Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report three cases of arthritis occurring after treatment with BCG immunotherapy for bladder disease. This complication is observed in 0.5 to 1% of treated patients and affects the small joints within 1 to 5 months of the first BCG injection. The clinical outcome is favourable with non-steroidal antiinflammatory drugs. This form of arthritis may be attributable to a cross-reaction between antigenic components of cartilaginous proteoglycan and BCG, influenced by a particular HLA-DR pattern, and with the intervention of a heat shock protein.
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PMID:Three cases of arthritis after BCG therapy for bladder cancer. 803 89

Immunization of Lewis rats with heat-killed Mycobacterium tuberculosis (Mt) in mineral oil induces adjuvant arthritis (AA), associated with T cell responses to residues 180-188 of the mycobacterial 65-kDa heat shock protein (hsp65). Preimmunization with hsp65 protects rats against AA and other forms of arthritis. Several explanations for these protective effects have been proposed, including enhanced responsiveness to protective epitopes in hsp65, down-regulation of T cell responses to the 180-188 epitope, and activation of self-hsp60-reactive T cells. To assess the potential of these hypotheses, we analyzed hsp65 T cell epitopes recognized after immunization of Lewis rats with Mt or hsp65. Here we identify nine RT1.B1-restricted T cell epitopes in hsp65. Mt immunization induced T cell responses in which the 180-188 epitope was dominant, whereas hsp65 immunization resulted in a co-dominance of this and two further epitopes, 216-225 and 226-235. Two minor epitopes were recognized after hsp65 but not Mt immunization. These results indicate that hsp65 preimmunization does not down-regulate responses to the AA-associated epitope, but does enhance responses to several hsp65 epitopes that are minor or absent after the AA-inducing immunization protocol. Cross-reactive T cell recognition of hsp65 and rat hsp60 was limited to a single epitope (256-265), recognized after hsp65 immunization, but poorly recognized after Mt immunization. This study provides the necessary basis for elucidating the T cell events involved in the protective effects of hsp65 preimmunization.
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PMID:Differential mycobacterial 65-kDa heat shock protein T cell epitope recognition after adjuvant arthritis-inducing or protective immunization protocols. 814 41

Adjuvant arthritis (AA) and type II collagen (CII)-induced arthritis (CIA) in the rat serve as models of chronic human arthritis. Adoptive transfer of AA was observed in 21 of 25 Lewis rats given concanavalin A (Con A)-treated spleen cells prepared from animals immunized with Mycobacterium butyricum in mineral oil (complete Freund's adjuvant, CFA). No arthritic changes were noted in rats given spleen cells obtained from donors that had received incomplete Freund's adjuvant (IFA, 0/22), type I collagen in IFA (CI-IFA, 0/6) or CII-IFA (0/28). Administration of spleen cells from IFA, CI-IFA or CII-IFA-injected animals did not modify the development of CIA when these rats were subsequently challenged with CII-IFA. However, partial protection against induction of AA was provided by the transfer of spleen cells prepared from rats immunized with CII-IFA (6/11) but not by those obtained from rats injected with IFA (1/15) or CI-IFA (0/3). Rats that did not develop clinically evident arthritis following the administration of spleen cells prepared from CFA-injected rats were also resistant to AA induction by CFA. Pre-treatment of rats with a synthetic peptide, corresponding to amino acids 180-188 of the Mycobacterium 65 kD heat shock protein (65 kD HSP), significantly delayed the onset of AA, but not that of CIA. Disease-specific resistance to AA, provided by spleen cells prepared from rats injected with CII-IFA and by pre-treatment with the 65 kD HSP 180-188 peptide, may result from the induction of protective tolerance to arthritogenic epitopes present in the Mycobacterium and CII preparations.
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PMID:Relationship between collagen-induced and adjuvant arthritis in the Lewis rat. 815 51

The IgG of patients with rheumatoid arthritis and mice with pristane induced arthritis (PIA) tends to lack the terminal galactose normally on the conserved N-acetylglucosamine linked beta 1-2 to mannose in IgG. The terminal N-acetylglucosamine (GlcNAc) residues of oligosaccharides on agalactosyl IgG may be an important component of the action of these glycoforms. Here, administration of ovomucoid, a glycoprotein rich in terminal GlcNAc, before pristane injection was found to reduce the incidence of PIA. This observation is the second report of an intraperitoneally administered antigen that reduces the incidence of PIA, mycobacterial 65-kD heat shock protein (hsp65) being the first. The suppressive effect of ovomucoid was not transferred from protected to naive recipients by spleen cells at the dose tested. By contrast, transfer of spleen cells from hsp65-protected mice to naive recipients conferred protection and this protection may be antibody-mediated. It is considered that ovomucoid and hsp65 protect against the development of PIA by different mechanisms.
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PMID:Comparison between the protective effects of mycobacterial 65-kD heat shock protein and ovomucoid in pristane-induced arthritis: relationship with agalactosyl IgG. 822 14

