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)

We investigated the effect of HLA-DQw6 genes on collagen-induced arthritis (CIA) in mice, based on our previous observation that the frequency of HLA-DR4-Dw15-DQw4 haplotype was increased in the patients with rheumatoid arthritis (RA) in the Japanese whereas the frequency of HLA-DR2-Dw12-DQw6 was decreased in them significantly. We utilized the HLA-DQw6 genes of transgenic C57BL/6 mice (DQw6-B6) and their F1 progenies with or without DQw6 genes derived from the matings between DBA/1 mice and HLA-DQw6 hemizygous transgenic DQw6-B6 mice. Mice were immunized with bovine type II collagen (C II) followed by boost immunization 3 weeks later. The development of arthritis was observed and the levels of IgG specific to C II were evaluated on ELISA every week until 10 weeks after the first immunization. The incidence of arthritic mice in DQw6(+)-F1 decreased significantly (P less than 0.05) as compared with that in DQw6(-)-F1 42.9% vs. 80.0%). The incidence of arthritic limbs in DQw6(+)-F1 decreased significantly (P less than 0.01) as compared with that in DQw6(-)-F1 (30.2% vs. 58.3%). The level of IgG specific to C II on the 5th week in DQw6(+)-F1 decreased significantly (P less than 0.01) as compared with that in DQw6(-)-F1 (218.6 +/- 39.2 micrograms/ml, mean +/- SEM, n = 21 vs. 431.3 +/- 58.8 micrograms/ml, mean +/- SEM, n = 20). Thus these results suggested that HLA-DQw6 genes suppressed the development of CIA most likely due to the reduction of the production of IgG specific to type II collagen.
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PMID:[The suppressive effect of HLA-DQw6 genes on collagen-induced arthritis in mice]. 202 63

Monoclonal anti-idiotypic antibodies previously shown to react with a cross-reactive idiotope of anti-collagen II auto-antibodies were used for in vivo treatment of DBA/1 mice receiving immunization with arthritogenic native rat collagen type II. Injection of 100 micrograms of the anti-idiotypic antibody 3 weeks before the collagen immunization resulted in a significant suppression of collagen arthritis, compared with mice treated with a monoclonal control antibody. The treatment with anti-idiotypic antibody 3 weeks before collagen immunization could also cause a marked down-regulation of the total serum levels of anti-collagen II antibodies. When the anti-idiotypic antibodies were administered near the time for induction of arthritis (2 days after collagen immunization) a significant effect was seen on the collagen arthritis, but not on the levels of anti-collagen antibody. As collagen-induced arthritis is a disease where both T- and B-cell mediated immunity are believed to play critical roles, the present effects of the in vivo anti-idiotype treatment on arthritis development could provide an interesting system for the study of idiotype regulation on both B- and T-cell arthritis-associated autoimmunity.
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PMID:Down-regulation of collagen arthritis after in vivo treatment with a syngeneic monoclonal anti-idiotypic antibody to a cross-reactive idiotope on collagen II auto-antibodies. 203 11

SWR mice are resistant to collagen-induced arthritis but produce antibodies to type II collagen. To determine if these antibodies have arthritogenic potential, serum from collagen-immunized mice was concentrated and passively transferred to DBA/1 mice. The recipients developed severe arthritis within 72 hours. To evaluate the role of complement, SWR mice were bred with congenic inbred B10.D2/oSn (complement deficient) and B10.D2/nSn (complement normal) mice. Collagen-immunized (SWR x B10.D2/nSn)F1 mice had high levels of C5 and were susceptible to arthritis, while (SWR x B10.D2/oSn)F1 mice were deficient in C5 and were resistant to arthritis.
Arthritis Rheum 1991 Jun
PMID:SWR mice are resistant to collagen-induced arthritis but produce potentially arthritogenic antibodies. 205 25

