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

Type II collagen-induced arthritis is dependent on the activation of T-helper cells and is modulated by female sex hormones. It is shown that treatment of castrated female DBA/1 mice with beta-estradiol decreases the incidence (32% vs 88%) as well as the severity of the disease. The estrogen-induced suppression of both the development of collagen arthritis and T-cell immunity were not dependent on the thymus. Thus, estrogen treatment of thymectomized and castrated female mice suppressed the incidence (21% versus 100% in controls) and severity of arthritis. Similarly, estrogen treatment of thymectomized and castrated female mice suppressed both antigen-specific delayed-type hypersensitivity and T-cell proliferative responses. These data suggest that the estrogen-mediated suppression of arthritis and T-cell immunity is not dependent on the presence of an intact thymus.
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PMID:Estrogen-induced suppression of collagen arthritis. III. Adult thymectomy does not affect the course of arthritis or the estrogen-mediated suppression of T-cell immunity. 323 56

Arthritis induced with type II collagen in DBA/1 mice, was analyzed by immunohistochemical techniques. In the earliest detectable pathologic changes, before any macroscopic signs, an accumulation of Mac1+, macrophage-like cells, and an increased expression of major histocompatibility class II antigens were observed focally in the synovial lining layer. In these foci, CD4+ and interleukin 2 receptor expressing T lymphocytes were regularly detected, but not usually other sets of lymphocytes such as B lymphocytes and CD8+ lymphocytes. In clinically detectable arthritis, there was a prominent infiltration of Mac1+ cells, both polymorphonuclear-like and macrophage-like cells. T cells were relatively few, suggesting that they do not play a primary effector role, but rather that they may regulate or permit the self-perpetuative inflammation.
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PMID:Early appearance of activated CD4+ T lymphocytes and class II antigen-expressing cells in joints of DBA/1 mice immunized with type II collagen. 325 83

Immunization of DBA/1 mice with type II collagen resulted in typical and progressive arthritis, which is associated with the production of high titer of anti-collagen antibody and the induction of cell-mediated immunity as exemplified by delayed type hypersensitivity response as well as lymphokine production. In contrast, administration of heat-denatured collagen into DBA/1 mice failed to induce the arthritis. These mice produced only marginal antibody, whereas they developed comparable cell-mediated immunity to that induced by immunization with native collagen, and therefore the inoculation of heat-denatured collagen provided the regimen capable of inducing preferentially cell-mediated immunity without the generation of high level of antibody. Inasmuch as administration of antibody induced only marginal and transient joint swelling not associated with typical histologic lesion, the synergistic effect of humoral and cell-mediated immunities was investigated using antibody preparation and the regimen to induce selectively cell-mediated immunity. The results demonstrate that administration of antibody into DBA/1 mice pre-sensitized with heat-denatured collagen resulted in potent and progressive arthritis. Such synergy was further confirmed by the induction of arthritis in T cell-depleted DBA/1 mice that had been adoptively transferred with antibody and lymphoid cells from heat-denatured collagen-sensitized mice. Moreover, it was revealed that the nature of cells capable of transferring cell-mediated immunity was of Thy-1+ and L3T4+ Lyt-2-. These results indicate that anti-collagen antibody and L3T4+ T cell-mediated cellular immunity are crucially required for the perpetuated development of type II collagen-induced arthritis.
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PMID:Type II collagen-induced murine arthritis. I. Induction and perpetuation of arthritis require synergy between humoral and cell-mediated immunity. 325 78

