Cellular Immunity in Rheumatic Diseases I. Rheumatoid Arthritis

Waxman, Jack; Lockshin, Michael D.; Schnapp, Jerome J.; Doneson, Ira N.

doi:10.1002/art.1780160410

Cited by 53 publications

(24 citation statements)

References 15 publications

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“…The decreased proliferative response of peripheral blood lymphocytes from RA patients to virus antigens which was demonstrated in the present study extends previous reports of diminished cellular immunity in RA (19)(20)(21)(22)(23)(24)28). Significantly fewer RA patients than controls responded to measles, rubella, and parainfluenza types 2 and 3 antigens, and the magnitude of response was significantly lower to rubella and parainfluenza types 1,2, and 3.…”

Section: 1 2 3 4 5 6supporting

confidence: 87%

“…In one study (12) R A synovial cells were observed to be less susceptible than other synovial cells to growth of rubella, a finding that suggests prior virus infection, but others (9.13.14) have not confirmed that observation. Although the studies mentioned here suggest a possible role for viruses in the pathogenesis of RA, numerous attempts to culture viruses from various tissues and fluids from R A patients have been unsuccessful Diminution of cell-mediated immunity in R A has been indicated by decreased responses in vitro to plant mitogens (19)(20)(21) and in vivo to skin test antigens (22,23) and by low levels of circulating thymus-dependent (T) lymphocytes (24) although conflicting results have been reported (25-27). A recent study (28) demonstrated a correlation between decreased response to mitogens and erosive R A , indicating an association with more advanced disease which could explain the varied results among studies from different laboratories.…”

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confidence: 99%

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Hyporesponsiveness of lymphocytes to virus antigens in rheumatoid arthritis

Wolf

1978

Arthritis & Rheumatism

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The immune response of peripheral blood lymphocytes to measles, rubella, parainfluenza types I , 2, and 3 RNA virus antigens, and to varicella-zoster and herpes virus type 1 DNA virus antigens was evaluated in 14 patients with rheumatoid arthritis (RA) and 14 matched controls by assessing SH-thymidine incorporation. The results demonstrated hyporesponsivenss of lymphocytes from RA patients to virus antigens and phytohemagglutinin (PHA), which did not appear to be nonspecific because of a lack of correlation between response to virus antigens and response to mitogens. The pattern of decreased responsiveness was suggestive of a relative restriction of hyporesponsiveness to RNA virus antigens.A possible relationship between virus infection and rheumatoid arthritis (RA) has been considered on From the Dallas Veteran's Administration

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confidence: 87%

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confidence: 99%

Hyporesponsiveness of lymphocytes to virus antigens in rheumatoid arthritis

Wolf

1978

Arthritis & Rheumatism

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“…Several investigators have reported depressed skin reactivity to common antigens in RA patients (Wasz-H6ckert, 1951;Houba et al, 1964;Hayes et al, 1970;Bacon, 1970;Bitter, 1971;Waxman, et al, 1973;Toh et al, 1973), and Epstein and Jessar (1959) have reported a decreased capacity for sensitization in these patients. A correlation between anergy and long duration of disease has been reported (Waxman et a!., 1973), but whether there is any relation between skin reactivity and the course of the disease has not been determined. This study taking salicylates, indomethacin or paracetamol.…”

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confidence: 99%

Cell-mediated immunity in rheumatoid arthritis.

Andrianakos¹,

Sharp²,

Person³

et al. 1977

Annals of the Rheumatic Diseases

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SUMMARY Cell-mediated immunity in rheumatoid arthritis (RA) was assessed by skin testing with six antigens in 107 patients, 94 of whom were age, sex, and race-matched with healthy individuals or patients with diseases unrelated to immunological abnormalities. 20 % of RA patients were anergic. Impaired cell-mediated immunity in the RA patients was manifested by a decrease in the magnitude of skin reactivity as well as a decrease in the incidence of positive reactions to multiple antigens. Depression in cell-mediated immunity was related to age but not to sex, duration of disease, or dise4se activity. A slight correlation was found between absolute peripheral lymphocyte counts and the number of positive skin tests, and was confirmed by finding an association between lymphocyte counts and the size of skin reactions. A correlation was also found between lymphocyte counts and disease activity.Four explanations of the observed depression in cell-mediated immunity in RA were considered: (1) a preoccupation of the immune mechanism of the host with cell-mediated immunity reactions related to the pathogenesis of the disease; (2) a depression of cell-mediated immune reactivity by a virus infection; (3) depression of cell-mediated immunity by therapy; and (4) immune complex suppression of cell-mediated immunity. No effect of gold therapy was found. The near universal use of salicylates or other anti-inflammatory drugs did not permit investigation of the effect of these drugs on cell-mediated immunity.