Pregnancy is known to influence the course of rheumatoid arthritis (RA) in women, as well as type II collagen-induced arthritis (CIA) in DBA/1 mice. A characteristic feature is the remission during gestation and the exacerbation of the diseases during the post-partum period. In the case of CIA in DBA 1 mice, two hormonal changes have been assumed to be critical for the induction of the post-partum flare: (i) the fall in steroid hormone levels from those present during pregnancy; and (ii) surges of prolactin (PRL) release at and after delivery. Our results show that treatment with oestradiol during a short period immediately after parturition protects the mouse from a post-partum flare of the disease, and that treatment with bromocriptine, a drug known to inhibit the endogenous PRL release, has a significant though less marked effect. Studies of lactating (i.e. animals with physiological stimulation of endogenous PRL release) and non-lactating arthritic mice revealed no clear-cut differences, indicating that PRL is of minor importance for the induction of the post-partum flare. Some steroids other than oestradiol, which may be implicated in the exacerbation of arthritis, namely progesterone and hydrocortisone, had no clinical effect. Analyses of agalactosyl IgG levels in mice with CIA, and anti-collagen II antibodies in sera collected at the end of the experiments revealed no significant differences between the oestradiol and the control groups. The successful oestradiol treatment of the mice indicates that the drop in endogenous oestradiol levels prior to delivery ends the oestrogen-mediated protection against arthritis during pregnancy.
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PMID:Maintained pregnancy levels of oestrogen afford complete protection from post-partum exacerbation of collagen-induced arthritis. 207 May 61

The importance of T-cell receptor (TcR) V beta gene haplotype and complement component C5 deficiency for the resistance to collagen-induced arthritis (CIA) in the SWR mouse was studied. Firstly, the immune responses against heterologous and autologous type II collagen (CII) were compared between SWR mice and arthritis-susceptible and major histocompatibility complex (MHC)-identical DBA/1 mice. Secondly, F1 and F2 crosses were made between the two strains and studied for arthritis development, V beta gene usage and C5 presence. After immunization with heterologous rat CII, both strains reacted with a strong autoantibody response. Immunization with mouse CII, on the other hand, gave a much lower response in both strains, with DBA/1 mice having the strongest response. A collection of B-cell hybridomas was created from the draining lymph nodes of SWR mice 9 days after immunization with rat CII. This hybridoma collection showed similarity to previous data from the DBA/1 mouse, by its high frequency of B cells producing IgG specific for CII and with a high degree of cross-reactivity with autologous mouse CII. After immunization with heterologous CII, both T cells specific for heterologous CII as well as T cells cross-reacting with autologous CII could be demonstrated. F1 crosses between SWR and DBA/1 were relatively resistant to CIA (8%), while in the F2 generation 72% of the mice developed arthritis. No correlation between V beta haplotype or C5 and development of arthritis in the F2 mice was found. It is concluded that the resistance to CIA in the SWR mouse is not related to either V beta haplotype or C5 deficiency. Instead we postulate the involvement of two or more genes which are important for the induction and maintenance of tolerance to own CII.
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PMID:T-cell receptor V beta haplotype and complement component C5 play no significant role for the resistance to collagen-induced arthritis in the SWR mouse. 207 Nov 65

The relationship between the functional affinity of antibodies against type II collagen (CII) and the development of arthritis was studied in mice with collagen-induced arthritis. The responses of DBA/1 strain mice were compared with those of mice selectively bred to produce antibodies of high functional affinity (HA mice) and low functional affinity (LA mice). HA and LA mice did not develop arthritis in response to immunization with CII whereas 86% of DBA/1 mice did, with 33% showing severe and 53% mild disease. Anti-CII antibodies of the highest titre, the lowest functional affinity, and the greatest affinity heterogeneity were associated with the development of the severest arthritis in DBA/1 mice: even in DBA/1 mice with moderate or no disease the amount of antibody and heterogeneity were higher and functional affinity lower than in either HA or LA mice. Antibodies of the G1, 2a, 2b and 3 subclasses were produced in all mice, and none of these alone accounted for the overall difference in IgG antibody titres or affinity in the groups of mice. Antibodies of the IgG2a subclass showed the closest association with the development of arthritis in the different groups. It is concluded that anti-CII antibodies of low functional affinity, and presumably also of the IgG2a subclass, influence the disease process in collagen arthritis.
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PMID:Low affinity antibodies against collagen type II are associated with pathology in collagen-induced arthritis in mice. 208 89

