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Philip J. Cooper

Researcher at Liverpool School of Tropical Medicine

Publications -  33
Citations -  2726

Philip J. Cooper is an academic researcher from Liverpool School of Tropical Medicine. The author has contributed to research in topics: Ascaris lumbricoides & Interleukin 5. The author has an hindex of 22, co-authored 33 publications receiving 2581 citations. Previous affiliations of Philip J. Cooper include Pontificia Universidad Católica del Ecuador & National Institutes of Health.

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A line of non-tumorigenic mouse melanocytes, syngeneic with the B16 melanoma and requiring a tumour promoter for growth.

TL;DR: An immortal line of pigmented melanocytes, “melan‐a”, has been derived from normal epidermal melanoblasts from embryos of inbred C57BL mice, providing an excellent parallel non‐tumorigenic line for studies of the cellular and molecular basis of melanoma malignancy.
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Reduced risk of atopy among school-age children infected with geohelminth parasites in a rural area of the tropics.

TL;DR: Active infections with geohelminth parasites and the presence of serologic markers of chronic infections are independent protective factors against allergen skin test reactivity among school-age children living in an endemic region of the rural tropics.
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Human Infection with Ascaris lumbricoides Is Associated with Suppression of the Interleukin-2 Response to Recombinant Cholera Toxin B Subunit following Vaccination with the Live Oral Cholera Vaccine CVD 103-HgR

TL;DR: Findings indicate that vaccination with CVD 103-HgR is associated with a Th1 cytokine response (IL-2 and IFN-γ) to CT-B, that infection with A. lumbricoidesdiminishes the magnitude of this response, and that albendazole treatment prior to vaccination was able to partially reverse the deficit in IL-2.
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Impaired Tetanus-Specific Cellular and Humoral Responses following Tetanus Vaccination in Human Onchocerciasis: A Possible Role for Interleukin-10

TL;DR: It is indicated that concurrent infection with O. volvulus can diminish the immune response to an unrelated antigen (TT) by a mechanism that is likely to involve interleukin-10.