Increased expression of Ia antigens on resting B cells: an additional role for B-cell growth factor.

Noelle, Randolph J.; Krammer, Peter H.; Ohara, Junichi; Uhr, Jonathan W.; Vitetta, Ellen S.

doi:10.1073/pnas.81.19.6149

Cited by 387 publications

(163 citation statements)

References 23 publications

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“…IL-4 signaling promotes Ig isotype switch [32], a phenomenon mediated by Stat6 [33]. IL-4 also promotes the up-regulation of MHC class II molecules [34] and the viability of murine B lymphocytes in vitro [35]. Here we demonstrate that IL-4 is also implicated in promoting the presentation of MHC class I-restricted peptides to CD8 T cells by B lymphocytes.…”

Section: Discussionmentioning

confidence: 53%

“…Moreover, since CD8 T cell priming in the presence of IL-4 down-regulates IFN-c [37] the upregulation of IFN-c observed herein rules out a direct activation of CD8 T cells by IL-4. Finally, although IL-4 signaling is known to up-regulate MHC class II molecules in B lymphocytes [33,34], to the best of our knowledge there are no reports showing that IL-4 up-regulates MHC class I molecules. Further studies will have to address these issues in greater detail to investigate the possible role of IL-4 in promoting to transcriptional activation of MHC class I genes and/or enhancing antigen processing.…”

Section: Discussionmentioning

confidence: 91%

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CD8 T cell priming by B lymphocytes is CD4 help dependent

Castiglioni¹,

Gerloni²,

Cortez-Gonzalez³

et al. 2005

Eur J Immunol

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While it is generally accepted that B lymphocytes can present antigen and activate CD4 T cells, priming of CD8 T cells by B lymphocytes remains controversial. Recently, we showed that mice injected with genetically programmed B lymphocytes generate antigen specific CD4 and CD8 T cell responses in vivo that could also be induced in mice lacking functional dendritic cells. To gain further insights into the requirements for T cell priming by antigen-presenting B lymphocytes, in vitro experiments were performed using ovalbumin (OVA) and OVA-specific TCR-transgenic CD4 and CD8 T cells. We found that while B lymphocytes can directly prime CD4 T cells, the activation of CD8 T cells requires T cell help. Transfer experiments show that help can either be contact dependent or be mediated by soluble factors in the supernatants of activated OVAspecific CD4 T cells. Furthermore, the effect of activated CD4 T cells can be replaced by soluble recombinant IL-4. Collectively, the data show the existence of different requirements for priming of CD4 and CD8 T cells and point to the previously unappreciated fact that the induction of CD8 T cell responses by B lymphocytes requires T cell help.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 91%

CD8 T cell priming by B lymphocytes is CD4 help dependent

Castiglioni¹,

Gerloni²,

Cortez-Gonzalez³

et al. 2005

Eur J Immunol

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“…Recent evidence (7,8) has established that BSF-1 is a potent activation factor for resting B cells. In contrast, BSF-1 has little or no capacity to sustain proliferation of B cell blasts after treatment with anti-Ig (9) or anti-~ plus BSF-1 (20).…”

Section: Discussionmentioning

confidence: 99%

Serological, biochemical, and functional identity of B cell-stimulatory factor 1 and B cell differentiation factor for IgG1.

Vitetta

Ohara

Myers

et al. 1985

The Journal of Experimental Medicine

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379

149

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By three criteria, we have demonstrated that B cell stimulatory factor (BSF-1) and B cell differentiation factor (BCDF-gamma) are the same lymphokine. Highly purified preparations of high performance liquid chromatography-purified or affinity-purified BSF-1 had BCDF-gamma activity but not BCDF-mu activity. A monoclonal anti-BSF-1 antibody coupled to Sepharose depleted both BSF-1 and BCDF-gamma activity but not BCDF-mu activity from two different T cell supernatants. Soluble monoclonal anti-BSF-1 blocked the BSF-1 and BCDF-gamma but not the BCDF-mu responses. These results suggest that BSF-1 acts on both resting and activated B cells to induce different effects.

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“…[6][7][8] Like many cytokines, interleukin-4 (IL-4) has pleiotropic effects on immune cells of multiple lineages and therefore its potential to induce immunoreactivity to CNS tumors has been explored. IL-4 increases surface major histocompatibility complex class II antigens in B cells, 9 stimulates the growth of both normal helper and cytotoxic T cells, 10 including tumor infiltrating lymphocytes 11 and upregulates the expression of vascular cell adhesion molecule 1 (VCAM-1) on activated endothelia. 12 In addition, the local production of IL-4 from genetically engineered tumor cells induces potent protective 13,14 and therapeutic immunity 15,16 in non-CNS animal models.…”

Section: Introductionmentioning

confidence: 99%

Effective cytokine gene therapy against an intracranial glioma using a retrovirally transduced IL-4 plus HSVtk tumor vaccine

Okada

Giezeman‐Smits

Tahara³

et al. 1999

Gene Ther

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To explore the potential for molecular immunotherapies in rejected the same challenge with wild-type 9L. More the treatment of malignant gliomas, we evaluated the effiimportantly, treatment of established (day 3) intracranial 9L cacy of subcutaneous tumor cell vaccines in the treatment tumors with genetically engineered tumor cells resulted in of intracranial 9L tumors, using 9L gliosarcoma cell lines long-term survival (Ͼ100 days) for 25-43% of 9L-IL4-Tk stably transduced with the murine interleukin-4 cDNA (9L-immunized animals and for 27% of nonirradiated 9L-IL4 IL4), the herpes simplex virus-thymidine kinase cDNA (9L-immunized animals. In striking contrast, no 9L-Tk, 9L-neo Tk) or both (9L-IL4-Tk). The expression of multiple genes or irradiated 9L-IL4 immunized animals survived for more from a single transcript was achieved by incorporating than 33 days. As a marker of a cellular immune response, internal ribosomal entry site (IRES) cassettes in the retrovisplenocytes from nonirradiated 9L-IL4, 9L-Tk or 9L-IL4-Tk ral constructs. Subcutaneous immunization of rats with immunized animals produced interferon-gamma (IFN-␥) in nonirradiated 9L-IL4 cells or 9L-IL4-Tk cells followed by greater amounts than those from 9L-neo immunized or treatment with ganciclovir (GCV) completely protected the Hank's balanced salts solution (HBSS) treated animals animals from a subsequent intracranial challenge with wildwhen stimulated with wild-type 9L in vitro. Our findings suptype 9L cells. In contrast, only 50% of animals immunized port the use of tumor cell vaccines expressing the IL-4 and with 9L-Tk cells and 0% of 9L-neo immunized animalsHSVtk genes for the treatment of malignant gliomas.

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Increased expression of Ia antigens on resting B cells: an additional role for B-cell growth factor.

Cited by 387 publications

References 23 publications

CD8 T cell priming by B lymphocytes is CD4 help dependent

CD8 T cell priming by B lymphocytes is CD4 help dependent

Serological, biochemical, and functional identity of B cell-stimulatory factor 1 and B cell differentiation factor for IgG1.

Effective cytokine gene therapy against an intracranial glioma using a retrovirally transduced IL-4 plus HSVtk tumor vaccine

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