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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental model of human chronic inflammatory arthritis, adjuvant arthritis may be induced only in several strains of inbred Rats: it is well developed in LEW and practically absent in WAG. After adjuvant injection, the PHA-stimulable lymphocytes subpopulation quite disappears from the blood, if polyarthritis is well developed. These cells are probably capted in the tissues implicated in immunological conflict. On the contrary, the ConA-stimulable subpopulation is enhanced in both strains after adjuvant injection, earlier and more intense in WAG than in LEW and that phenomenon is probably linked to a stimulation of suppressor T lymphocytes. Treatment with prednisone or gamma rays inhibits partially and delays the appearance of arthritis in LEW, acting essentially on ConA-stimulable subpopulation.
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PMID:[Lymphocyte subpopulations in adjuvant arthritis of rats. Effects of corticoids and gamma irradiation]. 9 95

Evaluation of lymphocyte response has been undertaken in adjuvant-induced arthritis in rats. Lymphocyte reactivity was studied by evaluating lymphocyte transformation in mixed lymphocyte-chondrocyte cultures as well as the response to PHA and M. tuberculosis. It was found that animals immunized with Freund's complete adjuvant showed increased transformation when challenged with M. tuberculosis powder. However, there was a depressed response to PHA and a markedly depressed response in mixed lymphocyte-chondrocyte cultures.
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PMID:Altered lymphocyte response in adjuvant-induced arthritis. 11 49

Knee joint arthritis is induced among rabbits previously immunized by intradermal injection with egg albumin (EA) emulsified in adjuvant containing either M. tuberculosis or M. butyricum, then by intra-articular injection with EA. Arthritis evolution involves two phases, an early one during the first 2 months and a late one from 3 months to 1 year. During the early phase, arthritis intensities are similar no matter which Mycobacterium is used. However, during the late phase, only rabbits immunized with M. tuberculosis develop self-perpetuating arthritis. Among more than 50% of arthritic rabbits, immunological lesions of aortic artery and cardiac valvules are found. Among the rabbits immunized with M. tuberculosis, the humoral anti-EA antibody level remains constant during the whole arthritis evolution; but, among the rabbits immunized with M. butyricum, the arthritis intensity decreases from 3 months of evolution. The correlation between arthritis index (AI) and humoral antibody level is only significant among the rabbits with early arthritis. The intradermally immunized rabbits show a positive skin test with EA and tuberculin. The more intense the cutaneous reactions, the greater the chances of developing self-perpetuating arthritis after the EA intra-articular injection. The fluorescent anit-EA antibodies in the synovia and spleen are found only among the early arthritis. After 2 months of evolution, fluorescent antibodies disappear whatever the immunization may be. Among the immunized rabbits, it is probable that antigenic EA does not persist in the synovia. Indeed, the autologous inflamed synovia transplantation, from the donor-challenged knee joint, does not develop an inflammatory reaction in the non-challenged knee joint. The fluorescent immunoglobulins IgG and IgM in the synovium of arthritic rabbits are found with the same percentages as fluorescent anti-EA antibodies. The lymphocyte response to EA, PHA and PWM are positive whatever the immunization and arthritis evolution may be. There is no correlation between AIs and lymphocyte responses to specific and nonspecific mitogens. It is probable that self-perpetuation depends closely on M. tuberculosis whose adjuvant power is much superior than M. butyricum and not on antigenic EA whose essential role would be to trigger the inflammatory process.
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PMID:Physiopathological aspect of Glynn's type of experimental arthritis. 12 12

A naturally occurring T-lymphocytotoxic autoantibody (Hu-NTA) in serum from a patient with systemic lupus erythematosus (SLE) showed a differential cytotoxic effect on functionally different T cell subsets as did natural thymocytotoxic autoantibody (NTA) of NZB mice. When the normal peripheral blood lymphocytes were treated, in the presence of complement, with Hu-NTA at a dilution that eliminated 25 to 30% of Hu-NTA-sensitive T cells, there was a marked reduction or a total depletion in the ability of resultant cells to show Con A-activated suppression on the proliferative response of responder cells in mixed lymphocyte reaction. The treatment of PBL in the same manner also resulted in a marked reduction in its responsiveness to Con A and PHA. However, the responder cells to allogeneic stimulator cells in MLR were found to be much more resistant to the cytotoxicity of Hu-NTA than other functional T cell subsets tested. These results suggest that Hu-NTA is responsible for the selective loss of certain functional T cell subsets including suppressor T cells in patients with SLE.
Arthritis Rheum 1979 Feb
PMID:Differential sensitivity of functional subsets of T cells to the cytotoxicity of natural T-lymphocytotoxic autoantibody of systemic lupus erythematosus. 15 30

Administration of thymosin fraction V to NZB/NZW F1 mice, an animal model for human SLE, accelerated the appearance of proteinuria and anti-nDNA antibodies, increased deposition of immunoglobulins in kidneys, and significantly shortened survivals. Although the addition of thymosin to in vitro cultures of spleen and lymph node cells from thymosin-treated mice increased DNA synthesis in response to stimulation with Con A, in vivo treatment with thymosin did not affect the Con A response. There was no effect on in vitro responses to PHA or LPS, or on IgM antibody formation to SRBC (T cell dependent) or SSS III (T cell independent) immunizations. Antibodies to thymosin or contamination of our thymosin preparations with nucleic acids could not be demonstrated. The acceleration of autoimmune disease produced by thymosin treatment could not be explained by alteration of the T and B cell functions studied.
Arthritis Rheum 1978 Mar
PMID:Effect of altered lymphocyte function on immunologic disorders in NZB/NZW mice. III. Acceleration of disease by thymosin. 30 81