The 60-kD heat shock protein (hsp60) has been implicated in the etiology and pathogenesis of both experimental and naturally occurring autoimmune diseases such as juvenile chronic arthritis (JCA). Human hsp60 is expressed in inflamed synovial tissue, and T lymphocytes both from peripheral blood and synovial fluid show reactivity to human hsp60. Because the anti-hsp60 B lymphocyte response has been less well studied, we have determined the occurrence of IgG anti-human hsp60 antibodies in patients with JCA and various other autoimmune diseases of childhood. Serum IgG anti-human hsp60 antibodies in JCA patients were significantly higher compared with control children (358 and 163 U/mL, respectively). Within the group of JCA patients, the highest antibody titers were found in the subgroup with a polyarticular onset of JCA. IgG anti-human hsp60 antibody levels in synovial fluid were 3- to 4-fold higher compared with paired serum samples. Because this difference was not found for total IgG or for irrelevant antibodies (anti-polyribosylribitol phosphate), this suggests local anti-hsp60 antibody production in the synovial compartment. The occurrence of anti-hsp60 antibodies is not specific for JCA but also is found in children with systemic lupus erythematosus and in cystic fibrosis, whereas mixed connective tissue disease and insulin-dependent diabetes are negative in this respect. Whether the anti-human hsp60 antibodies are directed toward species-specific sequences or to conserved sequences of the hsp60 molecule remains to be determined.
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PMID:Antibodies to human HSP60 in patients with juvenile chronic arthritis, diabetes mellitus, and cystic fibrosis. 825 71

Synovial fluid and peripheral blood mononuclear cells from juvenile chronic arthritis (JCA) patients have previously been shown to exhibit substantial proliferative responses to both human and mycobacterial heat shock protein (hsp) 65. We investigated the nature of the antibody response to mycobacterial and E. coli hsp 65 and human and E. coli hsp 70 in 56 JCA patients using an ELISA. Elevated levels of antibodies to both human and E. coli hsp 70 were demonstrated. With hsp 65, raised levels of antibodies to the mycobacterial but not the E. coli protein were detected. Overall, 48% of patient serum samples contained antibodies of at least one isotype to mycobacterial hsp 65. These antibodies were predominantly of IgG and IgM isotype, a finding in contrast to adult rheumatoid arthritis, where IgA and IgG isotypes are most often detected.
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PMID:Antibody response of restricted isotype to heat shock proteins in juvenile chronic arthritis. 832 62

We have recently reported antigenic (B-cell) cross-reactivity between the mycobacterial 65 kDa heat shock protein (hsp65) and human lactoferrin (LF) and we suggested that this cross-reactivity might have a role in mycobacteria-associated autoimmune disease. Here, we have searched for anti-LF T-cell reactivity in Lewis rats submitted to a mycobacteria-triggered autoaggressive disorder (adjuvant arthritis, AA), an autoimmune disorder characterized by high anti-hsp65 reactivity. We have quantified the in vitro proliferative response to LF of lymph node and spleen cells of Lewis rats killed 9, 14 and 21 days after the immunization with the AA-triggering, mycobacteria-containing adjuvant (complete Freund's adjuvant, CFA). We found that LF induced significant proliferation of lymph node T cells of rats undergoing AA. This T-cell proliferation was not as marked as the one provoked by hsp65; it was, nevertheless, significantly higher (P < 0.05) than that produced by a non-arthritogenic antigen (i.e. albumin). T cells from naive or mineral oil (incomplete Freund's adjuvant, IFA) injected rats did not respond to LF or hsp65. These data indicate that LF may work as an accessory stimulatory factor of the T-cell autoreactivity associated with mycobacteria-induced arthritis.
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PMID:Lactoferrin triggers in vitro proliferation of T cells of Lewis rats submitted to mycobacteria-induced adjuvant arthritis. 834 15

