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Christopher J. Paige

Researcher at Princess Margaret Cancer Centre

Publications -  148
Citations -  12781

Christopher J. Paige is an academic researcher from Princess Margaret Cancer Centre. The author has contributed to research in topics: B cell & Progenitor cell. The author has an hindex of 48, co-authored 147 publications receiving 12379 citations. Previous affiliations of Christopher J. Paige include University Health Network & Ontario Institute for Cancer Research.

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TRAF6 deficiency results in osteopetrosis and defective interleukin-1, CD40, and LPS signaling

TL;DR: It is reported that mice deficient in TNF receptor-associated factor 6 (TRAF6) are osteopetrotic with defects in bone remodeling and tooth eruption due to impaired osteoclast function, and it is demonstrated that TRAF6 is crucial not only in IL-1 and CD40 signaling but also, surprisingly, in LPS signaling.
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Profound block in thymocyte development in mice lacking p56lck.

TL;DR: The results illustrate the crucial role of this T-cell-specific tyrosine kinase in the thymocyte development, as Lck-deficient mice show a pronounced thymic atrophy, with a dramatic reduction in the double-positive (CD4+CD8+) thymocytes population.
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Deregulated T cell activation and autoimmunity in mice lacking interleukin-2 receptor beta

TL;DR: In mice lacking the interleukin-2 receptor beta chain (IL-2R beta), T cells were shown to be spontaneously activated, resulting in exhaustive differentiation of B cells into plasma cells and the appearance of high serum concentrations of immunoglobulins G1 and E as well as autoantibodies that cause hemolytic anemia.
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B Cell Development in the Spleen Takes Place in Discrete Steps and Is Determined by the Quality of B Cell Receptor–Derived Signals

TL;DR: It is shown that selection into the mature pool is an active process and takes place in the spleen, and two populations of splenic B cells were identified as precursors for mature B cells.
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Normal development and function of CD8+ cells but markedly decreased helper cell activity in mice lacking CD4.

TL;DR: In these mice, the development of CD8+ T cells and myeloid components is unaltered, indicating that expression of CD4 on progenitor cells and CD4+CD8+ (double positive) thymocytes is not obligatory, which is important to the understanding of immune disorders, including AIDS.