune responses. See also the authors’ previous article, “CD28 deficiency exacerbates joint inflammation upon Borrelia burgdorferi infection, resulting in the development of chronic Lyme arthritis.” ]

Lyme disease is a debilitating infection that is caused upon a bite of Borrelia burgdorferi (Bb)-infected ticks. One of the most prominent clinical manifestations is the development of chronic Lyme arthritis.

Months after Bb infection, approximately 60% of untreated Lyme patients experience intermittent arthritic attacks that may last for years.

The use of the CD28(-/-) [deficient] mouse in Bb infection has helped to shed light into the mechanisms that govern this inflammatory process, which seems to be tightly regulated. [Unlike “wild” mice but as with humans, a majority of this CD28 deficient mutant breed develops chronic Lyme arthritis after infection, so is useful as an animal model for the study of the inflammatory process.]

In this current review, the effect of immunoregulation, as well as CD28 deficiency in the development of chronic Lyme arthritis is discussed.

Source: Immunopharmacology and Immunotoxicology, Sep 2008;15:1-12. [Epub ahead of print] PMID: 18792834, by Iliopoulou BP, Huber BT. Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, USA. [E-mail: Brigitte.huber@tufts.edu ]

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