Extended reports
Absence of peripheral blood T cell responses to `shared
epitope' containing peptides in recent onset rheumatoid arthritis
a The Walter and Eliza Hall Institute of Medical
Research, Melbourne, Australia , b Roche Milano Ricerche, Milan, Italy
Correspondence to: Dr G J McColl, Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital PO, Parkville, Victoria 3050, Australia.
Accepted for publication 21 January 1997
OBJECTIVES
To determine if peptides containing
the `shared epitope' sequence, QKRAA, from either endogenous,
HLA-DR
1(0401), or exogenous, Escherichia coli dnaJ,
sources activate T cells in recent onset rheumatoid arthritis (RA).
METHODSPeripheral blood mononuclear cell (PBMC)
proliferative and whole blood cytokine responses to shared epitope
containing peptides from DR1(0401) and E coli dnaJ, to
control peptides from DR1(0402) and hsp40 and to the recall antigen,
tetanus toxoid, were tested in 20 untreated, recent onset RA subjects,
20 HLA, age, and sex matched healthy controls and 18 other subjects
with inflammatory arthritis. PBMC proliferative responses to a second
E coli dnaJ peptide (with the shared epitope at the
N-terminus) and two peptides from type II collagen with high affinity
for DR4(0401) were tested in a further 16 recent onset RA and 17 control subjects.
RESULTSPBMC proliferation and whole blood
interferon 
or interleukin 10 production in response to the shared
epitope containing and control peptides were not different between the
disease and control groups. On the other hand, compared with controls,
RA subjects had significantly higher proliferation to a collagen II (aa
1307-1319) peptide, but significantly lower proliferation and
interferon production to tetanus toxoid.
CONCLUSIONRecent onset RA subjects had no
demonstrable increase in peripheral blood T cell reactivity to shared
epitope containing peptides. However, a proportion had increased T cell
reactivity to a peptide of similar length from a candidate RA
autoantigen, collagen type II. Their impaired responses to tetanus are
in keeping with evidence for general T cell hyporesponsiveness in RA.
© 1997 by Annals of the Rheumatic Diseases
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