Inhibition of the Production of Anti-OspA Borreliacidal Antibody with T Cells from Hamsters Vaccinated against<i>Borrelia burgdorferi</i>

Jensen, Jani R.; Chateau, Brian K. Du; Munson, Erik; Callister, Steven M.; Schell, Ronald F.

doi:10.1128/iai.66.4.1507-1512.1998

Cited by 5 publications

(2 citation statements)

References 50 publications

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“…In addition, the development of anti‐OspA borreliacidal antibody was not significantly affected compared with controls. These findings suggest that TGF‐β and IL‐6 work together to augment the development of arthritis in Borrelia ‐vaccinated and ‐challenged mice even in the presence of antibody known to eliminate B. burgdorferi (Jensen et al ., 1998).…”

Section: Discussionmentioning

confidence: 99%

“…Anti‐OspA borreliacidal antibodies were detected by a flow cytometric procedure (Callister et al ., 1996; Jensen et al ., 1998). We showed previously that sera from Borrelia‐ vaccinated and ‐challenged animals (0–3 weeks after infection) have no borreliacidal activity after absorption with recombinant OspA (Jensen et al ., 1998), demonstrating that the killing antibodies detected by borreliacidal antibody assay have specificity for OspA. Viable B. bissettii organisms in the logarithmic growth phase were enumerated with a Petroff–Hausser counting chamber and diluted with fresh BSK medium to a concentration of c .…”

Section: Methodsmentioning

confidence: 99%

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Role of IL-17, transforming growth factor-β, and IL-6 in the development of arthritis and production of anti-outer surface protein A borreliacidal antibodies inBorrelia-vaccinated and -challenged mice

Nardelli

Luk

Kotloski

et al. 2008

FEMS Immunol Med Microbiol

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We showed recently that the adaptive immune events leading to the development of arthritis in Borrelia burgdorferi isolate 297-vaccinated and Borrelia bissettiichallenged mice involve IL-17. Here, we show in Borrelia-vaccinated and -challenged mice that two cytokines known to induce the production of IL-17, IL-6 and transforming growth factor (TGF)-b, are also involved in the development of arthritis. Vaccinated and challenged mice administered either anti-TGF-b or anti-IL-6 antibodies developed histopathologic changes of the hind paws similar to or greater than untreated control mice. By contrast, simultaneous blockage of these cytokines reduced the severity of arthritis in Borrelia-vaccinated and -challenged mice. Moreover, administration of anti-IL-17 antibodies to these dual-antibodytreated mice completely prevented the development of histopathologic changes of the ankle joints, significantly reduced edema of the hind paws, and prevented the production of anti-outer surface protein A borreliacidal antibodies. These findings demonstrate a role for the combined effects of IL-17, IL-6, and TGF-b in the adaptive immune events leading to the development of Borrelia-induced arthritis.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Role of IL-17, transforming growth factor-β, and IL-6 in the development of arthritis and production of anti-outer surface protein A borreliacidal antibodies inBorrelia-vaccinated and -challenged mice

Nardelli

Luk

Kotloski

et al. 2008

FEMS Immunol Med Microbiol

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The Important and Diverse Roles of Antibodies in the Host Response to Borrelia Infections

LaRocca¹,

Benach²

2008

Current Topics in Microbiology and Immunology

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Neutralization of Gamma Interferon Augments Borreliacidal Antibody Production and Severe Destructive Lyme Arthritis in C3H/HeJ Mice

Munson

DeCoster

Nardelli

et al. 2004

Clin Vaccine Immunol

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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-␥). When lymph node cells capable of producing borreliacidal antibody were cultured with anti-murine IFN-␥, an eightfold increase in borreliacidal antibody production was obtained. However, anti-IFN-␥ treatment of these cells also enhanced their ability to adaptively induce arthritis. When anti-IFN-␥-treated lymph node cells producing borreliacidal antibody were infused into C3H/HeJ mice and the mice were then challenged with B. burgdorferi, the mice developed severe destructive Lyme arthritis. Additional studies are needed to delineate the immune response responsible for the induction of arthritis and production of borreliacidal antibody. These studies are needed to ensure an effective and safe vaccine against infection with B. burgdorferi.Vaccination with Borrelia burgdorferi or its components can induce antibodies that prevent infection with the Lyme disease spirochete (1, 6, 8-10, 13, 27, 34). These vaccine-induced antibodies kill B. burgdorferi in the presence of complement (17,24). Specifically, it has been shown that antisera raised against recombinant outer surface protein OspA can prevent borrelial infection by passive immunization (8, 17, 31, 34), kill B. burgdorferi in vitro (13, 17, 18, 20, 24, 27, 29, 30), and sterilize B. burgdorferi-infected ticks (11). However, anti-OspA borreliacidal activity wanes rapidly after active immunization. Padilla et al. (24) reported that vaccination of experimental animals with recombinant OspA induced a borreliacidal antibody response that peaked 6 weeks after vaccination and declined rapidly. Moreover, human volunteers administered several doses of recombinant OspA produced borreliacidal antibody that rapidly decreased (24). Only one vaccinee had antibody 6 months after vaccination. The poor OspA-borreliacidal antibody response may have been a factor in prompting withdrawal of the vaccine for use in humans.Very little is currently known about the immunologic events that might promote and maintain a sustained borreliacidal antibody response after vaccination. Therefore, we developed an in vitro system to determine the effects of immunological mediators on production of borreliacidal activity. Several cytokines have been evaluated, including interleukin (IL)-4, a known B-lymphocyte stimulator (26), and its antagonist, gamma interferon (IFN-␥) (25). However, these cytokines failed to induce high levels of borreliacidal antibody (21, 22).Here, we report that treatment of lymph node cells containing borreliacidal antibody-producing cells with anti-murine IFN-␥ augments the production of anti-B. burgdorferi antibody. Unfortunately, treatment of these cells with anti-murine IFN-␥ also enhances their ability to induce arthritis. MATERIALS AND METHODSMice. Inbred C3H/HeJ mice 8 to 12 weeks old were obtained fro...

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Inhibition of the Production of Anti-OspA Borreliacidal Antibody with T Cells from Hamsters Vaccinated againstBorrelia burgdorferi

Cited by 5 publications

References 50 publications

Role of IL-17, transforming growth factor-β, and IL-6 in the development of arthritis and production of anti-outer surface protein A borreliacidal antibodies inBorrelia-vaccinated and -challenged mice

Role of IL-17, transforming growth factor-β, and IL-6 in the development of arthritis and production of anti-outer surface protein A borreliacidal antibodies inBorrelia-vaccinated and -challenged mice

The Important and Diverse Roles of Antibodies in the Host Response to Borrelia Infections

Neutralization of Gamma Interferon Augments Borreliacidal Antibody Production and Severe Destructive Lyme Arthritis in C3H/HeJ Mice

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