Passive transfer of arthritis by purified anticollagen immunoglobulin: Localization of 125I-labeled antibody

Kerwar, S.S.; Gordon, Samuel; McReynolds, Richard A.; Oronsky, Arnold L.

doi:10.1016/0090-1229(83)90033-8

Cited by 20 publications

(3 citation statements)

References 7 publications

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“…Deposits of IgG and C3 are found after the serum transfer [1]. Interestingly, C3 depletion of recipient rats with cobra venom factor prevented passive transfer of arthritis with anti-CII antibodies [101]. Similarly, C3 deficient mice developed less severe disease compared to C3 sufficient mice, although both systemic and local C3 and C5 cleavage would be absent in these mice [97].…”

Section: Collagen Antibody-induced Arthritismentioning

confidence: 99%

Untitled

2006

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During the development of rheumatoid arthritis (RA) autoantibodies to IgG-Fc, citrullinated proteins, collagen type II (CII), glucose 6 phosphoisomerase (G6PI) and some other self-antigens appear. Of these, a pathogenic effect of the anti-CII and anti-G6PI antibodies is well demonstrated using animal models. These new antibody mediated arthritis models have proven to be very useful for studies involved in understanding the molecular pathways of the induction of arthritis in joints. Both the complement and FcγR systems have been found to play essential roles. Neutrophils and macrophages are important inflammatory cells and the secretion of tumour necrosis factor-α and IL-1β is pathogenic. The identification of the genetic polymorphisms predisposing to arthritis is important for understanding the complexity of arthritis. Disease mechanisms and gene regions studied using the two antibody-induced arthritis mouse models (collagen antibody-induced arthritis and serum transfer-induced arthritis) are compared and discussed for their relevance in RA pathogenesis. IntroductionBoth genetic and environmental factors interact and contribute to the development of autoimmune diseases. One such disease debilitating joint architecture is rheumatoid arthritis (RA). Arthritis in the joint involves a multicellular inflammatory process, including infiltration of lymphocytes and granulocytes into the articular cartilage, proliferation of synovial fibroblasts and macrophages and neovascularization of the synovial lining surrounding the joints. This proliferative process not only induces swelling, erythema, and pain in multiple joints but also progresses to joint destruction and causes loss of bone density and architecture. Many cellular components (macrophages, dendritic cells, fibroblast-like synoviocytes, mast cells, eosinophils, neutrophils, T cells and B cells), cell surface molecules (adhesion molecules, integrins), signaling components (ZAP70, PTPN22, JAK, mitogen activated protein kinase and Stat1) and humoral mediators (antibodies, cytokines, chemokines, metalloproteinases, serine proteases and aggrecanases) interact and aid in the disease progression, leading to digestion of extracelluar matrix and destruction of articular structures.The importance of B cells in RA pathogenesis stems not only from the original finding of high titers of rheumatoid factors (RFs), but also from the observation that arthritis is mediated in experimental animals via B cells and anti-collagen type II (anti-CII) antibodies [1][2][3][4][5]. Interest in studying the role of B cells in arthritis has returned as a result of successful anti-CD20 therapy [6][7][8]. In addition, the two widely used mouse models of antibody-initiated arthritis, collagen antibodyinduced arthritis (CAIA; induced with anti-CII antibodies) and the newly developed serum transfer-induced arthritis (STIA; induced with anti-glucose 6 phosphoisomerase (anti-G6PI) anti-sera) have been better characterized. B cells can contribute to the disease pathogenesis as antigen presenti...

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Section: Collagen Antibody-induced Arthritismentioning

confidence: 99%

Untitled

2006

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“…Following the "elimination" strategy, it was demonstrated that both B and T cellmediated immunity contribute significantly to the arthritis by showing that on one hand nude rats did not acquire CIA [50] and mice treated with anti-CD4 antibodies were prevented from disease [74], and on the other that rats depleted of B cells with anti-~t antibodies [28] or complement-depleted with cobra venom factor were also protected from disease [67]. Following the reconstitution strategy, both transfer of anti-collagen antibodies from diseased mice or rats [45,81] and transfer of T cells reactive with collagen II [30,42] were shown to cause arthritis. Interestingly however, the arthritis seen after such transfer was never as severe as after immunization with collagen, indicating a synergy between B and T cell immunity to collagen in the active disease.…”

Section: Further Pathogenetic Studies On Cia In Rodentsmentioning

confidence: 99%

What can we learn about rheumatoid arthritis from animal models?

Klareskog

1989

Springer Semin Immunopathol

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“…One interpretation of these results posits that the manipulations are necessary to overcome the resistance of the normal host synovium to the induction of inflammation by the transferred cells, in contrast to actively induced AA, in which the pro-inflammatory adjuvant has been shown to disseminate to joint tissues (18). We reasoned that, if local synovial alterations promote arthritis induced by AA lymphoid cells, then the administration of antibody to type II collagen, which has been shown to bind rapidly in vivo wherever there is articular cartilage (19) and to produce transient inflammation in large joints (3)(4)(5), should augment the severity of the arthritis passively transferred with AA cells.…”

Section: Discussionmentioning

confidence: 99%

Synergy between adjuvant arthritis and collagen-induced arthritis in rats.

Taurog

Kerwar

McReynolds

et al. 1985

The Journal of Experimental Medicine

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Adjuvant arthritis (AA) in rats is susceptible to cell-mediated passive transfer. Collagen-induced arthritis (CIA) in rats is susceptible to passive transfer with antibody to type II collagen. We report here the development of strikingly severe arthritis in Lewis rats as the result of synergy between passively transferred antibody to type II collagen from rats with CIA and concanavalin A (Con A)-stimulated lymph node or spleen cells from syngeneic rats with AA. Similar synergy was seen in rats with AA given anticollagen antibody, in rats with CIA given Con A-stimulated adjuvant spleen cells, and in rats actively immunized with CII and complete Freund's adjuvant. The synergistic process caused a very severe polyarthritis, characterized by marked swelling and erythema in all the joints of the distal extremities, with histologic and radiographic evidence of early, extensive erosion of articular cartilage. Synergy was apparent if the lymphoid cells from AA rats were given up to 1 mo after a single injection of anticollagen antibody. No synergy was seen when normal rat immunoglobulin or anti-ovalbumin antibody was substituted for anticollagen antibody, when Con A-stimulated lymphoid cells from normal rats or donors with CIA were used, or when Con A-stimulated AA lymphoid cells were irradiated before transfer. Synergy between separate immune effector mechanisms may represent a general phenomenon in the pathogenesis of inflammatory joint disease.

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Passive transfer of arthritis by purified anticollagen immunoglobulin: Localization of 125I-labeled antibody

Cited by 20 publications

References 7 publications

Untitled

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What can we learn about rheumatoid arthritis from animal models?

Synergy between adjuvant arthritis and collagen-induced arthritis in rats.

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