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Ability of T cells from patients with rheumatoid arthritis to respond to immunoglobulin G
Author(s) -
Allison K. Lang,
L M Macht,
John R. Kirwan,
David C. Wraith,
C. J. Elson
Publication year - 1999
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1999.00852.x
Subject(s) - peripheral blood mononuclear cell , immunology , rheumatoid arthritis , medicine , antibody , immunoglobulin g , rheumatoid factor , antigen , immunoglobulin e , stimulation , biology , in vitro , biochemistry
The ability of T cells from rheumatoid factor (RF)‐positive patients with rheumatoid arthritis (RA) to respond to immunoglobulin G (IgG) was assessed. Peripheral blood mononuclear cells (PBMC) from RA patients and normal individuals were cultured with and without human IgG or Mycobacterium tuberculosis‐ purified protein derivative (PPD) for 7 days and their proliferative response measured at intervals by their ability to take up tritiated thymidine. PBMC from 14/26 RA patients proliferated in response to IgG (taking a stimulation index of 3 or above as positive). The peak response varied between individuals but usually occurred on day 5, the same day, or 1 day later than the peak response to PPD. By contrast, PBMC from a significantly lower proportion (1/9) of normal individuals and patients with other arthritides (0/6) responded to IgG, although all responded to PPD. PBMC from 9/14 RA patients responded to Fab fragments of IgG but only 3/9 to the Fc fragment. Higher proliferative responses from RA PBMC were elicited by IgG aggregates than the original IgG preparation, but PMBC from 5/5 normal individuals and 5/6 patients with other arthritides failed to respond to the aggregates. The response to IgG was human leucocyte antigen (HLA)‐DR restricted and mediated by CD4 + T cells. It is considered that these results advance the hypothesis that IgG‐reactive T cells contribute to the initiation or perpetuation of RA.

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