T cell responses to human type II collagen in patients with rheumatoid arthritis and healthy controls

Snowden, Neil; Reynolds, I.; Morgan, K; Holt, Lennox

doi:10.1002/1529-0131(199707)40:7<1210::aid-art4>3.0.co;2-t

Cited by 40 publications

(25 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our culture conditions were different from those in previous studies in terms of the dose of antigen and the number of antigen-presenting cells (17,32). This result supports the recent report that the response of PBMC to purified protein derivative (PPD) and tetanus toxoid did not differ significantly between healthy controls and patients with early RA or late RA (31).…”

supporting

confidence: 79%

Shift toward T helper 1 cytokines by type II collagen–reactive T cells in patients with rheumatoid arthritis

Park

Min

Cho

et al. 2001

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. To investigate the impact of type II collagen (CII)-reactive T cells on the Th1/Th2 cytokine balance in patients with rheumatoid arthritis (RA).Methods. T cell proliferative responses to bovine CII were examined in synovial fluid mononuclear cells (SFMC) and peripheral blood mononuclear cells (PBMC) by mixed lymphocyte culture. CII-reactive T cell lines were generated from the SFMC and PBMC. Interferon-␥ (IFN␥), interleukin-12 (IL-12), and IL-4 were measured by enzyme-linked immunosorbent assay in the SF, sera, and culture supernatants of PBMC and SFMC that had been stimulated with CII.Results. The frequency of CII-reactive T cells was higher in the PBMC from RA patients than in that from osteoarthritis patients and healthy control subjects. In RA patients, CII-reactive T cells were more prevalent in SFMC than in PBMC. The mean level of IFN␥ and the ratio of IFN␥ to IL-4 were significantly higher in the culture supernatants of T cells stimulated with CII; these differences were more prominent in SFMC. Levels of IL-12 in the culture supernatants of SFMC and PBMC stimulated with CII were significantly higher than those in unstimulated supernatants. T cell responsiveness correlated well with the level of type 1 cytokines in culture supernatants from RA T cells stimulated with

show abstract

supporting

confidence: 79%

Shift toward T helper 1 cytokines by type II collagen–reactive T cells in patients with rheumatoid arthritis

Park

Min

Cho

et al. 2001

Arthritis & Rheumatism

View full text Add to dashboard Cite

show abstract

“…Against this deduction, a substantial proportion of RA patients did not have PBMC which responded to IgG. However, T cells from RA patients respond more frequently than those from normal individuals to other joint antigens including type II collagen 19 and peptides corresponding to the sequence of cartilage glycoprotein 39 16 . It may therefore be that T cells reactive with different joint antigens can trigger the same or similar final common pathways.…”

Section: Discussionmentioning

confidence: 99%

“…Despite these results, the majority of RA patients do not appear to harbour type II collagen reactive T cells 17 . T cells from RA patients respond rarely to human hsp 60 18 , 19 and PBMC from many RA individuals fail to respond to cartilage glycoprotein peptides 16 . It could be argued therefore either that RA is neither initiated nor perpetuated by T cells reacting with joint antigens or that other antigens remain to be identified.…”

Section: Introductionmentioning

confidence: 98%

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

et al. 1999

View full text Add to dashboard Cite

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.

show abstract

“…The involvement of CII in RA has, however, had a rather chequered history. Although there is now general consensus that humoral immunity to CII is associated with RA, it has been much more difficult to establish a direct role for CII-reactive T cells in the pathogenesis of RA (for example, see [4,5]). Moreover, treatment of RA patients with oral CII has not been as successful as expected on the basis of results obtained from similar trials in collagen-induced arthritis in animals [6].…”

Section: Full Textmentioning

confidence: 99%

Untitled

Fugger

2000

Arthritis Res

View full text Add to dashboard Cite

show abstract

T cell responses to human type II collagen in patients with rheumatoid arthritis and healthy controls

Cited by 40 publications

References 42 publications

Shift toward T helper 1 cytokines by type II collagen–reactive T cells in patients with rheumatoid arthritis

Shift toward T helper 1 cytokines by type II collagen–reactive T cells in patients with rheumatoid arthritis

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

Untitled

Contact Info

Product

Resources

About