In an attempt to examine the in vivo proinflammatory properties of IL-1, the effects of rIL-1 beta on the development of collagen-induced arthritis in mice were investigated. The results presented in this paper demonstrated that the administration of rIL-1 beta via mini-osmotic pumps into DBA/1 mice which were suboptimally immunized with native chick type II collagen (NcII) markedly accelerated the onset as well as the progression of the arthritic disease. When IL-1-containing osmotic pumps were s.c. implanted onto mice 18 days post-collagen immunization, clinical signs of arthritis appeared within 3 to 4 days after the implant with the pumps. Maximal incidence of arthritis which was usually 80 to 100% occurred between the 6th and 7th day after the administration of rIL-1 beta. Histologic analyses revealed that the knee and ankle joints from mice which were treated with rIL-1 beta for 7 days were most severely and consistently affected. Furthermore, these IL-1-treated mice exhibited granulocytic hyperplasia within the marrow as well as marked peripheral blood neutrophilia. By contrast, arthritis was not observed during the 7-day course of the IL-1 study in the following control groups: 1) mice that were only immunized with NcII, and 2) collagen-immunized mice which received osmotic pumps containing PBS. A substantial number of these collagen-immunized mice which were not treated with IL-1 eventually developed arthritis but at later times after the incidence of arthritis had peaked in the IL-1-treated group. In addition, unimmunized mice failed to develop arthritis upon treatments with IL-1 beta. Moreover, the humoral responses to NcII were not altered in the IL-1-treated mice. Thus, these in vivo studies suggest that IL-1 is potentially capable of triggering the various inflammatory events of collagen-induced arthritis, and thereby, contribute to the pathogenesis of murine arthritis.
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PMID:In vivo administration with IL-1 accelerates the development of collagen-induced arthritis in mice. 326 Sep 13

An IgG2a hybridoma antibody (BC-10) was obtained by a myeloma fusion with lymphocytes from B10.RIII mice immunized against native bovine type II collagen. This anti-collagen monoclonal exhibited extensive cross-reactivity with several type II collagen species. BC-10 was found to have self-associating properties, but not the specificity of a typical IgG rheumatoid factor, inasmuch as this mAb bound to F(ab')2 fragments of itself and of normal mouse IgG. Self binding was inhibited by the association of BC-10 with type II collagen, and inhibition assays indicated that antibodies with the capacity to inhibit BC-10 binding to collagen were present in the sera from B10.RIII arthritic mice, but not from DBA/1 LacJ arthritic mice. Joint inflammation and histopathologic features consistent with arthritis were observed in mice injected with the BC-10 hybridoma.
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PMID:A monoclonal anti-type II collagen antibody with cross-reactive anti-Ig activity specific for the F(ab')2 fragment. 326 35

Intradermal injection of 100 micrograms of native homologous type II collagen (CII) into DBA/1-susceptible mice induced a progressive and chronic polyarthritis. This experimental autoimmune arthritis (EAA) closely mimicked the clinical evolution of human rheumatoid arthritis (RA) except for the sex linkage. Males were highly susceptible to EAA induction even when the amount of autoantigen injected was reduced to 25 micrograms. Conversely, females remained resistant to the disease even when a booster injection of 50 micrograms was administered. With regard to age, no major difference in the incidence was observed, although younger males developed a more severe arthritis than older ones. Anti-CII autoantibodies were detected in all immunized animals, regardless of the presence or absence of joint pathology. However, in arthritic mice, the onset of the disease was associated with a predominance of IgG2a autoantibodies. Kinetic studies revealed that females as well as males exhibited early histological lesions and detectable humoral responses toward mouse CII as of the second week postimmunization. Moreover, a specific cellular autoreactivity to homologous CII occurred in different lymphoid organs with a higher intensity in females than in males. Taken together, these findings suggest that homologous CII injection induces an early subclinical arthritis that develops progressively in all immunized mice, but would be down-regulated several weeks after priming, exclusively in females.
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PMID:Experimental autoimmune arthritis in mice. II. Early events in the elicitation of the autoimmune phenomenon induced by homologous type II collagen. 339 Sep 71

