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Updated: Jun 1, 2026

Development and Functional Characterization of Murine Tolerogenic Dendritic Cells
Published on: May 18, 2018
Immunomodulatory effects of lactobacillus and Bifidobacterium on both murine and human mitogen-activated T cells
Chia-Yang Li1, Hung-Chih Lin, Chih-Ho Lai
1Division of Infectious Diseases, National Health Research Institutes, Miaoli, Taiwan, ROC.
Background:
Beneficial effects of probiotics have been reported for patients with allergic diseases and intestinal disorders. There is increasing interest in studying the role of different strains or combined probiotic administration on immunoregulation. In this study, we investigated whether probiotics modulate the immune response through regulating T cell proliferation and differentiation.
Methods:
We examined the effect of probiotic I (a combination of Lactobacillus acidophilus and Bifidobacterium bifidus) and probiotic II (a combination of L. acidophilus and B. infantis) on cell survival and proliferation, the progression of the cell cycle, and the production of Th1/Th2 cytokines by mitogen-stimulated murine spleen cells and human peripheral blood mononuclear cells (PBMCs).
Results:
Our experimental results showed that high concentrations (≥ 1 × 10(6) CFU/ml) of probiotic I or II inhibited mitogen-induced cell proliferation and arrested the cell cycle at the G0/G1 stage in both mitogen-stimulated spleen cells and PBMCs. In the results of low concentrations (<1 × 10(6) CFU/ml), probiotic I or II enhanced the production of IFN-γ but inhibited the production of IL-4. Our results indicated that high concentrations of probiotic I or II treatment could attenuate mitogen-induced overactive immune responses. On the other hand, low concentrations of probiotic I or II treatment could promote a shift in the Th1/Th2 balance toward Th1-skewed immunity.
Conclusion:
Dose selection is an important issue for probiotic studies. Our results indicated that probiotics have beneficial effects on regulating T cell-mediated immune responses by attenuating mitogen-induced overactive immune responses and promoting Th1 immune responses.
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