PMID: 9423867Jan 10, 1998Paper

Modulation of murine Lyme borreliosis by interruption of the B7/CD28 T-cell costimulatory pathway

Infection and Immunity
M C ShanafeltL K Bockenstedt

Abstract

Recent studies have implicated cytokines associated with Th2 cells in the genetic resistance to murine Lyme borreliosis. Because the B7/CD28 costimulatory pathway has been shown to influence the differentiation of Th-cell subsets, we investigated the contribution of the B7 molecules CD80 and CD86 to the Th2 cytokine profile and development of arthritis in BALB/c mice infected with Borrelia burgdorferi. Effective blockade of CD86/CD28 interaction was demonstrated by elimination of interleukin 4 (IL-4) and upregulation of gamma interferon (IFN-gamma) responses by B. burgdorferi-specific T cells and by reduction of B. burgdorferi-specific immunoglobulin G. Despite the shift toward a Th1 cytokine pattern, which others have associated with disease susceptibility, the severity of arthritis was unchanged. Moreover, combined CD80/CD86 blockade by using anti-CD80 and anti-CD86 monoclonal antibodies or CTLA-4Ig enhanced IFN-gamma production over that seen with CD86 blockade alone, yet augmentation of this Th1-associated cytokine did not enhance disease. These results demonstrate that IL-4 production by T cells in B. burgdorferi-infected BALB/c mice is dependent upon CD86/CD28 interaction and that this cytokine does not contribute signifi...Continue Reading

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Citations

Jul 9, 2003·The Journal of Immunology : Official Journal of the American Association of Immunologists·Charles R BrownChristie M Loiacono
Dec 18, 2007·FEMS Immunology and Medical Microbiology·Xiaohui WangJanis J Weis
Oct 25, 2000·The Journal of Immunology : Official Journal of the American Association of Immunologists·H KumarL K Bockenstedt
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Sep 17, 2008·Immunopharmacology and Immunotoxicology·Bettina Panagiota Iliopoulou, Brigitte T Huber
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Jun 22, 1999·Infection and Immunity·C R Brown, S L Reiner

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