Extended reports
Rheumatoid arthritis: autoreactive T cells recognising a novel
68k autoantigen
a Department of
Medicine III, Rheumatology and Clinical Immunology, Charité
University Hospital, Humboldt University of Berlin, Germany
, b Institute of Haemostasis and
Transfusion Medicine , c Department of Rheumatology , d Institute for Genetics
, e Heinrich Heine University of
Düsseldorf, Germany
Correspondence to: Dr S Bläß, Immunologisch-Rheumatologisches Labor, Charité, Tucholskystr 2, D-10117 Berlin, Germany.
Accepted for publication 21 January 1997
OBJECTIVE
A 68k autoantigen has been identified
by specific antibodies from patients with rheumatoid arthritis (RA).
This study considered whether or not this antigen is a target for T
cells and thus may play a part in T cell mediated immunopathology of
active RA.
METHODSThe 68k antigen was isolated and used in
a nitrocellulose bound form to stimulate T cells. Proliferation of T
lymphocytes of peripheral blood as well as synovial fluid was measured.
RESULTSPeripheral blood T cells specifically
proliferating against the 68k antigen were detected in 19 of 27 patients with RA (70%). For T cells isolated from peripheral blood,
proliferation peaked on day 10. When T cells were isolated from
actively inflamed synovial fluid, the proliferation kinetics shifted to
a peak on day 3. Blockade of HLA class II antigens resulted in an
increase of proliferation in the case of HLA-DP. Applying HLA-DP
specific antibodies capable of inhibiting antigen presentation mediated
by this molecule, T cells of 17 of 27 RA patients (63%) proliferated
to a higher extent than with the 68k antigen alone. The phenomenon that
an increased proliferation occurred upon blockade of a particular HLA
class II family member was also demonstrated for DQ and DR: the 68k
antigen likewise stimulated T cells restricted for DP or DQ, respectively.
CONCLUSIONSThe novel 68k antigen is a target of
both T and B cellular immune responses and as such could play a part in
the immune dysfunction of RA. The finding that blocking of certain HLA
class II molecules functioning in antigen presentation (for example,
via HLA-DQ) results in a higher instead of lower proliferation in
vitro, may argue for the presence of antigen specific suppressive T cells.
© 1997 by Annals of the Rheumatic Diseases
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