Chronic Allogeneic Disease

Gleichmann, Helga; Gleichmann, Ernst; André-Schwartz, J; Schwartz, Robert S.

doi:10.1084/jem.135.3.516

Cited by 44 publications

(9 citation statements)

References 11 publications

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“…They appeared to be similar to those described by other authors (13,24,49) who ascribe them to circulating antigenantibody complexes. In the other cases, advanced pyelonephritis prevented any recognition of possible immune-type renal lesions.…”

Section: Discussionsupporting

confidence: 73%

Lymphomas as Sequelae of the Transplantation of CO<sub>2</sub> -Treated Skin Autografts in Mice

Goldsmith¹,

Narváez²

1975

Oncology

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Inbred strains BALB/c and CBA and noninbred Swiss mice were used for transplanting skin autografts exposed before transplantation for approximately 48 h to (a) culturing in room air and (b) culturing in 45–48 % CO₂ in air. These pre-transplantation manipulations of skin autografts led to malignant lymphomas in the hosts. The lymphoma incidence was highest in the recipients of the CO₂-treated grafts; moreover, it was greater than the spontaneous incidence even in the recipients of grafts exposed to culturing in air alone, in some types of mice. The following abnormalities of the reticuloendothelial system were noted: (1) proliferation of lymph follicles into irregular masses of pleomorphic cells, (2) hyperplasia with concomitant atrophy of the lymphoid tissue, (3) replacement of the lymph follicles by malignant lymphoid cells. Renal lesions resembling membranous glomer-ulitis occurred occasionally. The occurrence varied in different strains.

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Section: Discussionsupporting

confidence: 73%

Lymphomas as Sequelae of the Transplantation of CO<sub>2</sub> -Treated Skin Autografts in Mice

Goldsmith¹,

Narváez²

1975

Oncology

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“…cGVHD recipient mice develop advanced immune complex-mediated glomerulonephritis with associated elevated urine protein levels (proteinuria) [21]. To assess the implication of miR-21 deficiency on the development of cGVHD-induced kidney disease, we collected urine samples from recipient mice pre-cGVHD induction and at six weeks post-induction and quantified urine protein concentrations as described in Materials and Methods.…”

Section: Resultsmentioning

confidence: 99%

MicroRNA-21 deficiency protects from lupus-like autoimmunity in the chronic graft-versus-host disease model of systemic lupus erythematosus

Garchow

Kiriakidou

2016

Clinical Immunology

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MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression primarily at the post-transcriptional level. Emerging evidence supports a regulatory role for miRNAs in the immune response and autoimmunity. In this work, we investigated the implication of miR-21 in the experimentally inducible bm12→B6 cGVHD model of systemic lupus erythematosus (SLE). cGVHD host mice deficient in miR-21 show a 2-fold reduction in splenomegaly, significantly reduced autoantibody titers and down-regulated components of the CD40:CD40L and CD28:CD80/86 co-stimulation pathways. Furthermore, we demonstrate that miR-21-deficient hosts have reduced CD4(+) IL-17(+) cell populations and an expanded CD4(+) CD25(+) FoxP3(+) cell compartment. We propose that miR-21 has a pluripotent role, serving to link distinct lymphocyte signaling pathways and acting as a "rheostat" for signals that promote B and T cell activation in lupus. Collectively, our experiments demonstrate that miR-21 deficiency in cGVHD host mice is sufficient to protect from lupus-like autoimmunity.

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“…Interestingly, the VH'ofBXW-16 is also derived from aJ558 subfamily with a 91% match to the VH ofA6. 1 (58,59). Until more mouse strains are tested with our pathogenic autoantibodies, we do not know whether MHClinked genes are involved in susceptibility.…”

Section: Resultsmentioning

confidence: 99%

Structural characteristics of the variable regions of immunoglobulin genes encoding a pathogenic autoantibody in murine lupus.

Tsao¹,

Ebling²,

Roman³

et al. 1990

J. Clin. Invest.

119

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We have studied several monoclonal anti-double-stranded (ds) DNA antibodies for their ability to accelerate lupus nephritis in young NZB X NZW Fl female mice and to induce it in BALB/c mice. Two identified as pathogens in both strains have characteristics previously associated with nephritogenicity: expression of IgG2a isotype and IdGN2 idiotype. Both pathogenic antibodies used the combination of genes from the VHJ558 and VK9 subfamilies. Two weak pathogens failed to accelerate nephritis in young BW mice, but induced lupus nephritis in BALB/c mice. They both express IdGN2; one is cationic and an IgG3, the other is an IgG2a. Additional MAbs (some IgG2a, one IdGN2-positive) did not accelerate or induce nephritis. We have cloned and sequenced the variable regions of the immunoglobulin genes of one pathogenic autoantibody. No unique V, D, or J gene segments and no evidence of unusual mechanisms in generating diversity were used to construct this antibody. These data argue against use of unique abnormal Ig genes by systemic lupus erythematosus individuals to construct pathogenic autoantibody subsets. Instead, the major abnormality may be immunoregulatory. (J. Clin. Invest. 1990. 85:530-540.) immunoglobulin gene * pathogenic autoantibody * systemic lupus erythematosus

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Chronic Allogeneic Disease

Cited by 44 publications

References 11 publications

Lymphomas as Sequelae of the Transplantation of CO<sub>2</sub> -Treated Skin Autografts in Mice

Lymphomas as Sequelae of the Transplantation of CO<sub>2</sub> -Treated Skin Autografts in Mice

MicroRNA-21 deficiency protects from lupus-like autoimmunity in the chronic graft-versus-host disease model of systemic lupus erythematosus

Structural characteristics of the variable regions of immunoglobulin genes encoding a pathogenic autoantibody in murine lupus.

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