Vasoactive intestinal peptide induces S(alpha)/S(mu) switch circular DNA in human B cells.

Fujieda, Shigeharu; Waschek, James A.; Zhang, K; Saxon, Andrew

doi:10.1172/jci118944

Cited by 50 publications

(37 citation statements)

References 61 publications

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“…These binding data are in close agreement with the VPAC 1 and VPAC 2 mRNA expression studies (Qian et al, 2001). There are few VPAC receptor binding studies in nontransformed and isolated B cells (Ottaway et al, 1990;Tatsuno et al, 1991) despite the biological effects mediated throughout VPAC receptors (Kimata et al, 1992(Kimata et al, , 1996Fujieda et al, 1996;Shimozato and Kincade, 1997). Available data came from transformed B cell lines, i.e., SKW 6.4 B cells with a K d of 59 nM , Raji B cells with a K d of 0.8 nM (Robichon et al, 1993), Nalm 6 preB cells with a K d of 12.6 nM, and Dakiki plasma cells with a K d of 9.1 nM (O'Dorisio et al, 1989(O'Dorisio et al, , 1992.…”

Section: B Biochemical Pharmacological and Signaling Key Features supporting

confidence: 78%

The Significance of Vasoactive Intestinal Peptide in Immunomodulation

Delgado

Pozo²,

Ganea³

2004

Pharmacol Rev

371

319

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Section: B Biochemical Pharmacological and Signaling Key Features supporting

confidence: 78%

The Significance of Vasoactive Intestinal Peptide in Immunomodulation

Delgado

Pozo²,

Ganea³

2004

Pharmacol Rev

371

319

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“…This κB site neither induces nor enhances the activation of I α promoters 55 , suggesting that NF-κB regulates IgA CSR at a level other than germline C α gene transcription. Most likely, NF-κB mediates the Remarkably, CD40L can induce IgA class switching in combination with cytokines other than TGFβ1, including interleukin-2 (IL-2), IL-4, IL-5, IL-6, IL-10 and VIP (vasoactive intestinal peptide) 58,60,61,67,69,70 . These cytokines may enhance the production of endogenous TGFβ1 by B cells exposed to CD40L, thereby triggering IgA CSR through an autocrine TGFβ1-dependent loop 61 .…”

Section: Role Of Cd40l In Csr To C αmentioning

confidence: 99%

“…Remarkably, CD40L can induce IgA class switching in combination with cytokines other than TGFβ1, including interleukin-2 (IL-2), IL-4, IL-5, IL-6, IL-10 and VIP (vasoactive intestinal peptide) 58,60,61,67,69,70 . These cytokines may enhance the production of endogenous TGFβ1 by B cells exposed to CD40L, thereby triggering IgA CSR through an autocrine TGFβ1-dependent loop 61 .…”

