Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody.

CD4+ CD25+ T cells are a population of regulatory T cells responsible for active suppression of autoimmunity. Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-gamma degrees ) C57BL/6 mice challenged with the Lyme spirochete.

Neutralization of gamma interferon augments borreliacidal antibody production and severe destructive Lyme arthritis in C3H/HeJ mice.

Development of a high level of sustained borreliacidal antibody is paramount for maintaining protection against infection with Borrelia burgdorferi. We show that production of borreliacidal antibody can be enhanced by preventing the effects of gamma interferon (IFN-gamma). When lymph node cells capable of producing borreliacidal antibody were cultured with anti-murine IFN-gamma, an eightfold increase in borreliacidal antibody production was obtained.

Primary pulmonary glomus tumor with contiguous spread to a peribronchial lymph node.

Glomus tumors are uncommon soft tissue tumors. Rare occurrences in visceral organs including the respiratory tract have been reported. The vast majority of these tumors are biologically benign.

Inhibition of interleukin-17 prevents the development of arthritis in vaccinated mice challenged with Borrelia burgdorferi.

We showed that Borrelia burgdorferi-vaccinated interferon gamma-deficient (IFN-gamma(0)) mice challenged with the Lyme spirochete developed a prominent chronic severe destructive osteoarthropathy. The immune response underlying the development of the severe destructive arthritis involves interleukin-17 (IL-17). Treatment of vaccinated IFN-gamma(0) mice challenged with B.

Destructive arthritis in vaccinated interferon gamma-deficient mice challenged with Borrelia burgdorferi: modulation by tumor necrosis factor alpha.

We found that Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-gamma(0)) mice challenged with B. burgdorferi developed prominent chronic destructive osteoarthropathy. When these mice were treated with anti-tumor necrosis factor alpha (TNF-alpha) antibody, the severity of the destructive osteoarthritis was enhanced and affected the mobility of the animals.