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The outer surface lipoprotein OspA of Borrelia burgdorferi provides co-stimulatory signals to normal human peripheral CD4+ and CD8+ T lymphocytes.

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By Knigge H, Simon MM, Meuer SC, Kramer MD, Wallich R • www.ProHealth.com • October 1, 1996


Abstract

Studies in man and mice have indicated that T cells induced during Borrelia burgdorferi infection are involved in the pathogenesis of the disease. We analyzed the ability of B. burgdorferi to provide co-stimulatory signals to highly enriched normal human CD2+ T lymphocytes in the presence of suboptimal concentrations of immobilized anti-CD3 antibodies. Here we show that the lipid-containing recombinant outer surface lipoprotein A (rlip-OspA) of B. burgdorferi but not its delipidated derivative rNS1-OspA augmented CD3-induced T cell proliferation in a dose-dependent manner and at levels similar to that obtained with anti-CD28 antibodies. Lipopolysaccharide had no effect in this system at any concentration tested, suggesting that the active principle of co-stimulation is associated with the lipid moiety of rlip-OspA and distinct from conventional lipid A. Furthermore, incubation of CD2+ T cells or selected CD4+ as well as CD8+ subpopulations with rlip-OspA, but not with rNS1-OspA led to the production of interferon (IFN)-gamma, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha, but not IL-4. In contrast, co-stimulation of the respective T cell populations with anti-CD28 antibodies resulted in the generation of IFN-gamma, IL-4 and TNF-alpha, but not IL-6. This indicated that the signal transduction pathway induced by rlip-OspA is distinct from that elicited via the CD28 receptor. Co-stimulation of T cells with rlip-OspA also resulted in the development of cytolytic effector cells. In light of the fact that inflamed tissues of B. burgdorferi-infected hosts contain blood leukocytes together with spirochetes, their degradation products, or both, these results suggest that infiltrating CD4+ and CD8+ T cells of any specificities, including spirochetes, autoantigens, or both, participate in the pathogenesis of Lyme disease.

Eur J Immunol. 1996 Oct;26(10):2299-303. Research Support, Non-U.S. Gov't





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