A comparative immunologic analysis of several murine strains with autoimmune manifestations

Theofilopoulos, Argyrios N.; McConahey, Patricia J.; Izui, Shozo; Eisenberg, Robert A.; Pereira, Aparecido B.; Creighton, W D

doi:10.1016/0090-1229(80)90039-2

Cited by 76 publications

(26 citation statements)

References 64 publications

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“…BXSB autoimmuneprone mice are also small compared to other autoimmuneprone mice (i.e., B/W, MRL/lpr, and NZB). BXSB male mice develop an inflammatory vascular disease of the heart and autoimmune or immune complex-based renal disease that is somewhat different in distribution and manifestation than the diseases characteristic of mice of other autoimmuneprone strains (9).…”

mentioning

confidence: 99%

The effects of dietary restriction on immune function and development of autoimmune disease in BXSB mice.

Kubo

Gajar

Johnson

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

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Chronic energy intake restriction (CEIR) prolonged the median life span and inhibited autoimmunity and development of autoimmune disease in BXSB mice, as has been established for mice of several other autoimmune-prone, short-lived strains. Whether imposed just after weaning or delayed until manifestations of disease had appeared, CEIR inhibited or reversed development of autoimmunity and immune complex-based renal disease in male BXSB mice. CEIR also prevented the formation of anti-DNA antibodies and prevented the increase in circulating immune complex levels that is typically observed in male mice of this strain. Moreover, CEIR inhibited development of splenomegaly and prevented the normal age-associated decline of a number of immunological functions, including interleukin 2 production, cellmediated cytotoxic responses, and mixed lymphocyte reactivity. The observed improvement in cell-mediated immune responses was attributed largely to the capacity of CEIR to inhibit development of the splenomegaly that occurs concomitant with expansion of a non-T, non-B lymphoid cell population. These findings emphasize that CEIR, even when imposed relatively late in life in BXSB mice, can influence expression of autoimmunities and autoimmune diseases of different genetic origins and presumed pathogenetic bases.

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mentioning

confidence: 99%

The effects of dietary restriction on immune function and development of autoimmune disease in BXSB mice.

Kubo

Gajar

Johnson

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

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“…3A). Separate analyses were done with the males and females, as we found that females had higher Ab levels than males, an observation that has not been reported before in the MRL-Fas lpr model, although it has been noted previously that MRL/ϩ Fas-lpr females have slightly worse mortality than males (28). The elevated Ig concentrations in the B6.MRLc7 animals were considerably more striking at 6 mo of age than at 12.…”

Section: Autoantibody Productionmentioning

confidence: 58%

The Centromeric Region of Chromosome 7 from MRL Mice (Lmb3) Is an Epistatic Modifier of Fas for Autoimmune Disease Expression

Kong

Morel

Croker

et al. 2004

The Journal of Immunology

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Lupus is a prototypic systemic autoimmune disease that has a significant genetic component in its etiology. Several genome-wide screens have identified multiple loci that contribute to disease susceptibility in lupus-prone mice, including the Fas-deficient MRL/Faslpr strain, with each locus contributing in a threshold liability manner. The centromeric region of chromosome 7 was identified as a lupus susceptibility locus in MRL/Faslpr mice as Lmb3. This locus was backcrossed onto the resistant C57BL/6 (B6) background, in the presence or absence of Fas, resulting in the generation of B6.MRLc7 congenic animals. Detailed analysis of these animals showed that Lmb3 enhances and accelerates several characteristics of lupus, including autoantibody production, kidney disease, and T cell activation, as well as accumulation of CD4−CD8− double-negative T cells, the latter a feature of Fas-deficient mice. These effects appeared to be dependent on the interaction between Lmb3 and Fas deficiency, as Lmb3 on the B6/+Fas-lpr background did not augment any of the lupus traits measured. These findings confirm the role of Lmb3 in lupus susceptibility, as a modifier of Faslpr phenotype, and illustrate the importance of epistatic interaction between genetic loci in the etiology of lupus. Furthermore, they suggest that the genetic lesion(s) in MRLc7 is probably different from those in NZMc7 (Sle3/5), despite a significant overlap of these two intervals.

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“…They also reported that there were two types of B cells in ( (26)(27)(28). The expression of Ia antigens on B cells also seems to be higher in old female NZB mice than in young NZB mice.…”

Section: Expression Of Class II Molecules On Stimulator B Cellsmentioning

confidence: 93%

B‐B Cell Interactions in the Spontaneous Activation of B Cells in Autoimmune NZB Mice

Saito

Tanaka

Ota

et al. 1991

Microbiology and Immunology

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We analyzed the mechanism of spontaneous B cell activation in lupus mice by using anticlass-II antibody in vitro. The in vitro culture of B cells from old NZB mice markedly produced Ig without any stimulation, while B cells from NZW mice did not. The addition of anticlass-II antibody (anti-Iad antibody) to the culture inhibited Ig production of NZB B cells in a concentration-dependent manner. On the other hand, the addition of anticlass-I antibody (anti-H-2Dd antibody) and anticlass-II antibody with different specificity (anti-Iak) gave no effect on the Ig production of NZB B cells. When mitomycin C-treated B cells were added to in vitro culture of responder B cells as a stimulator, Ig production of responder B cells was enhanced in a concentration-dependent manner. However, the enhancing effect of the stimulator B cells was abrogated by the pretreatment with anticlass-II antibody. The stimulator B-cell activity to NZB B cells was marked . in NZB B cells, moderate in NZB/W F1 B cells, and weak in NZW B cells. Furthermore, the stimulator B-cell activity with regard to NZB B cells was marked in old female NZB B cells, moderate in old male NZB B cells, and weak in young NZB B cells. The expression of class II antigens on the surface of old female NZB B cells was significantly higher than that of old male NZB and young NZB B cells. These results suggest that in lupus mice the spontaneous B-cell activation is induced by an abnormal B-B cell interaction mediated by class II antigens.

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A comparative immunologic analysis of several murine strains with autoimmune manifestations

Cited by 76 publications

References 64 publications

The effects of dietary restriction on immune function and development of autoimmune disease in BXSB mice.

The effects of dietary restriction on immune function and development of autoimmune disease in BXSB mice.

The Centromeric Region of Chromosome 7 from MRL Mice (Lmb3) Is an Epistatic Modifier of Fas for Autoimmune Disease Expression

B‐B Cell Interactions in the Spontaneous Activation of B Cells in Autoimmune NZB Mice

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