Kimberly D. Dyer, Ph.D.

Staff Scientist, Inflammation Immunobiology Section, LAD

Dr. Dyer received her Ph.D. from Georgetown University in Washington, DC. Prior to joining the Laboratory of Allergic Diseases in 2003 as a staff scientist, Dr. Dyer held a similar position in the Laboratory of Host Defenses at the National Institutes of Health.

Description of Research Program

Eosinophil researchers are handicapped by the relative rarity of eosinophils. We have developed a method for generating eosinophils from unselected bone marrow in large numbers and high purity. This protocol has facilitated eosinophil research worldwide. To generate bone marrow eosinophils (bmEos), bone marrow cells are collected from the femur and the tibia, the red blood cells removed, and the remaining cells put into culture with two cytokines that support the maintenance and proliferation of hematopoietic stem cells. After four days, the cells are cultured in interleukin-5, a cytokine known to support the differentiation of eosinophils. By day 12, the cultures approach 100 percent purity. Phenotypically, these cells look like eosinophils and produce typical eosinophil transcripts, express typical surface markers, release typical cytokines, and exhibit chemotaxis toward eotaxin. We have shown that this method works well in several strains of mice.

Specifically, the Inflammation Immunobiology Section is interested in the role that eosinophils play in mediating host defenses against viral pathogens. We have used bmEos to demonstrate that eosinophils are a target of pneumonia virus of mice (PVM). Infection with PVM stimulated the release of proinflammatory cytokines in response to the replication of the virus, and this effect was mediated by MyD88.

In collaboration with other eosinophil researchers, we examined the response of bmEos to platelet activating factor (PAF), a known secretagogue for human eosinophils. PAF stimulated the release of the granule protein eosinophil peroxidase from mouse bmEos. Unexpectedly, PAF-stimulated degranulation was independent of the known PAF receptor, suggesting the existence of a second PAF receptor.

Soon we will be taking these cells in vivo and using them to answer questions of eosinophil biology and function in models of eosinophil-deficient mice in the face of challenges that lead to the development of eosinophilia in wild-type mice. Toward this goal, we have generated a flow-based method that will allow us to identify resting and activated eosinophils in mouse tissues.

Memberships

• The American Association of Immunologists
• The American Society of Cell Biologists
• The International Eosinophil Society

Selected Recent Publications

To view a complete listing, visit PubMed.

Dyer KD, Garcia-Crespo KE, Killoran, KE, Rosenberg HF. Antigen profiles for the quantitative assessment of eosinophil in mouse tissues by flow cytometry. J Immunol Methods. 2011 Jun 30;369(1-2):91-7.

Dyer KD, Percopo CM, Xie Z, Yang Z, Kim JD, Davione F, Lacy P, Druey KM, Moqbel R, Rosenberg HF. Mouse and human eosinophils degranulate in response to platelet-activating factor (PAF) and lysoPAF via a PAF-receptor-independent mechanism: evidence for a novel receptor. J Immunol. 2010 Jun 1;184(11): 6327-34.

Dyer KD, Percopo CM, Fisher ER, Gabryszewski SJ, Rosenberg HF. Pneumoviruses infect eosinophils and elicit MyD88-dependent release of chemoattractant cytokines and interleukin-6. Blood. 2009 Sep 24;114(13): 2649-56. Dyer KD, Percopo CM, Rosenberg HF. Generation of eosinophils from unselected bone marrow progenitors: wild-type, TLR- and eosinophil-deficient mice. Open Immunol J. 2009 Jan 1;2:163-7.

Dyer KD, Moser JM, Czapiga M, Siegel SJ, Percopo CM, Rosenberg HF. Functionally competent eosinophils differentiated ex vivo in high purity from normal mouse bone marrow. J Immunol. 2008 Sep 15;181(6): 4004-9.

Dyer KD, Czapiga M, Foster B, Foster PS, Kang EM, Lappas CM, Moser JM, Naumann N, Percopo CM, Siegel SJ, Swartz JM, Ting-De Ravin S, Rosenberg HF. Eosinophils from lineage-ablated Delta dblGATA bone marrow progenitors: the dblGATA enhancer in the promoter of GATA-1 is not essential for differentiation ex vivo. J Immunol. 2007 Aug 1;179(3):1693-9.

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