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At least 19 recordsLinked to original sources
PubMed1985

Functional consequences of perceived interleukin deficiencies? Analysis employing NZB x C58 recombinant inbred mice.

NZB mice have previously been shown to be deficient in the production of interleukins 1 and 2 (IL-1, IL-2) during the development of autoimmune disease. One or both of these defects have been inherited in certain of the NZB X C58 recombinant inbred strains (N X 8 RI). Certain of these strains have been selected to examine further the effect of decreased production of IL-1 and/or IL-2. The interleukin deficiencies found in vitro were not due to the presence of an inhibitor/suppressor nor was any activity found intracellularly upon water lysis of stimulated cells. Despite profound IL-1 and/or IL-2 deficiencies measured in vitro, all of the N X 8 RI lines examined were found to be capable of producing IL-1 in vivo as shown by their serum amyloid A response to endotoxin injection. We conclude from these studies that defects in IL-1 production measured in vitro do not reflect inability to produce this lymphokine in vivo. Young, IL-1 deficient NZB mice generated CTL to TNP-self but old, IL-2 deficient NZB mice did not. Since all other strains were found to generate cytotoxic T cells to TNP-self regardless of interleukin defects, we also conclude that the cytotoxic T cell defect in NZB mice is due to some presently unknown factor in addition to IL-2 deficiency. The relationship of decreased production of interleukins to the development of autoimmunity remains undefined.

Animals↗
PubMed1984

Cytokine production by NZB, C58, and NZB X C58 recombinant inbred mice.

Humans with autoimmune disease and autoimmune mouse strains such as NZB have been shown to produce reduced levels of the cytokines interleukin 1 and interleukin 2. The NZB X C58 recombinant inbred (N X 8 RI) strains exhibit certain of the autoimmune characteristics of the NZB strain. Their abilities to produce interleukin 1 and interleukin 2 have been tested. Deficiencies in the production of one or both of these cytokines were observed in the N X 8 RI strains. Decreased interleukin 2 production was not due to inability to respond to concanavalin A or allogeneic stimulation, nor to altered kinetics of the response. No correlation was observed between cytokine deficiencies and the inherited autoimmune characteristics previously studied in these strains. One especially interesting strain was N X 8 RI 16, which made high amounts of interleukin 2 but no detectable interleukin 1.

Animals↗
PubMed1982

Independent segregation of NZB immune abnormalities in NZB x C58 recombinant inbred mice.

The study of NZB x C58 recombinant inbred mouse strains has revealed independent segregation of naturally occurring thymocytotoxic antibody and Coombs' anti-erythrocyte autoantibody. The lack of concordance of either of these autoantibodies with known heavy and light chain markers suggests that the autoantibodies are produced as a result of regulatory gene defects rather than alterations of antibody structural genes. Further, lack of concordance of the various autoimmune traits with each other or with H-2 or virus expression suggests that the autoimmune phenotype is not the result of a single "autoimmunity' gene but rather the outcome of faulty regulation of a number of independently segregating genes.

Aging↗
PubMed1977

Quantitative estimation of serum Ss level: changes upon the development of autoantibodies, environment and acute inflammation in inbred mice.

The level of the fourth complement component was quantitated in sera from several inbred strains of mice of various ages. In NZB and NC mice, which are known to produce autoantibodies spontaneously, the level of C4 increased from one month to six months of age, maintained high C4 levels until 10 months but showed a gradual decrease in serum C4 beginning at one year of age. Direct and indirect Coombs' antibodies were detected after 6 months of age in both strain. C4 level in BALB/c and C57BL/6J mice were relatively constant throughout their life span. In order to determine whether or not antigen-antibody complexes induce the elevation of serum C4 level, either rabbit anti-mouse IgG serum or normal rabbit serum was injected intravenously into BALB/c mice. Sera obtained at various times were tested for C3 and C4 by single radial immunodiffusion. The results indicate that the C4 level elevated after the injection of rabbit anti-mouse IgG, but C3 levels did not change after the same treatment. Normal rabbit serum did not induce a detectable change in C3 and C4 level under the conditions used.

Age Factors↗
PubMed1988

The role of splenic colony-forming units in autoimmune disease.