Section: Role Of Cd40l In Csr To C αmentioning

confidence: 99%

The regulation of IgA class switching

2008

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IgA class switching is the process whereby B cells acquire the expression of IgA, the most abundant antibody isotype in mucosal secretions. IgA class switching occurs via both T-celldependent and T-cell-independent pathways, and the antibody targets both pathogenic and commensal microorganisms. This Review describes recent advances indicating that innate immune recognition of microbial signatures at the epithelial-cell barrier is central to the selective induction of mucosal IgA class switching. In addition, the mechanisms of IgA class switching at follicular and extrafollicular sites within the mucosal environment are summarized. A better understanding of these mechanisms may help in the development of more effective mucosal vaccines.IgA has been selected throughout evolution to provide a first line of immune protection at mucosal surfaces -vulnerable frontline sites that are exposed to potentially harmful commensal, airborne, ingested and sexually transmitted agents. Growing evidence indicates that IgA uses a high-affinity binding system to neutralize microbial toxins and pathogens, and a low-affinity binding system to prevent commensal bacteria from breaching the mucosal surface 1 . This latter process is known as immune exclusion and has a fundamental role in the intestine, which is home to a number of commensal bacteria exceeding that of human cells by an estimated order of magnitude 2 .Remarkably, intestinal IgA achieves both immune protection and immune exclusion in a non-inflammatory manner, thereby promoting the establishment of a sustainable hostmicrobial mutualism 3 . The complex relationship between IgA and the intestinal microbiota is further exemplified by the fact that IgA responses are highly dependent on intestinal colonization by commensal microorganisms. Indeed, the number of IgA-secreting B cells is dramatically reduced in the intestine of germ-free animals and these cells are virtually absent in neonates before their exposure to bacteria 3 .In this Review, I summarize recent advances in our understanding of the function, regulation and geography of IgA class switching. In addition to analysing the signalling pathways underlying IgA class switching, I discuss new evidence indicating that commensal bacteria Competing interests statementThe author declares no competing financial interests. DATABASES Function of IgA class switchingAntibody diversification is essential for the immune system to mount protective humoral responses. B cells diversify their antibody repertoire through three main genetic alterations that occur in two distinct phases of B-cell development. In the antigen-independent phase, B-cell precursors lodged in the bone marrow generate antigen recognition diversity by assembling the exons that encode immunoglobulin heavy (H) and light (L) chain variable regions from individual variable (V), diversity (D) and joining (J) gene segments through V(D)J gene recombination 4 . This process is initiated by a lymphoid-cell-and sequencespecific RAG1 (recombination-activating gene 1...

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“…Then, 1 ml of the resulting first-strand cDNA was used for each PCR. The primers for human HDAC3 and b-actin (Fujieda et al, 1995) were used in the reactions. The primers were as follows: HDAC3 upstream, 5 0 -GTCGATGTTATTTCCCCAGC-3 0 (nucleotides 79-98 of human HDAC3 cDNA), HDAC3 downstream, 5 0 -CCGATTT GGTGATGGGTGTT-3 0 (nucleotides 862-881).…”

Section: Rt-pcr Analysismentioning

confidence: 99%

Inhibition of histone deacetylase 3 stimulates apoptosis induced by heat shock under acidic conditions in human maxillary cancer

et al. 2005

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To elucidate the molecular mechanisms for the enhancement of heat-induced apoptosis on exposure to acidic conditions, human maxillary carcinoma IMC-3 cells were heat-shocked at 441C for 30 min at either pH 7.4 or 6.7. Analyses with cDNA arrays, the reverse transcriptionpolymerase chain reaction (RT-PCR), and Western blotting were performed. We found that histone deacetylase 3 (HDAC3) was specifically induced after hyperthermia at 441C for 30 min at pH 6.7. Although the cytotoxicity of heating at 441C for 30 min was enhanced by decreasing the pH from 7.4 to 6.7, it was enhanced even more by antisense RNA oligonucleotides for HDAC3. The induction of G 2 /M arrest after heating occurred earlier at pH 6.7 than at pH 7.4. The inhibition of HDAC3 by the antisense RNA oligonucleotides suppressed partially the induction of G 2 /M arrest, resulting in an enhancement of the apoptosis caused by the heating under acidic conditions. Antisense RNA oligonucleotides for HDAC3 enhanced apoptosis 48 h after hyperthermia at 431C for 30 min in vivo. Analyses of p65 activity suggested that NF-jB is involved in this enhancement of hyperthermia. HDAC3 may be a novel target enhancing hyperthermia and combined treatment with hyperthermia and HDAC inhibitors is a possible modality for cancer therapy.

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Vasoactive intestinal peptide induces S(alpha)/S(mu) switch circular DNA in human B cells.

Cited by 50 publications

References 61 publications

The Significance of Vasoactive Intestinal Peptide in Immunomodulation

The Significance of Vasoactive Intestinal Peptide in Immunomodulation

The regulation of IgA class switching

Inhibition of histone deacetylase 3 stimulates apoptosis induced by heat shock under acidic conditions in human maxillary cancer

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