T-bet regulates IgG class switching and pathogenic autoantibody production

Peng, Stanford L.; Szabo, Susanne J.; Glimcher, Laurie H.

doi:10.1073/pnas.082114899

Cited by 432 publications

(458 citation statements)

References 45 publications

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“…ELISA measurements showed that non-smoking diabetic women in group 2 had a higher level of serum IgA, IgG and IgM compared to normal women in group 1. The dramatic increase determined by ELISA was expected due to diabetic complications in support to previous studies (26)(27)(28). It has been estimated that exposure to environmental tobacco smoke in pregnancy results in birth weight reduction by approximately 20-30g (29,30).…”

Section: Discussionsupporting

confidence: 90%

The influence of tobacco smoking on humoral immune response in insulin dependent diabetic pregnancy

Haroun

2006

Indian J Clin Biochem

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Section: Discussionsupporting

confidence: 90%

The influence of tobacco smoking on humoral immune response in insulin dependent diabetic pregnancy

Haroun

2006

Indian J Clin Biochem

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“…We also analyzed mice for deposition of IgG2b and IgG2c, as these (in combination with IgG3) are believed to be the major pathogenic IgG isotypes. 14 We found no differences in the amount and pattern of either IgG2b or IgG2c staining between IFNAR þ / þ and IFNAR À/À B6.Nba2 mice (Figure 3a).…”

Section: Resultsmentioning

confidence: 79%

Type I interferon signaling is involved in the spontaneous development of lupus-like disease in B6.Nba2 and (B6.Nba2 × NZW)F1 mice

et al. 2007

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Several studies have described a role for type I interferons (IFNab) in the initiation and/or prolongation of autoimmune diseases. Most pronounced has been the association of disease activity with what is now known as 'the interferon signature' of gene expression in peripheral blood mononuclear cells from lupus patients. In correlation, studies have shown that inhibition of IFNab signaling abrogates disease in various mouse models of lupus. New Zealand black (NZB) and B6.Nba2 congenic mice spontaneously develop elevated levels of serum anti-nuclear autoantibodies (ANAs). Nevertheless, neither of these strains develop fatal renal disease. The female F1 offspring of NZB or B6.Nba2 crossed with New Zealand white (NZW) mice do, however, develop kidney disease. We have previously shown that increases in endogenous IFNab levels in (B6.Nba2 Â NZW)F1 mice leads to accelerated development of renal disease in an IFNab-dependent manner. We now show that B6.Nba2 and (B6.Nba2 Â NZW)F1 mice deficient for the IFNab-receptor fail to develop ANA and renal disease, although the mice have substantial immune complex deposition in the glomeruli. Thus, endogenous IFNab might influence disease by affecting B-cell activation and differentiation, as well as the kidneys' susceptibility to damage, the latter perhaps through induction of a local inflammatory milieu.

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“…These results were confirmed by the generation of T-bet-deficient mice, which lack Th1 cells and instead exhibit an enlarged Th2 compartment (6). In addition to Th1 cells, T-bet is detected in several other immune cells, including CD8 ϩ T cells (3,5,6), dendritic cells (7), B cells (8), NK cells and NKT cells (9 -11). T-bet regulates expression of numerous immune systemassociated genes, including cytokines (4), cytokine receptors (9 -12), chemokines (7,11), chemokine receptors (4,11,13) and cytotoxicity (9,11).…”

Section: Temporal Dissection Of T-bet Functionsmentioning

confidence: 79%

Temporal Dissection of T-bet Functions

Matsuda

George²,

Hagman

et al. 2007

The Journal of Immunology

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T-bet is a transcription factor of the T-box family that regulates the expression of numerous immune system-associated genes. T-bet directs the acquisition of the Th1-associated genetic program in differentiating CD4+ lymphocytes. It also influences the development of NK and NKT cells through its regulation of the IL-2/IL-15Rβ-chain (CD122) and the trafficking of these lymphocytes through CxCR3. The temporal requirements of T-bet activity for the production of IFN-γ and the regulation of CD122 and CxCR3 expression remain undefined. We produced an ectopically controllable form of T-bet by fusing its C-terminal domain with a mutated ligand-binding domain of human estrogen receptor α. By temporally controlling the expression of T-bet-estrogen receptor α by the addition or removal of 4-hydroxytamoxifen (4-HT), we show that IFN-γ, CD122, and CxCR3 are direct gene targets of T-bet whose expression are acutely regulated by T-bet activity.

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T-bet regulates IgG class switching and pathogenic autoantibody production

Cited by 432 publications

References 45 publications

The influence of tobacco smoking on humoral immune response in insulin dependent diabetic pregnancy

The influence of tobacco smoking on humoral immune response in insulin dependent diabetic pregnancy

Type I interferon signaling is involved in the spontaneous development of lupus-like disease in B6.Nba2 and (B6.Nba2 × NZW)F1 mice

Temporal Dissection of T-bet Functions

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