Stem cell activity in murine lupus was investigated by analyzing endogenous splenic colony-forming units in sublethally irradiated inbred, congenic, and consomic mice as well as F1 crosses. Splenic colony-forming units (CFU-s) were elevated (greater than 100) in young NZB mice as compared with nonautoimmune-prone mice (less than 10). In lpr/lpr and gld/gld mice, elevated levels of CFU-s were in association with disease manifestations. F1 crosses of inbred lpr/lpr mice often showed an excess of CFU-s in females when compared with male littermates. The autoimmunity accelerating factor on the Y chromosome of BXSB mice led to high numbers of CFU-s relative to female littermates. The xid gene, which does not alter stem cell activity but, instead, interferes with terminal lymphocyte maturation, had no effect on CFU-s in congenic mice. These studies demonstrate that there is a strong association between increased numbers of CFU-s and the development of generalized autoimmunity; increased stem cell division may be important for the development of murine lupus.

Animals↗
PubMed1982

Analysis of recombinant inbred lines derived from "autoimmune" (NZB) and "high leukemia" (C58) strains: independent multigenic systems control B cell hyperactivity, retrovirus expression, and autoimmunity.

The relationship of B cell hyperactivity and retrovirus expression to other autoimmune traits were examined in recombinant inbred (N X 8 RI) lines derived from NZB and C58 progenitor strains. Although both NZB and C58 mice expressed high levels of xenotropic virus, the RI lines segregated in virologic phenotype, as high or low expressors of the endogenous virus. The expression of the C58-derived ecotropic virus occurred in only one-half of the RI lines, and its expression in the remaining lines of mice appeared to be suppressed by the NZB-derived allele at the Fv-1 locus. The inheritance of B lymphocyte abnormalities of the NZB progenitor strain was investigated by studying spontaneous and SRBC-induced production of IgM by the spleen cells of the RI lines. These two phenotypes of B cell hyperactivity were found to be determined by independently segregating genes and they were not linked to immunoglobulin structural gene loci. The strain distribution patterns of virus expression and B cell hyperactivity in the RI lines did not match with each other or with the inheritance patterns of other immunologic abnormalities, such as defective AMLR and production of autoantibodies.

Animals↗
PubMed1983

Differences in maternal lineages of New Zealand Black mice defined by restriction endonuclease analysis of mitochondrial DNA and by expression of maternally transmitted antigen.

Two substrains of New Zealand Black (NZB) mice have been compared with respect to expression of a maternally transmitted cell surface antigen, Mta, defined by cloned cytolytic T cells, and for restriction enzyme polymorphisms of mitochondrial DNA (mtDNA). These independent assays of maternal cytoplasmic inheritance provide strong evidence for genetic contamination of the NZB/BlPt substrain (NZB/Bl mice from Michael Potter's separate colony at the National Institutes of Health), in which the typical NZB immunologic abnormalities are at least partially ameliorated. The decisive data are the restriction enzyme maps of mtDNA for NZB/BlPt, which were identical with those of the common "old inbred" strains and quite different from those of NZB/BlN (NZB/Bl mice from the breeding facility at the National Institutes of Health). It is probable that the contamination of the NZB/BlPt substrain is related to phenotypic changes in their autoimmune state. More interestingly, the data are consistent with, although they do not prove, involvement of the mitochondrial genome in expression of a cell surface molecule.

Animals↗
PubMed2002

Quantitative trait locus mapping of genes that regulate HDL cholesterol in SM/J and NZB/B1NJ inbred mice.

To investigate the quantitative trait loci (QTL) regulating plasma cholesterol, the female progeny of an (SMxNZB/ B1NJ)xNZB/B1NJ backcross were fed an atherogenic diet. After 18 wk, plasma total cholesterol and high-density lipoprotein cholesterol (HDL-C) was measured. HDL-C concentrations were greater in NZB than in SM mice. For standard chow-fed mice, QTL were found near D5Mit370 and D18Mit34. For mice fed an atherogenic diet, a QTL was found near D5Mit239. The QTL for chow-fed and atherogenic-fed mice on chromosome 5 seem to be two different loci. We used a multitrait analysis to rule out pleiotropy in favor of a two-QTL hypothesis. Furthermore, the HDL-C in these strains was induced by the high-fat diet. For inducible HDL-C, one significant locus was found near D15Mit39. The gene for an HDL receptor, Srb1, maps close to the HDL-C QTL at D5Mit370, but the concentrations of Srb1 mRNA and SR-B1 protein and the gene sequence of NZB/B1NJ and SM/J did not support Srb1 as a candidate gene. With these QTL, we have identified chromosomal regions that affect lipoprotein profiles in these strains.

Animals↗