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T Cells Respond to Borrelia burgdorferi Lipoproteins and Lipidated Hexapeptides1
,
*
Divisions of Immunobiology and Rheumatology, Department of Medicine, University of Vermont College of Medicine, Burlington, VT 05405; Departments of
Internal Medicine and
Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75235;
§
Department of Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, NJ 08903; and
¶
Lymphocyte Biology Section, Division of Rheumatology and Immunology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115
Lyme arthritis synovial fluid contains a large proportion of 
T cells that proliferates upon stimulation with the causative
spirochete, Borrelia burgdorferi. A panel of
Borrelia-reactive T cell clones was derived from
synovial fluid of two patients with Lyme arthritis. Each of six
clones from one patient used the V1 TCR segment but had otherwise
unique CDR3 sequences and diverse V segment usage. Stimulation of
the V1 clones was optimal in the presence of
Borrelia, dendritic cells, and exogenous IL-2, which was
reflected by proliferation, TCR down-modulation, as well as induction
of CD25 and Fas ligand expression. Stimulation by B.
burgdorferi-pulsed dendritic cells withstood chemical fixation
and was not restricted to class I or class II MHC, CD1a, CD1b, or CD1c.
In contrast, anti- antibody potently inhibited proliferation.
Extraction of B. burgdorferi lipoproteins with Triton
X-114 enriched for the stimulatory component. This was confirmed using
lipidated vs nonlipidated hexapeptides of Borrelia outer
surface proteins. These observations suggest that synovial V1 T
cells may mediate an innate immune response to common lipoprotein
products of spirochetes.
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