Role for interleukins 5 and 6 in IgA synthesis

Beagley, Kenneth W.; Eldridge, John H.; Aicher, Wilhelm K.; Hirano, Toshio; Kishimoto, Tadamitsu; Lee, F; Kiyono, Hiroshi; McGhee, Jerry R.

doi:10.1007/978-94-009-1848-1_31

Cited by 4 publications

(5 citation statements)

References 8 publications

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“…The increase in AOCC numbers in loops treated with exogenous IL‐6 is consistent with the role identified for this cytokine as a B cell growth factor 8 , 9 . However, in view of the evidence that IL‐6 acts preferentially in enhancing IgA expression in vitro 3 , 10 and experiments performed by Pockley and Montgomery, who demonstrated a significant increase in IgA production in rat tears and in cultures of ex vivo lacrimal glands after topical application of IL‐6 together with IL‐5, 11 it is surprising that there was not a more pronounced effect on IgA‐AOCC numbers in the experiments reported here. A significant effect may have been observed if a larger number of animals had been included in the experiment.…”

Section: Resultssupporting

confidence: 80%

“…We have shown previously in in vitro studies that surface IgA + cells (but not sIgA − cells) from mouse Peyer's patch (PP) produce copious amounts of IgA when cultured in the presence of recombinant murine IL‐6 3 . The potential role of IL‐6 in antibody expression in the intestine is supported by our data from in vivo studies of IL‐6 expression and function.…”

Section: Introductionsupporting

confidence: 68%

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Exogenous IL‐6 promotes enhanced intestinal antibody responses in vivo

et al. 1998

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It is well documented that IL-6 plays a critical role in B cell terminal differentiation, and in mucosal sites it stimulates proliferation and large-scale secretion of immunoglobulin by B cells, especially those committed to IgA production. The close juxtaposition of IL-6 mRNA+ cells to plasma cells in the intestinal lamina propria supports the proposition that IL-6 production in situ is an important factor determining the outcome of antibody responses at that site. However, it has not been established previously whether exogenous IL-6 could boost antibody responses in the intestine if administered with a challenge antigen. Using a resected gut loop (Thiry-Vella loop) model, we have been able to demonstrate that in mice with double loops, antibody containing cell responses to lumenal administration of ovalbumin were 50% greater in loops given intralumenal recombinant IL-6 with the challenge antigen, than in loops challenged with antigen alone. This demonstrates the efficacy of IL-6 in promoting accumulation of antibody secreting cells in the gut, and suggests a potential therapeutic role for IL-6 to enhance responses to mucosal vaccines.

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Section: Resultssupporting

confidence: 80%

Section: Introductionsupporting

confidence: 68%

Exogenous IL‐6 promotes enhanced intestinal antibody responses in vivo

et al. 1998

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“…Based on the finding that IL-6 promotes IgA secretion by Peyer's patches (33) and that IL-6-/-mice fail to develop strong mucosal antibody responses to viral infection (34), we examined the course ofGI candidiasis in IL-6-/and IL-6+/+ mice. Course and outcome of GI infection are influenced by the host mucosal immune status (25).…”

Section: Resultsmentioning

confidence: 99%

Impaired neutrophil response and CD4+ T helper cell 1 development in interleukin 6-deficient mice infected with Candida albicans.

Romani

Mencacci

Cenci

et al. 1996

The Journal of Experimental Medicine

297

185

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To define the role of interleukin (IL)6 in Candida albicans infection, IL-6 deficient mice were assessed for susceptibility to systemic or gastrointestinal infection, as well as for parameters of elicited T helper cell (Th) immunity. IL-6-deficient mice were more susceptible than wild-type mice to either type of infection caused by virulent C. albicans. In response to systemic challenge with a live vaccine strain of yeast, IL-6-deficient mice failed to mount Th1-associated protective immunity, but the resulting Th2-biased response could be redirected to the Th1 phenotype by IL-10 neutralization. Severe impairment of the macrophage and neutrophil response to infection was observed in IL-6-deficient mice, but administration of IL-6 would increase both neutrophil response and resistance to infection. IL-6 seems to oppose the Th2-promoting role of IL-10 in candidiasis, its early regulatory activity involving effects on neutrophil function.

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“…CD4 + o#[3 T cells have been shown to be essential for IgA B cell responses (for review see reference 20), whereas the results of this study suggest that ~//8 T cells also may regulate the mucosal IgA immune response. The helper T cells that preferentially produce IL-4, IL-5, IL-6, and IL-10, the Th2 subset of CD4 + cells, promote IgA responses (16,(21)(22)(23). Our earlier studies indicated that oral immunization of normal mice with the combined TT and CT vaccine induced Th2-type cells in the IgA mucosal response (16), and TCR-[3 -/-mice are essentially devoid of mucosal IgA-producing cells (Fujihashi, K., M.-N. Kweon, M. Marinaro, K. Imaoka, R.J. Jackson, J.R. McGhee, and H. Kiyono, manuscript in preparation).…”

Section: Discussionmentioning

confidence: 99%

gamma/delta T cell-deficient mice have impaired mucosal immunoglobulin A responses.

Fujihashi

McGhee

Kweon

et al. 1996

The Journal of Experimental Medicine

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171

123

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Mucosal tissues of mice are enriched in T cells that express the gamma/delta T cell receptor. Since the function of these cells remains unclear, we have compared mucosal immune responses in gamma/delta T cell receptor-deficient (TCRdelta-/-) mice versus control mice of the same genetic background. The frequency of intestinal immunoglobulin (Ig) A plasma cells as well as IgA levels in serum, bile, saliva, and fecal samples were markedly reduced in TCRdelta-/- mice. The TCRdelta-/- mice produced much lower levels of IgA antibodies when immunized orally with a vaccine of tetanus toxoid plus cholera toxin as adjuvant. Conversely, the antigen-specific IgM and IgG antibody responses were comparable to orally immunized control mice. Direct assessment of the cells forming antibodies against the tetanus toxoid and cholera toxin antigens indicated that significantly lower numbers of IgA antibody-producing cells were present in the intestinal lamina propria and Peyer's patches of TCRdelta-/- mice compared with the orally immunized control mice. The selective reduction of IgA responses to ingested antigens in the absence of gamma/delta T cells suggests a specialized role for gamma/delta cells in mucosal immunity.

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Role for interleukins 5 and 6 in IgA synthesis

Cited by 4 publications

References 8 publications

Exogenous IL‐6 promotes enhanced intestinal antibody responses in vivo

Exogenous IL‐6 promotes enhanced intestinal antibody responses in vivo

Impaired neutrophil response and CD4+ T helper cell 1 development in interleukin 6-deficient mice infected with Candida albicans.

gamma/delta T cell-deficient mice have impaired mucosal immunoglobulin A responses.

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