Infectious arthritis and immune dysregulation: lessons from Lyme disease.

[Guest guest]

Curr Opin Rheumatol. 2010 Apr 6. [Epub ahead of print]

 

Infectious arthritis and immune dysregulation: lessons from Lyme disease.

 

Iliopoulou BP, Huber BT.

 

Department of Pathology, Tufts University School of Medicine, Boston,

Massachusetts, USA.

 

Abstract

 

PURPOSE OF REVIEW:

Borrelia burgdorferi colonization of the joints induces an inflammatory

response, which in some individuals progresses to chronic arthritis. In this

review, we discuss novel pathways that are implicated in disease

development by modulating host defenses to B. burgdorferi infection.

 

RECENT FINDINGS: The use of transgenic mice and gene expression analyses

has revealed novel pathways involved in pathogenesis of Lyme disease. It is

now clear that B. burgdorferi exploits an array of salivary gland proteins

of the tick to evade immune responses in the mammalian host. The spirochete

also modulates its surface protein profile upon infection and induces

anti-inflammatory cytokines, favoring survival of the pathogen. The host

defense involves toll-like receptors (TLRs), such as TLR2 and others, in B.

burgdorferi recognition. To further dissect the genetic predisposition to

treatment-refractory Lyme arthritis, HLA-DR transgenic mice have been used.

 

SUMMARY: The cause and pathogenesis of Lyme arthritis are complex.

Elucidating the mechanisms that govern this chronic inflammatory response will

provide direct insights into other infectious arthritides and the development

of novel therapeutic approaches against B. burgdorferi infection.

 

PMID: 20375899