Pristane-induced arthritis (PIA) is unique among the animal arthritides in that a non-infectious, non-antigenic oil induces a chronic immune based arthritis with a prolonged delay between exposure to the inciting agent and development of the disease. Mice with pristane-induced arthritis have elevated T cell and humoral responses to the 65 kDa heat shock protein derived from Mycobacterium bovis (hsp65) and in common with several other models of autoimmune diseases the incidence of PIA is markedly suppressed by preimmunisation with hsp65 in Freund's incomplete adjuvant (Thompson et al. (1990) Eur. J. Immunol. 20, 2479). Recent studies have investigated how autoimmune reactions to heat shock proteins are involved in the development of arthritis. Arthritic CBA/Igb mice given pristane alone develop antibodies to both hsp65 and GroEl (bacterial 60 kDa heat shock proteins) and to hsp58 (the mammalian equivalent). Moreover, the splenic T cells of such mice proliferate vigorously in response to both bacterial and mammalian 60 kDa heat shock proteins. Remarkably, the anti-hsp65 antibody response in normal mice rises rapidly with age, directly correlating with the age related incidence of PIA. In addition, specific pathogen free mice (SPF) maintained in an isolator have negligible anti-hsp65 responses but these convert to positive responses if the animals are exposed to the open part of the animal facility (Thompson et al. (1992) Arthritis Rheum. 35, 139).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Susceptibility to pristane-induced arthritis is altered with changes in bowel flora. 834 17

The immune response to the mycobacterial 65-kDa heat shock protein (hsp65) is considered an important event in the induction of adjuvant arthritis (AA) in rats; this induction probably occurs through a molecular mimicry mechanism involving cross-reactivity against the rat homolog hsp60. To analyze the role of mammalian molecule hsp60 in arthritis, we generated a recombinant vaccinia virus (hsp60-VV) carrying the human hsp60 gene inserted into the thymidine kinase locus under the control of the 7.5k vaccinia virus promoter. Human hsp60 is almost identical to its rat homolog (97.4% linear amino acid homology) and shares about 50% of amino acid positions with Mycobacterium tuberculosis hsp65. The latter supposedly carries a critical epitope for AA induction that is not present in human hsp60. Infections with hsp60-VV of monkey cell cultures led to the expression of the human hsp60 molecule, as evidenced by immunoblotting analysis with specific monoclonal antibodies. Also, Lewis rats infected with hsp60-VV produced specific antibodies, demonstrating the in vivo expression of human hsp60 in the infected animals. Therefore, we used hsp60-VV to analyze whether the delivery of hsp60 could affect the induction of AA in Lewis rats. hsp60-VV clearly reduced and retarded arthritic symptoms when administered to rats at day 7 after AA induction. In contrast, inoculation of rats with a control recombinant vaccinia virus did not affect the course of the disease. The improvement in AA with hsp60-VV administration was associated with a specific immune response, as determined by the presence of antibodies to hsp60 in the sera and the proliferation induced by hsp60 of T cells from popliteal lymph nodes. These results support a critical role for immunity to heat shock proteins in AA. Since the protective construct is virtually identical to rat homolog hsp60, we conclude that immunity directed to conserved areas of this family of proteins is directly involved in the pathogenesis of AA.
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PMID:Modulation of adjuvant arthritis in Lewis rats by recombinant vaccinia virus expressing the human 60-kilodalton heat shock protein. 840 10

An association of microbial agents and autoimmunity has been suggested for the pathogenesis of psoriasis. Mycobacteria are common environmental microbes and their antigens, especially the highly conserved mycobacterial 65-kDa heat shock protein (hps65), have been implicated in the pathogenesis of autoimmune arthritis and other idiopathic diseases. In this context, we investigated a possible mycobacterium-induced humoral immune response in psoriasis. Sera from 17 patients with chronic plaque-type psoriasis were studied by immunoblotting using the whole sonicate of Mycobacterium tuberculosis and purified recombinant mycobacterial hsp65. Immunoblot analysis demonstrated that 58% of the psoriasis patients compared to patients with acne and DLE, and normal controls showed strong antibody activity to 65-kDa and 48/45 doublet antigens from M. tuberculosis sonicate, whereas 47% of the patients showed antibody activity to mycobacterial hsp65. Only 10-20% of the patients had an antibody response to 16-kDa and 80-kDa antigens. Similar antibody activity to 65 kDa and 48/45 kDa was also found consistently with eight different sonicated mycobacterial species by immunoblotting, indicating that these seroreactive antigens are crossreactive and are present in common environmental mycobacteria. Antibody activities to both mycobacterial 65-kDa and hsp65 showed a positive correlation (r = 0.76) with the psoriasis disease activity, whereas antibodies to 48/45-kDa doublet antigens showed a weak correlation (r = 0.54). By enzyme-linked immunosorbent assay (ELISA), 47% of the psoriasis patients showed significantly elevated antibody titers to hsp65 (p < 0.003) as compared to control groups, and the antibody response by ELISA also showed a significant positive correlation (r = 0.76) with disease activity. Anti-mycobacterial antibody activity may be related to severity of disease and may be useful in monitoring disease activity in psoriasis.
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PMID:Antibodies to mycobacterial 65-kDa heat shock protein and other immunodominant antigens in patients with psoriasis. 842 5


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