B-Cell Stimulatory Factor-1/Interleukin 4

Paul, W E; Ohara, Junichi

doi:10.1146/annurev.iy.05.040187.002241

Cited by 554 publications

(154 citation statements)

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“…Besides adding another item to a long list of diverse IL-4 functions (52,53), results presented in this report support the notion that functional T cell longevity can be regulated by cytokines during initial antigen encounter and provide a foundation on which rational and possibly CTL-specific vaccine development can be approached. These potentials are made more relevant in view of the critical role played by CD8 ϩ T cells in combating cancer and virus infection and the relative paucity of effective antivirus and anticancer drugs.…”

Section: Resultssupporting

confidence: 71%

Potent induction of long-term CD8+ T cell memory by short-term IL-4 exposure during T cell receptor stimulation

Huang

Chen²,

Chen³

et al. 2000

Proceedings of the National Academy of Sciences

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An important goal of vaccination is to achieve long-term survival of functional memory T cells. Using a MHC-compatible adoptive transfer system, we show here that a short, 3-day IL-4 but not IL-2 or IL-12 exposure during in vitro T cell receptor stimulation of naive CD8 ؉ T cells induced long-lasting in vivo memory. Such long-term memory CD8 ؉ T cells expressed antigen-specific cytotoxicity and the potential for IFN-␥ and IL-4 production. Our results support the concept that functional T cell longevity can be regulated by cytokines during initial antigen encounter and provide a rational foundation for vaccine development. They also may have implications in formulating optimal therapeutic regimens of ex vivo expanded autologous cancer-and HIV-specific CD8 ؉ T cells. In addition, the availability of large numbers of memory CD8 ؉ T cells generated through our high-efficiency system should facilitate progress in the molecular dissection of CD8 ؉ T cell memory development.

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Section: Resultssupporting

confidence: 71%

Potent induction of long-term CD8+ T cell memory by short-term IL-4 exposure during T cell receptor stimulation

Huang

Chen²,

Chen³

et al. 2000

Proceedings of the National Academy of Sciences

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“…CSR from IgM to IgG, IgE, and IgA results from recombination between the donor S region and one of the recipient ␥, , or ␣ S regions and is induced when surface receptors are engaged by different combinations of mitogens and cytokines (42,43). The resulting signals lead to transcription of GLT (44).…”

Section: Discussionmentioning

confidence: 99%

Differential regulation of histone acetylation and generation of mutations in switch regions is associated with Ig class switching

Luo

Scharff

2004

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

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Class switch recombination (CSR) allows B cells to make effective protective antibodies. CSR involves the replacement of the constant region with one of the downstream constant regions by recombination between the donor and recipient switch (S) regions. Although histone H3 hyperacetylation in recipient S regions was recently reported to coincide with CSR, the relative histone H3 and H4 acetylation status of the donor and recipient S regions and the relationship between the generation of mutations and histone hyperacetylation in S regions have not been addressed. Here we report that histone H3 and H4 were constitutively hyperacetylated in the donor S region before and after different mitogen and cytokine treatments. We observed an increased frequency of mutations in hyperacetylated S␥ DNA segments immunoprecipitated with anti-acetyl histone antibodies. Furthermore, time course experiments revealed that the pattern of association of RNA polymerase II with S regions was much like that of H3 hyperacetylation but not always like that of H4 hyperacetylation. Collectively, our data suggest that H3 and H4 histone hyperacetylation in different S regions is regulated differently, that RNA polymerase II distribution and H3 hyperacetylation reflect the transcriptional activity of a given S region, and that transcription, hyperacetylation, and mutation are not sufficient to guarantee CSR. These findings support the notion that there are additional modifications and͞or factors involved in the complex process of CSR.H igh-affinity IgG, IgA, and IgE antibodies protect higher organisms from infection by pathogenic organisms and other environmental threats. The generation of effective protective antibodies requires B cells to carry out somatic hypermutation (SHM) and class switch recombination (CSR), two related but quite different DNA transactions (1). SHM introduces many point mutations in the variable (V) regions of the Ig heavy and light chain genes that encode the antigen-binding site of the antibody molecule (2). In contrast to SHM, CSR is a region-specific recombinationdeletion process that requires the generation of double-stranded DNA breaks (DSB) (3). These DSB are generated in the donor switch (S) region that is just upstream of the constant (C) region gene and in a downstream recipient ␥, , or ␣ S region (4, 5). Recombination then brings one of those downstream C regions into proximity to the V region. This allows the mutated heavy chain V region to be expressed with one of the C regions so that each antigen-binding site will be able to mediate different effector functions and be distributed throughout the body.Despite the different outcomes of SHM and CSR, activationinduced cytidine deaminase (AID) is required for both processes (6) presumably because of its ability to deaminate deoxycytidine to deoxyuridine on single-stranded DNA (ssDNA) (7-11). Both SHM and CSR require transcription (12), suggesting that the ssDNA substrate for AID is created by the generation of transcription bubbles (7) and͞or perhaps triplex RNA...

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“…In NOG mice, the lack of detectable serum Igs might be due to inactivation of IL-4 and IL-7 receptors. The IL-7 receptor is essential for the development of B cells, in particular for the developmental progression from pro-B cells to pre-B cells [18], and IL-4 plays an important role in B cell activation [14]. The inactivation of IL-4 and IL-7 receptors sharing IL-2Rγ as a subunit in NOG mice may result in the suppression of B cell development in these mice.…”

mentioning

confidence: 99%

Immunodeficient NOD-scid IL-2R.GAMMA.null Mice Do Not Display T and B Cell Leakiness

et al. 2011

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[7]. These characteristics indicate that NOG mice constitute an excellent humanized mouse model in which engrafted cells and tissues function as they do in humans [8]. At present, various studies using humanized mouse models based on NOG mice have been carried out in various fields of human disease research [10,11,19], where they have proved to be very useful tools. The immunological deficiencies that underlie the high engraftment levels of NOG mice are derived from three immunodeficient mice. Reduced macrophage function and complement activity originate from a NOD inbred strain [17], T and B cell deficiencies from SCID mice with the scid mutation [1], and NK cell deficiency and multiple cytokine dysfunction from null KO mice [13]. Among these immunodeficiencies, the lack of functional T and B cells in mice with the scid mutation is a result of defective gene recombination events in T cell receptors (TCR) and immunoglobulins [16]. These mice -Note-

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B-Cell Stimulatory Factor-1/Interleukin 4

Cited by 554 publications

References 0 publications

Potent induction of long-term CD8+ T cell memory by short-term IL-4 exposure during T cell receptor stimulation

Potent induction of long-term CD8+ T cell memory by short-term IL-4 exposure during T cell receptor stimulation

Differential regulation of histone acetylation and generation of mutations in switch regions is associated with Ig class switching

Immunodeficient NOD-scid IL-2R.GAMMA.null Mice Do Not Display T and B Cell Leakiness

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