Modulation of human IgE synthesis by transforming growth factor-β

Wu, Cheng-Hung; Brinkmann, Volker; Cox, David A.; Heusser, C.; Delespesse, Guy

doi:10.1016/0090-1229(92)90103-u

Cited by 20 publications

(7 citation statements)

References 36 publications

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“…IL-13 and IL-10), even suppression of IgE is environment directed. It has been reported that at a later stage of differentiation, IgE B cells are refractory to the inhibitory effect of TGFβ, as shown by the slight but significant increase in the spontaneous secretion of IgE by PBMC of atopic patients [30]. Finally, TGFβ1 downregulation of IgE may be a mechanism where Th2 inflammation may still be prominent, with no increase in IgE, a situation that might be seen in intrinsic asthma for example.…”

Section: Discussionmentioning

confidence: 99%

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Association of Transforming Growth Factor-β1 Single Nucleotide Polymorphism C-509T with Allergy and Immunological Activities

Meng

Thongngarm²,

Nakajima³

et al. 2005

Int Arch Allergy Immunol

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Background: A single nucleotide polymorphism (SNP) C-509T within the tumor growth factor β1 (TGFβ1) gene has been associated with atopic asthma and asthma severity. To further understand the mechanisms involved, the association of C-509T with allergy, T-lymphocyte proliferation and plasma TGFβ1 concentration has been explored in a case-control study with allergic and non-allergic subjects. Methods: The recruited subjects including allergic (n = 38) and nonallergic (n = 25) participants have been genotyped for C-509T using allele discrimination assay. Association of C-509T with allergy status was examined using logistic regression analysis in both dominant and recessive models. Association of C-509T with T-cell proliferation in control and antigen-stimulated peripheral blood mononuclear cells (PBMCs), plasma TGFβ1 and total IgE level were tested by multiple regression analysis. Results: Individuals with homozygous mutant TT genotype showed a higher risk of allergy (TT: odds ratio = 5.099, 95% confidence limit: 1.355–19.190, p = 0.016) after covariates were adjusted. A trend to increased plasma TGFβ1 in subjects with T allele has been discovered. In the meantime, the T allele is associated with lower T cell proliferation in controls and maximum response to above antigens. A low T-cell proliferation is correlated with higher plasma TGFβ1 concentration (p < 0.01). The in vitro studies confirmed the suppressing effect of TGFβ1 on T-cell proliferation at physiological range. A significant inhibitory effect on IL-4 production was also observed. Conclusions: A C to T base change in TGFβ1 SNP C-509T has been associated with a higher risk of allergy. The mechanisms are not clear. Elevated TGFβ1 levels associated with the C-509T polymorphism might suppress immune activation as well as Th2 cytokine production.

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Section: Discussionmentioning

confidence: 99%

“…This is because the TGFβ1-induced downregulation of the IL-2 receptor at both protein and mRNA level has been reported [29]. TGFβ1 has been shown to inhibit IL-2-induced tyrosine phosphorylation, activation of Jak-1 and Stat 5, and IL-2-induced expression of α and β chains of IL-2R [30]. Interaction of IL-4 and IFNγ has been reported.…”

Section: Discussionmentioning

confidence: 99%

Association of Transforming Growth Factor-β1 Single Nucleotide Polymorphism C-509T with Allergy and Immunological Activities

Meng

Thongngarm²,

Nakajima³

et al. 2005

Int Arch Allergy Immunol

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“…Since sCD23 and sCD54 did not reverse ATRA mediated inhibition of IgE synthesis completely (see Table 2), we searched for further molecules that might explain the effects of ATRA on this process by analysing the production of cytokines like IL-6, IL-8, IL-10, TGFb and IFNg which are all known to modulate IgE production in B cells [11,12,14,18]. Under these conditions, production of IL-8 and of IFNg remained unchanged in the presence of ATRA in unstimulated and anti-CD40 plus IL-4 stimulated B cells (data not shown).…”

Section: Down-regulation Of Il-6 Production By Atra In Anti-cd40 Plusmentioning

confidence: 99%

Retinoic acid inhibits CD40 plus IL-4 mediated IgE production through alterations of sCD23, sCD54 and IL-6 production

et al. 2005

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“…lL-5, IL-6 and hydrocortisone enhance IL-4-indueed IgE synthesis but are not capable of inducing IgE production in the absence of IL-4 (29)(30)(31). IgE produetion is inhibited by IFN-a, prostaglandin E,, IL-12, pafacether and TGF-p (32)(33)(34)(35)(36). IFN-y is a Thl or ThO cell-derived Lk that suppresses IgE production (32,33,37).…”

Section: Cd4+ T-cell Subsets Defined By Lymphokine Patternmentioning

confidence: 99%