Inhibition of experimental autoimmune renal tubulointerstitial disease in guinea pigs by depletion of complement with cobra venom factor

Rudofsky, Ulrich H.; Steblay, Raymond William; Pollara, Bernard

doi:10.1016/0090-1229(75)90027-6

Cited by 38 publications

(6 citation statements)

References 14 publications

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“…Complement activation is required for full expression of disease, as guinea pigs that are rendered complement deplete by treatment with cobra venom factor are protected from antibody-induced disease (327). Although antibody and complement initiate interstitial injury, lymphocytes are required for progression, as demonstrated by the fact that antibody transfer into lymphocyte-depleted animals causes C3 deposition in the interstitium but does not cause tubulointerstitial disease (324,327).…”

Section: Antibody-mediated Nephritogenic Responsesmentioning

confidence: 99%

Immunological Mechanisms of Interstitial Disease

Danoff

2008

Seldin and Giebisch's the Kidney

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Section: Antibody-mediated Nephritogenic Responsesmentioning

confidence: 99%

Immunological Mechanisms of Interstitial Disease

Danoff

2008

Seldin and Giebisch's the Kidney

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“…Some strain 2 recipients which had no lesions on day 9 developed moderate le sions by day 19. Although this inordinate delay is unusual in antibody-induced tissue injury, e.g., glomerulonephritis, we have ob served such delayed onset of RTD in cobra venom factor-treated recipients [9], The time-course and dose response data on the passive transfer of RTD in Albany guinea pigs [9, unpubl. observations] also indicate that onset, as well as severity, are dose dependent.…”

Section: Discussionmentioning

confidence: 99%

“…We have experimental evidence that the alterna tive pathway of complement participates in the accumulation of lymphocytes and ma crophages in the target tissue [8,9,13], A distinct strain difference in the induction of RTD has been observed [4,5]. Active im munization of strain 2 guinea pigs failed to induce an adequate immune response, while passive immunization with anti-TBM au toantibodies did not evoke an inflammato ry response.…”

Section: Introductionmentioning

confidence: 99%

Studies on the Pathogenesis of Experimental Autoimmune Renal Tubulointerstitial Disease in Guinea Pigs

Rudofsky¹,

McMaster²,

Pollara³

1979

Int Arch Allergy Immunol

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It has been reported that strain 2 guinea pigs do not develop experimental autoimmune renal tubulointerstitial disease (RTD) by active or passive immunization. Under our experimental conditions strain 2 guinea pigs are susceptible to the induction of RTD. Typical moderate to severe renal lesions were seen 22 days after immunization with rabbit tubular basement membrane in complete Freund’s adjuvant. Most Albany strain guinea pigs had severe RTD. Susceptibility to induction of RTD by passive transfer of antitubular basement membrane autoantibodies was studied in Albany (A) and strain 2 (2) guinea pigs, as well as in A→A, A→2, and 2→A radiation chimeras. Only some Strain 2 guinea pigs had mild to severe renal lesions by day 9, but by day 19 all had typical histologic renal abnormalities. Albany guinea pigs already had moderate to severe RTD by days 9–10. Strain 2 differed from Albany recipients by a noticeable delay in the onset of lesions. Bone marrow transplants between Albany and strain 2 did not affect these susceptibility differences. A→2 recipients responded like strain 2, and 2→A like Albany. This indicates that the delay of onset of RTD in strain 2 is not a defect in the bone marrow-derived inflammatory cells.

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“…The developing or fully formed interstitial lesion does not involve neutrophils (2, 3), but rather contains a variety of mononuclear cells (2,3), including macrophages (2, 4) and T cells (3) in association with kidney-bound (wTBM-Ab and complement (5,6). The interstitial lesions in guinea pigs can be transferred with aTBM-Ab (7), but not with cells (2).…”

Section: Introductionmentioning

confidence: 99%

Macrophage chemotaxis in anti-tubular basement membrane-induced interstitial nephritis in guinea pigs

Kennedy

Merrow

Phillips

et al. 1985

Clinical Immunology and Immunopathology

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Interstitial renal lesions containing T cells and macrophages develop after 14 days in guinea pigs immunized to produce anti-tubular basement membrane-induced interstitial nephritis. We serially examined the renal venous and systemic arterial sera from such animals to determine if chemotactic factors were released across their kidneys. Our findings demonstrated the presence of a macrophage-specific renal chemoattractant with peak detectability on Days 10-14, just subsequent to the deposition of uTBM-Ab, but prior to the development of significant renal injury. We propose that such factors may provide important communication signals in the immunopathogenesis of this form of inteI'Stitia1 ktjUry.

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Inhibition of experimental autoimmune renal tubulointerstitial disease in guinea pigs by depletion of complement with cobra venom factor

Cited by 38 publications

References 14 publications

Immunological Mechanisms of Interstitial Disease

Immunological Mechanisms of Interstitial Disease

Studies on the Pathogenesis of Experimental Autoimmune Renal Tubulointerstitial Disease in Guinea Pigs

Macrophage chemotaxis in anti-tubular basement membrane-induced interstitial nephritis in guinea pigs

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