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Divisions of
*
Dermatology and
Rheumatology, University of California School of Medicine, Los Angeles, CA 90095;
Division of Rheumatology, Immunology and Allergy, Brigham and Women’s Hospital, Boston, MA 02115;
§
Harvard School of Public Health, Boston, MA 02115; and
¶
Division of Rheumatology, Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461
To understand the mechanism of T cell help for IgG production in
systemic lupus erythematosus (SLE) we investigated the response of CD4-
and CD8-negative (double-negative (DN)) T cells because 1) DN T cells
are present at unusually high frequency in patients with SLE and can
induce pathogenic autoantibodies; 2) the DN T cell repertoire includes
cells restricted by CD1 Ag-presenting molecules; and 3) CD1c is
expressed on a population of circulating B cells. We derived DN T cell
lines from SLE patients and healthy individuals. In the presence of
CD1+ APCs, DN T cell lines from SLE patients produced both
IL-4 and IFN-
, whereas DN T cells from healthy donors produced
IFN-, but no IL-4. In general, cells from patients with highly
active disease produced high levels of IFN-; cells from those with
little activity produced high IL-4. Coculture of CD1c-directly reactive
T cells from healthy donors with CD1c+ B cells elicited IgM
Abs, but little or no IgG. In contrast, CD1c-directly reactive T cells
from SLE patients induced isotype switching, with a striking increase
in IgG production. Neutralizing Abs to CD1c inhibited the ability of DN
T cells to induce IgG production from CD1c+ B cells,
further indicating that CD1c mediated the T and B cell interaction. IgG
production was also inhibited by neutralizing Abs to IL-4, correlating
with the cytokine pattern of DN T cells derived from these patients.
The data suggest that CD1c-restricted T cells from SLE patients can
provide help to CD1c+ B cells for IgG production and could
therefore promote pathogenic autoantibody responses in
SLE.
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