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J. Paul Justice

Researcher at East Carolina University

Publications -  6
Citations -  448

J. Paul Justice is an academic researcher from East Carolina University. The author has contributed to research in topics: Interleukin 5 & Interleukin 10. The author has an hindex of 5, co-authored 6 publications receiving 437 citations.

Papers
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Journal ArticleDOI

IL-10 reduces Th2 cytokine production and eosinophilia but augments airway reactivity in allergic mice

TL;DR: It is demonstrated that IL-10 reduces Th2 cytokine levels and eosinophilic inflammation but augments airway hyperreactivity but could contribute to the decline in pulmonary function observed in asthma.
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Ablation of eosinophils leads to a reduction of allergen-induced pulmonary pathology

TL;DR: The ablation of virtually all pulmonary eosinophils in OVA-treated mice resulted in a significant decrease in mucus accumulation and abolished allergen-induced airway hyperresponsiveness, demonstrating a direct causative relationship between allergenic-mediated pulmonary pathologies and eos inophils.
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IL-10 gene knockout attenuates allergen-induced airway hyperresponsiveness in C57BL/6 mice

TL;DR: Evidence is provided that IL-10 expression promotes the development of allergen-induced smooth muscle hyperresponsiveness and adoptive transfer of mononuclear splenocytes toIL-10-sufficient severe combined immunodeficient mice indicated that lymphocytes were an important source of the IL- 10 impacting AHR development.
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Th1 adjuvant N-acetyl-D-glucosamine polymer up-regulates Th1 immunity but down-regulates Th2 immunity against a mycobacterial protein (MPB-59) in interleukin-10-knockout and wild-type mice.

TL;DR: Chitin has a unique Th1 adjuvant effect on the development of Th1 immunity against a mycobacterial antigen, which is greater in IL-10-KO mice than in WT mice and down-regulates the adjUvant effect of chitin.
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CD4(+) T cell-dependent airway mucus production occurs in response to IL-5 expression in lung.

TL;DR: Pulmonary expression of IL-5 alone is capable of inducing CD4(+) T cell-dependent goblet cell metaplasia, apparently mediated by IL-4 receptor alpha-subunit-ligand interactions, and represents a previously unrecognized novel pathway for augmenting allergen-induced mucus production.