K
Kenneth W. Beagley
Researcher at Queensland University of Technology
Publications - 289
Citations - 11877
Kenneth W. Beagley is an academic researcher from Queensland University of Technology. The author has contributed to research in topics: Immune system & Chlamydia. The author has an hindex of 55, co-authored 280 publications receiving 11048 citations. Previous affiliations of Kenneth W. Beagley include University of Queensland & University of Newcastle.
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Dextran sulfate sodium-induced colitis occurs in severe combined immunodeficient mice
TL;DR: Acute DSS-induced colitis does not require the presence of T cells or B cells because it occurred in C.B17 severe combined immunodeficient mice that lack these cells, and its induction may result from a toxicity of DSS for colonic epithelial cells.
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Immunological decision-making: how does the immune system decide to mount a helper T-cell response?
TL;DR: In this article, the authors focus on the pathways and key factors responsible for the differentiation of the various subsets of effector CD4 T cells, including Th1, Th2, and Th17 cells.
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Interleukins and IgA synthesis. Human and murine interleukin 6 induce high rate IgA secretion in IgA-committed B cells.
Kenneth W. Beagley,John H. Eldridge,F Lee,Hiroshi Kiyono,Michael P. Everson,William J. Koopman,Toshio Hirano,Tadamitsu Kishimoto,Jerry R. McGhee +8 more
TL;DR: It is concluded that IL-6 plays an important role in promoting the terminal differentiation of PP B cells to IgA-secreting plasma cells and in inducing a sharp increase in numbers of B cells secreting IgA.
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Regulation of innate and adaptive immunity by the female sex hormones oestradiol and progesterone.
TL;DR: What is currently known about the effects of the female sex hormones oestradiol and progesterone on innate and adaptive immune responses in order to provide a framework for understanding these sex differences is described.
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Toll-like receptor (TLR) expression and TLR-mediated cytokine/chemokine production by human uterine epithelial cells.
TL;DR: It is indicated that uterine epithelial cells are important sentinels of the innate immune system and that stimulation through specific TLRs mediates changes in the expression of key chemokines and pro‐inflammatory cytokines that aid in the defence of the uterus against potential pathogens.