Disease relevance of Ads1

• Here, we demonstrate that SPA-1(-/-) mice show an age-dependent increase in B220(high) B1a cells producing anti-dsDNA antibody and lupus-like nephritis [1].
• Higher serum levels of IgG, anti-dsDNA antibody, lower creatinine clearance, and slight splenomegaly also were found in Nrf2-deficient female mice [2].
• This result suggested that many Ids with anti-dsDNA antibody activity may contribute to lupus pathogenesis in this strain of mouse [3].
• Experimental parameters included life span, proteinuria, peripheral lymphocytes, anti-dsDNA antibody titers, and renal histopathology [4].
• RESULTS: Short term treatment with anti-alpha beta TCR Mab starting 2 days after cell transfer markedly reduced the serum anti-dsDNA antibody (IgG) titers and virtually abolished the induction of glomerulonephritis [5].

Psychiatry related information on Ads1

• T cells (CD8+) with specific suppressor activity against anti-dsDNA antibody (16/6 Id+) were generated in vitro [6].
• Some phenotypes, such as glomerulonephritis (GN) and anti-chromatin IgG antibody production, were more penetrant in females, but others, such as anti-dsDNA antibody production, did not show a gender bias [7].

High impact information on Ads1

• Thus, B cells from NZB.H-2bm12 mice, because of previous activation in vivo, can proceed to IgG anti-dsDNA antibody production in vitro without direct T cell interaction [8].
• We have identified a new murine V kappa family that contains five to seven members, one member of which encodes the L chain V region of an anti-dsDNA antibody produced by a BALB/c hybridoma, C8 [9].
• The present genetic studies using (NZB X NZW)F1 X NZW backcross mice and their second through fourth generation progeny revealed that Agp-1 and Ads-1 exist in common or are closely linked on chromosome 17 of NZB mice and are related to the occurrence of renal disease [10].
• A combined effect of 2 unlinked dominant NZB loci (Ads-1 and Ads-2) is required for the production of anti-double-stranded DNA (anti-dsDNA) antibodies in these mice [10].
• Anti-dsDNA antibody levels, however, were reduced in the absence of Ccr2 [11].

Biological context of Ads1

• The effects of anti-idiotypic antibody on antibody production and apoptosis of anti-dsDNA antibody producing cells [12].
• We observe that transgenic B cells secreting anti-dsDNA antibody in these mice are T independent and display a marginal zone like phenotype althought they do not reside in the MZ [13].
• RESULTS: Two types of anti-dsDNA antibody producing hybridomas (G1-2, gamma and kappa chains; M2-10, mu and kappa chains) were treated with anti-Id and it was found that: (1) the amount of anti-dsDNA antibody production decreased; (2) the rate of transcription and cellular proliferation did not decrease; and (3) the level of apoptosis increased [12].
• These results suggest that paclitaxel is beneficial in the suppression of autoimmunity in this strain of mice by reducing the anti-dsDNA antibody titer and the BUN, prolonging survival [14].
• Anti-dsDNA antibody up-regulates interleukin 6, but not cyclo-oxygenase, gene expression in glomerular mesangial cells: a marker of immune-mediated renal damage [15]?

Anatomical context of Ads1

• When we examined direct T cell help for the IgG anti-dsDNA antibody response, we found that we could distinguish the actions of the two cloned T cell lines studied [8].
• We demonstrate here that, in both lupus-prone and normal mouse strains, strong anti-dsDNA antibody responses can be induced by dendritic cells (DC) that have ingested syngeneic necrotic (DC/nec), but not apoptotic (DC/apo), cells [16].
• These data suggest that control of anti-dsDNA antibody production may rely on elements from both the innate and adaptive arms of the immune system [17].
• HBO(2) treatment resulted in increased survival, decreased proteinuria, alterations in lymphocyte-subset redistribution, reduced anti-dsDNA antibody titers, and amelioration of immune-complex deposition in groups A and B. Our data demonstrated that HBO(2) therapy attenuated disease severity in NZB/W F1 mice [4].
• A murine monoclonal anti-dsDNA antibody, mAb 3E10, was selectively transported into skeletal muscle cells in vivo [18].

Associations of Ads1 with chemical compounds

• However, they can be induced to secrete anti-dsDNA antibody following activation with T cell-derived factors as well as with lipopolysaccharide (LPS) and they can be recovered by somatic cell hybridization even in the absence of LPS stimulation prior to fusion [19].
• To investigate the effects of prostaglandin E1 (PGE1) on IgM and IgG class anti-dsDNA antibody production by young and aged female New Zealand black/white (NZB/W) F1 mouse spleen cells in vitro [20].
• Spleen cells brought to a microculture system using flat-bottomed polystyrene plates produced anti-dsDNA antibody clearly detectable by solid-phase radioimmunoassay [21].
• CONCLUSION: The anti-Id suppressed the production of anti-dsDNA antibody in two cells by inducing apoptosis, as did prednisolone [12].

Other interactions of Ads1

• Treatment with mAb IL-6R significantly reduced anti-dsDNA antibody levels after Week 2 of treatment, but these values rebounded at Week 4 [22].
• In this report we cloned and sequenced the heavy chain variable region (VH) of a monoclonal anti-dsDNA antibody, mAb 3E10, derived from MRL/lpr mice with lupus nephritis previously shown to express an idiotype associated with nephritis in murine and human lupus [23].
• Chemical induction of HO-1 suppresses lupus nephritis by reducing local iNOS expression and synthesis of anti-dsDNA antibody [24].
• Despite the improvement in survival, treatment with TNF-alpha did not inhibit anti-dsDNA antibody production [25].

Analytical, diagnostic and therapeutic context of Ads1

• A combination of the microculture system and solid-phase radioimmunoassay was recommended for the characterization of anti-dsDNA antibody-forming cells [21].
• Idiotypic vaccination with a murine anti-dsDNA antibody: phase I study in patients with nonactive systemic lupus erythematosus with nephritis [26].
• They were serially semiquantitated for proteinuria, and serum IgG anti-dsDNA antibody was measured by ELISA [27].

References