The mechanism of poor lymphocyte transformation to mitogens was studied in selected patients with rheumatoid arthritis and systemic lupus erythematosus. Low lymphocyte response to PHA and Con-A in media containing autologous and homologous sera was usually associated with poor response to the calcium ionophore A23187, which induces blastogenesis by a different mechanism. The low lymphocyte response to mitogens in patients with rheumatoid arthritis could be restored by in vivo treatment with the anthelmintic drug, levamisole. The present findings suggest that intrinsic defects are responsible for the decreased cellular response in patients with rheumatoid arthritis and systemic lupus erythematosus.
Arthritis Rheum 1978 Apr
PMID:Decreased lymphocyte response to PHA, Con-A, and calcium ionophore (A23187) in patients with RA and SLE, and reversal with levamisole in rheumatoid arthritis. 34 4

The lymphoblastic response (LTT) to non-specific mitogens (PHA, PWM and ConA) of peripheral lymphocytes was investigated at days 0, 7, 14, 21 and 28 after adjuvant injection in four strains of inbred rats: Wistar (WAG), Long Evans (LE), Lewis (LEW) and Brown Norway (BN). LTT was assessed by using 18 hours H3 TdR incorporation in 5 days cultures of whole blood (micromethod). The statistical treatment of data, using principal components multifactorial analysis and analysis of variance showed a striking difference between strains. In control animals the responses to PHA and PWM were correlated and were higher in LE and WAG than in LEW and BN (BN=LEW less than LE=WAG). The response to ConA was independent of that to the other mitogens. It was generally low, but significantly higher in LEW and BN than in WAG and LE. In adjuvant-injected animals the responses to PHA and PWM were still correlated, but modified compared to control: in LE and LEW, but not in WAG and BN, a marked decrease of the response was found, reaching a minimum value within days 7 and 14. In the same time the response to ConA increased in the four strains, later in LE than in the others. However the intensity of the ConA response varied from one strain to another: it was constantly low in LE and WAG compared to LEW and BN. So the most striking modification of LTT were observed in LE and LEW, which both developed the most severe arthritis. However these different behaviours after adjuvant injection were not explained by the initial level of LTT to the different mitogens. These data suggest that the development of intense arthritis is associated with the proliferation and the release into the blood stream of a lymphocyte subpopulation, which exhibits a low response to PHA and PWM and a high response to ConA. These LTT modifications are not paralleled by quantitative variations of B-cells assessed by surface Ig immunofluorescent staining and EAC rosetting.
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PMID:Adjuvant-induced arthritis in four inbred strains of rats. An in vitro study of peripheral T and B lymphocytes. 108 95

For each of 28 patients with RA and 27 normal controls, the in vitro lymphocyte responses to PHA and to Con A were simultaneously determined on aliquots of the same cell preparation. In the case of RA lymphocytes, the response to Con A was abnormally low when compared with the simultaneous response to PHA (P less than 0.01). Cells capable of responding to PHA were specifically killed with BUdR. The cells remaining after this procedure showed a relatively greater response to Con A than did the original population. In the case of RA lymphocytes, this relative increase in the response to Con A was significantly less than normal (0.02 greater than P greater than 0.01). These results suggest that a lymphocyte subpopulation, responding principally to Con A, is relatively reduced in RA.
Arthritis Rheum
PMID:Lymphocyte populations in rheumatoid arthritis. 108 49

Lymphocyte responses to the mitogens phytohemagglutinin P(PHA-P), concanavallin A (Con A), and pokeweed (PWM) were studied in 18 patients with progressive systemic sclerosis (PSS). A subgroup of these patients with multisystem involvement showed a significantly decreased lymphocyte response to both Con A and PWM when compared to normal controls. However those PSS patients with myositis, although having multisystem involvement, had normal lymphocyte response to all three mitogens. PHA-P stumulation was normal in all PSS patients. Antinuclear antibodies, elevated sedimentation rates, and positive latex fixation were noted only in the multisystem disease group with abnormal lymphocyte function.
Arthritis Rheum
PMID:Lymphocyte response to mitogens in progressive systemic sclerosis. 108 28

Cellular-mediated immunity was examined in 6 consecutive patients with active SLE, 6 patients with low active SLE 6 patients with DLE, 8 patients with other collagen diseases, and 9 healthy controls. The following parameters were measured: delayed hypersensitivity, in vitro lymphocyte blast transformation, and MIF production after stimulation with five common antigens, DNA, and two nonspecific mitogens (PHA, PWM). The 6 active SLE patients were anergic and had a markedly depressed response in vitro to the specific antigens and PWM (P less than 0.001). When CMI was retested in 5 patients as early as 5 days after the start of prednisone (60 mc/day), the results were significantly improved in 4 who also improved clinically, and they remained unchanged in a fifth patieht who failed to improve. There was a less marked impairment of CMI among the low active SLE group, whereas the DLE and OCD patients did not differ significantly from the control subjects. DNA did not cause significant stimulation of blast transformation in any of the study groups.
Arthritis Rheum
PMID:Depression of cellular-mediated immunity in systemic lupus erythematosus. relation to disease activity. 109 20


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