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“…Both humoral and cellular immune mechanisms have been shown to be involved in this process (Pekin et al, 1964;Smiley et al, 1968;Winchester et al, 1969;Rodman et al, 1967;Bacon et al, 1973;Waxman et al, 1973;Rothenberger and Thiele, 1970;Clot et al, 1973). It is therefore to be expected that synovial effusions will contain material released during such events.…”

Section: Discussionmentioning

confidence: 99%

Suppression and Stimulation of Immunoglobulin Synthesis by Agents Present in Rheumatoid Synovial Effusions

Rosenthal

1976

Rheumatology

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SUMMARY Synovia! effusions from 14 patients with rheumatoid arthritis contain factors capable of enhancing and suppressing the production of immunoglobulin when added to normal peripheral lymphocyte cultures in vitro. Utilizing a radioactive immune coprecipitation technique it could be demonstrated that enhancement was observed upon addition of relatively small amounts of synovial fluid, while addition of higher amounts resulted in suppression of immunoglobulin synthesis. Nine of ten non-rheumatoid joint effusions showed neither enhancing nor suppressing activities. The possible relationship of these events to lymphokine production in the joint is discussed.THE participation of immune mechanisms in the pathogenesis of rheumatoid arthritis (RA) is well established (Pekin et al., 1964;Smiley et al, 1968;Winchester et al, 1969;Rodman et al., 1967). Recently, we described the presence in rheumatoid synovial effusions of enhancing factors capable of stimulating immunoglobulin synthesis in peripheral-blood lymphocyte cultures in vitro (Rosenthal et al., 1976). The factors described are a low-molecular factor which elutes from an Agarose A 5m column with serum albumin, presumably a lymphokine, and a high-molecular factor, which elutes from such a column with an IgM marker, presumably an immune complex. The lowmolecular factor is non-specific and stimulates immunoglobulin synthesis in both rheumatoid and normal lymphocyte cultures. The high-molecular factor showed specificity in its exclusive stimulation of rheumatoid cells. Recently, evidence has accumulated that in the collaboration between T-B cells and macrophages, T cells not only have an enhancing effect on antibody response, but also have a suppressive effect on antibody formation (Baker et al., 1973;Hardin et al, 1973;Dutton, 1973;Herzenberg et al., 1973; SjSberg, 1972). The experiments presented here were designed to investigate the possibility that not only a B-cell enhancing function, but also B-cell suppression function is mediated by soluble factors. Such B-cell inhibitory factors may be produced in vivo by the inflamed synovium in rheumatoid arthritis and be present in the synovial effusion. MATERIALS AND METHODSKnee-joint effusions from 14 patients with classical or definite rheumatoid arthritis (RA) as defined by the A.R.A. criteria (Ropes et al., 1959) and from 10 non-rheumatoid patients were obtained. The non-rheumatoid patients included six with osteoarthritis, two with ankylosing spondylitis, one with Reiter's syndrome and one with post-traumatic effusion.The effusions were immediately centrifuged at 2500 rev./min for 20 minutes at room temperature to remove cellular elements and the cell-free effusions treated with 0.02 mg of hyaluronidase/ml of joint fluid (bovine testes hyaluronidase, type I, Sigma Chem.

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Cellular Immunity in Rheumatic Diseases I. Rheumatoid Arthritis

Cited by 53 publications

References 15 publications

Hyporesponsiveness of lymphocytes to virus antigens in rheumatoid arthritis

Hyporesponsiveness of lymphocytes to virus antigens in rheumatoid arthritis

Cell-mediated immunity in rheumatoid arthritis.

Suppression and Stimulation of Immunoglobulin Synthesis by Agents Present in Rheumatoid Synovial Effusions

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