Collagen type II (CII)-induced arthritis (CIA) can be induced in 78% of B10.RIII mice (H2r) by intradermal (id) immunization with CII of bovine origin in complete Freund's adjuvant (CFA), whereas immunization with CII of chick origin induces arthritis in less than 5% of these mice. Nevertheless, tolerization of B10.RIII mice with intravenously injected chick CII renders the animals resistant to induction of CIA by immunization with bovine CII. Such tolerization can be achieved either by intravenous injection of 500 micrograms chick CII 1 week prior to immunization with bovine CII in CFA or by such an intravenous injection of chick CII 2 weeks after immunization with bovine CII in CFA. Postimmunization treatment results in a significant decrease in the concentration of antibody to bovine CII. Preimmunization administration of chick CII causes a marked decrease in the antibody reactive with chick CII without a significant effect on the anti-bovine CII antibody concentration. In DBA/1 mice, a strain in which both bovine CII and chick CII can induce a high incidence of the disease, intravenous injection of bovine CII can also prevent arthritis induced by chick CII, even when given 7 or 14 days after immunization. The fact that chick CII as tolerogen is quite effective in preventing arthritis in B10.RIII mice, while as immunogen it is very ineffective in inducing arthritis in this strain, may be interpreted as evidence for interaction between different epitopes on CII in the pathogenesis of CIA.
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PMID:Tolerance induction by a poorly arthritogenic collagen II can prevent collagen-induced arthritis. 340 29

Sensitization of DBA-1 mice with Type II collagen (CII) in complete Freund's adjuvant can cause polyarthritis. A possible link between CII-induced arthritis and delayed type hypersensitivity (DTH) has been suggested, so we decided to investigate the susceptibility of DBA-1 mice to CII induced DTH reactions. The mice were primed with a dose of 10 micrograms CII i.p. 4 days before challenging with 40 micrograms CII in the ear. Swelling was measured 48 h later and was found to be reproducible. Responsiveness to CII could be transferred with whole spleen cell populations from primed animals or with enriched spleen T cells, thus confirming the cellular nature of the reaction. Lymph node cells from CII/CFA footpad immunized animals were restimulated with CII in vitro. These cells were able to passively transfer DTH sensitivity in vivo and exhibited specificity for this antigen in vitro in proliferation assays.
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PMID:Delayed type hypersensitivity (DTH) to type II collagen (CII) in DBA-1 mice. 349 9

Experimental animal models can be used to help understand how oestrogen modulates autoimmune arthritis. We have previously shown that castration of female DBA/1 mice exaggerates arthritis induced with type II collagen. This report shows that treatment of castrated DBA/1 mice with low doses (0.2 micrograms twice a week) of beta-oestradiol reduces the incidence (37% vs 78% in controls) and severity (3.9 vs 5.6 mean scores) of arthritis. Levels of IgG anti type II collagen antibodies are decreased whereas levels of IgM antibodies are increased in the beta-oestradiol treated mice. The T cell response, as measured by a 3H-thymidine assay, is reduced in the beta-oestradiol treated mice. The results suggest that treatment with low doses of beta-oestradiol exerts a suppressive effect on both development of collagen arthritis as well as T cell dependent immune reactivity towards type II collagen.
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PMID:Oestrogen induced suppression of collagen arthritis: I. Long term oestradiol treatment of DBA/1 mice reduces severity and incidence of arthritis and decreases the anti type II collagen immune response. 350 49

Bovine type II collagen administered to non-pregnant female DBA/1 mice caused arthritis in 55% of animals with a mean onset time of 70 days following immunization. Of collagen-treated females subsequently becoming syngeneically pregnant before the onset of arthritis, all developed the disease within 10 days of parturition, representing an earlier onset, compared to non-pregnant females, of 41 days. This earlier onset also occurred in females with an allogenic pregnancy, but did not occur in females resorbing their fetuses (only syngeneic pregnancies were examined). In females with arthritis at the time of conception a significant remission was observed during pregnancy followed by exacerbation post-partum. This sequence of remissions during pregnancy and exacerbations post-partum occurred with each pregnancy (parties of up to four studied). The treatment of multiparous females with collagen demonstrated that pregnancy does not provide long-term protection against the development or progression of arthritis, as such females were equally susceptible to post-partum onset of collagen-induced arthritis (CIA) and the remissions and exacerbations described above. The modifying effect of pregnancy on CIA in mice is complex and does not appear to be the result of a single pregnancy-associated phenomenon.
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PMID:Effect of pregnancy on collagen-induced arthritis in mice. 360 30


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