We have investigated the effects of recombinant murine interferon-gamma (rIFN-gamma) on type II collagen-induced arthritis (CA) in DBA/l mice. Therapeutic as well as prophylactic treatment with subcutaneous rIFN-gamma, at 10(5) U/mouse six times a week, inhibited the development of CA without any obvious side effects. The accompanying suppression of anti-CII antibody responses may partly explain the inhibition of CA by rIFN-gamma. The possible role of the anti-inflammatory effect of systemic IFN-gamma in the inhibition of CA is discussed.
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PMID:The effect of treatment with interferon-gamma on type II collagen-induced arthritis. 211 46

Type II collagen-induced arthritis (CIA) is believed to be dependent on T cells expressing a limited number of V beta chains. Two different methods were used to selectively eliminate T cells expressing a certain T-cell receptor (TcR) V beta chain in mouse strains susceptible to CIA. In vivo treatment with monoclonal anti-V beta 6 or anti-V beta 8.1,2 antibodies did not alter CIA, despite a reduction of the major part of the V beta 6+ or V beta 8.1,2+ lymph node cells (LNC), as measured by flow cytometric (FACS) analyses. The reduction was not due to complete elimination of V beta 6+ or V beta 8.1,2+ cells, since part of the V beta 6 and V beta 8.1,2 expressing cells returned later, even in mice that had been thymectomized first to prevent maturation of new T cells. In contrast, treatment with antibodies against CD4 efficiently abrogated development of CIA. In the (CBA x DBA/1J)F1 and the (BALB/c x DBA/1J)F1 mice, where M1s1a was combined with expression of I-E, the V beta 6+ LNC were deleted. In spite of the deletion, both F1 strains were highly susceptible to CIA.
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PMID:In vivo elimination of T cells expressing specific T-cell receptor V beta chains in mice susceptible to collagen-induced arthritis. 213 66

The effect of exposure of female DBA/1 mice to collagen II (CII) prior to breeding on the susceptibility of their offspring to CII-induced arthritis (CIA) was investigated. It was found that female offspring, born within 3 months after exposure of the mothers to CII, had a significantly reduced incidence of CIA, following immunization with CII. Just prior to this immunization, no anti-CII could be detected in the offspring. Offspring born more than 3 months after exposure of the mothers to CII showed no differences in susceptibility to induction of CIA, if optimal conditions for induction were used. However, when suboptimal conditions for induction of CIA were used, offspring of females that had been exposed to CII developed less severe arthritis and had a delayed onset of arthritis as compared with controls. It is concluded that exposure of female mice to CII prior to mating results in changes in the immune response to CII in the offspring, leading to a subtle decrease in susceptibility to CIA.
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PMID:Exposure of female mice to type II collagen reduces susceptibility to collagen-induced arthritis in offspring. 220 8

The objective of the present investigation was to examine the effects of an irreversible inhibitor of ornithine decarboxylase (2R,5R)-6-heptyne-2,5,diamine (methylacetylenic putrescine, MAP) on experimentally induced arthritis in mice. MAP (0.5-0.05%) was administered in drinking water to DBA/1 mice immunized with native chick type II collagen (CII). The development of arthritis was inhibited only in those mice receiving 0.5% MAP; lower doses were ineffective. Putrescine and spermidine levels were decreased and spermine levels were increased in spleen and lymph node cells from drug-treated mice compared to control arthritic mice. Furthermore, when control mice were developing arthritis, serum anti-CII antibody levels were lower in the MAP-treated group. MAP inhibited antibody production early in the immune response to CII; there was an association between inhibition of antibody production and inhibition of the development of arthritis. When MAP was discontinued, the nonarthritic, drug-treated mice did not develop the disease. Late administration of MAP (beginning 19 days after CII immunization) did not affect the incidence or the severity of the arthritis. Cyclophosphamide treatment begun at the same time significantly inhibited the development of the disease. In vitro T cell responses to denatured type II collagen (dCII) in untreated and MAP-treated mice were examined 14 days after immunization with CII. This is a time of peak T cell responsiveness in untreated animals. MAP treatment had no effect on the T cell response to dCII. These results indicate that MAP can prevent the development of CII-induced arthritis, possibly by inhibiting the autoantibody response. Therefore, inhibitors of polyamine biosynthesis deserve further investigation as potential immunosuppressive agents.
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PMID:Methylacetylenic putrescine (MAP), an inhibitor of polyamine biosynthesis, prevents the development of collagen-induced arthritis. 229 95


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