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Carl G. Feng

Researcher at University of Sydney

Publications -  110
Citations -  14294

Carl G. Feng is an academic researcher from University of Sydney. The author has contributed to research in topics: Mycobacterium tuberculosis & Tuberculosis. The author has an hindex of 48, co-authored 98 publications receiving 12575 citations. Previous affiliations of Carl G. Feng include Centenary Institute of Cancer Medicine and Cell Biology & National Institutes of Health.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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A Critical Role for IL-21 in Regulating Immunoglobulin Production

TL;DR: It is demonstrated that, although mice deficient in the receptor for IL-21 (IL-21R) have normal lymphoid development, after immunization, these animals have higher production of the immunoglobulin IgE, but lower IgG1, than wild-type animals, suggesting that these γc-dependent cytokines may be those whose inactivation is primarily responsible for the B cell defect in humans with XSCID.
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TLR9 regulates Th1 responses and cooperates with TLR2 in mediating optimal resistance to Mycobacterium tuberculosis

TL;DR: A previously unappreciated role for TLR9 is revealed in the host response to M. tuberculosis and TLR collaboration in host resistance to a major human pathogen is illustrated.
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Conventional T-bet(+)Foxp3(-) Th1 cells are the major source of host-protective regulatory IL-10 during intracellular protozoan infection.

TL;DR: In this article, the source of regulatory IL-10 in mice infected with the protozoan parasite Toxoplasma gondii was analyzed and it was found that the same IFN-10(+)IFN-gamma(gamma) population displayed potent effector function against the parasite while, paradoxically, also inducing profound suppression of IL-12 production by antigen-presenting cells.
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IL-23 plays a key role in Helicobacter hepaticus-induced T cell-dependent colitis

TL;DR: The data demonstrate that IL-23 and not IL-12 is essential for the development of maximal intestinal disease, and support a model in which IL- 23 drives both interferon γ and IL-17 responses that together synergize to trigger severe intestinal inflammation.