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William A. Kuziel
Researcher at University of Texas at Austin
Publications - 104
Citations - 14447
William A. Kuziel is an academic researcher from University of Texas at Austin. The author has contributed to research in topics: CCR2 & Chemokine. The author has an hindex of 65, co-authored 104 publications receiving 13741 citations. Previous affiliations of William A. Kuziel include Ludwig Maximilian University of Munich & University of Florida.
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Journal ArticleDOI
TNF/iNOS-producing dendritic cells mediate innate immune defense against bacterial infection.
Natalya V. Serbina,Thais P. Salazar-Mather,Christine A. Biron,William A. Kuziel,Eric G. Pamer +4 more
TL;DR: A TNF/iNOS-producing (Tip)-DC subset in spleens of Listeria monocytogenes-infected mice that is absent from CCR2-deficient mice is identified, indicating that Tip-DCs are not essential for T cell priming.
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Severe reduction in leukocyte adhesion and monocyte extravasation in mice deficient in CC chemokine receptor 2
William A. Kuziel,Sharon J. Morgan,Tracey C. Dawson,Stephanie Griffin,Oliver Smithies,Klaus Ley,Nobuyo Maeda +6 more
TL;DR: Results demonstrate that CCR2 is a major regulator of induced macrophage trafficking in vivo and shows enhanced early accumulation and delayed clearance of neutrophils and eosinophils.
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An animal model of age-related macular degeneration in senescent Ccl-2- or Ccr-2-deficient mice.
Jayakrishna Ambati,Akshay Anand,Stefan Fernandez,Eiji Sakurai,Bert C. Lynn,William A. Kuziel,Barrett J. Rollins,Balamurali K. Ambati +7 more
TL;DR: Mice deficient in monocyte chemoattractant protein-1 or its cognate C-C chemokine receptor-2 develop cardinal features of age-related macular degeneration, including accumulation of lipofuscin in and drusen beneath the retinal pigmented epithelium.
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Cc Chemokine Receptor 2 Is Critical for Induction of Experimental Autoimmune Encephalomyelitis
TL;DR: It is suggested that CCR2 expression on host-derived mononuclear cells is critical for disease induction, and adopted myelin oligodendrocyte glycoprotein 35-55–specific T cells lacking expression of C CR2 were able to induce EAE, whereas CCR 2−/− recipients of wild-type T cells failed to develop disease.
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Chemokine Expression by Glial Cells Directs Leukocytes to Sites of Axonal Injury in the CNS
TL;DR: It is concluded that leukocyte responses to CNS axonal injury are directed via innate glial production of chemokines, and CCR5 ligands are not critical to this response.