Ability of T cells from patients with rheumatoid arthritis to respond to immunoglobulin G

The ability of T cells from rheumatoid factor (RF)-positive patients with r heumatoid arthritis (RA) to respond to immunoglobulin G (IgG) was assessed. Peripheral blood mononuclear cells (PBMC) from RA patients and normal indi viduals were cultured with and without human IgG or Mycobacterium tuberculo sis-purified protein derivative (PPD) for 7 days and their proliferative re sponse measured at intervals by their ability to take up tritiated thymidin e. PBMC from 14/26 RA patients proliferated in response to IgG (taking a st imulation index of 3 or above as positive). The peak response varied betwee n individuals but usually occurred on day 5, the same day, or 1 day later t han 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 pa tients responded to Fab fragments of IgG but only 3/9 to the Fc fragment. H igher proliferative responses from RE 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. T he response to IgG was human leucocyte antigen (HLA)-DR restricted and medi ated by CD4(+) T cells. It is considered that these results advance the hyp othesis that IgG-reactive T cells contribute to the initiation or perpetuat ion of RA.