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?? T cells affect IL-4 production and B-cell tolerance.

ABSTRACT: ?? T cells can influence specific antibody responses. Here, we report that mice deficient in individual ?? T-cell subsets have altered levels of serum antibodies, including all major subclasses, sometimes regardless of the presence of ?? T cells. One strain with a partial ?? deficiency that increases IgE antibodies also displayed increases in IL-4-producing T cells (both residual ?? T cells and ?? T cells) and in systemic IL-4 levels. Its B cells expressed IL-4-regulated inhibitory receptors (CD5, CD22, and CD32) at diminished levels, whereas IL-4-inducible IL-4 receptor ? and MHCII were increased. They also showed signs of activation and spontaneously formed germinal centers. These mice displayed IgE-dependent features found in hyper-IgE syndrome and developed antichromatin, antinuclear, and anticytoplasmic autoantibodies. In contrast, mice deficient in all ?? T cells had nearly unchanged Ig levels and did not develop autoantibodies. Removing IL-4 abrogated the increases in IgE, antichromatin antibodies, and autoantibodies in the partially ??-deficient mice. Our data suggest that ?? T cells, controlled by their own cross-talk, affect IL-4 production, B-cell activation, and B-cell tolerance.

SUBMITTER: Huang Y

PROVIDER: S-EPMC4291655 | biostudies-literature | 2015 Jan

REPOSITORIES: biostudies-literature

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Publications

γδ T cells affect IL-4 production and B-cell tolerance.

Huang Yafei Y Heiser Ryan A RA Detanico Thiago O TO Getahun Andrew A Kirchenbaum Greg A GA Casper Tamara L TL Aydintug M Kemal MK Carding Simon R SR Ikuta Koichi K Huang Hua H Cambier John C JC Wysocki Lawrence J LJ O'Brien Rebecca L RL Born Willi K WK

Proceedings of the National Academy of Sciences of the United States of America 20141222 1

γδ T cells can influence specific antibody responses. Here, we report that mice deficient in individual γδ T-cell subsets have altered levels of serum antibodies, including all major subclasses, sometimes regardless of the presence of αβ T cells. One strain with a partial γδ deficiency that increases IgE antibodies also displayed increases in IL-4-producing T cells (both residual γδ T cells and αβ T cells) and in systemic IL-4 levels. Its B cells expressed IL-4-regulated inhibitory receptors (CD ...[more]

PMID: 25535377

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Project description:BACKGROUND: The adenoviral protein E1A has been proposed to play a role in the pathophysiology of COPD, in particular by increasing IL-8 gene transcription of lung epithelial cells in response to cigarette smoke-constituents such as LPS. As IL-8 production is also under tight post-transcriptional control, we planned to study whether E1A affected IL-8 production post-transcriptionally. The production of IL-6 by E1A-positive cells had not been addressed and was studied in parallel. Based on our previous work into the regulation of IL-8 and IL-6 production in airway epithelial cells, we used the lung epithelial-like cell line NCI-H292 to generate stable transfectants expressing either E1A and/or E1B, which is known to frequently co-integrate with E1A. We analyzed IL-8 and IL-6 production and the underlying regulatory processes in response to LPS and TNF-alpha. METHODS: Stable transfectants were generated and characterized with immunohistochemistry, western blot and flow cytometry. IL-8 and IL-6 protein production was measured by ELISA. Levels of IL-8 and IL-6 mRNA were measured using specific radiolabeled probes. EMSA was used to assess transcriptional activation of relevant transcription factors. Post-transcriptional regulation of mRNA half-life was measured by Actinomycin D chase experiments. RESULTS: Most of the sixteen E1A-expressing transfectants showed suppression of IL-6 production, indicative of biologically active E1A. Significant but no uniform effects on IL-8 production, nor on transcriptional and post-transcriptional regulation of IL-8 production, were observed in the panel of E1A-expressing transfectants. E1B expression exerted similar effects as E1A on IL-8 production. CONCLUSION: Our results indicate that integration of adenoviral DNA and expression of E1A and E1B can either increase or decrease IL-8 production. Furthermore, we conclude that expression of E1A suppresses IL-6 production. These findings question the unique role of E1A protein in the pathophysiology of COPD, but do not exclude a role for adenoviral E1A/E1B DNA in modulating inflammatory responses nor in the pathogenesis of COPD.

Dataset Information

?? T cells affect IL-4 production and B-cell tolerance.

Publications

γδ T cells affect IL-4 production and B-cell tolerance.

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