Applications are invited for a fellowship in translational innate immunity. Focus will be on investigating emerging roles for apolipoprotein L1 (APOL1), and genetic variants thereof, in innate immunity, inflammation, and disease. African Americans have a three-fold higher rate of chronic kidney disease compared to European Americans, and much of this health disparity is driven by genetic variants in APOL1. 13% of African Americans, ~6 million people, carry two APOL1 risk alleles and are at increased risk for kidney disease. These variants arose quite recently in evolution, likely to protect against Trypanosomal infection, but cause kidney disease in ~10-20% of 2-risk allele carriers. Despite the tremendous public health burden, the underlying mechanisms of the APOL1 risk alleles in human disease remain poorly described. A key unanswered question is whether APOL1 risk alleles augment inflammatory responses in immune cells.
Studies will involve biochemical/signaling studies in cultured macrophages and also in primary human leukocytes collected in the NIEHS Clinical Research Unit from subjects with selected genetic polymorphisms of interest. Some studies may also include in vivo immune challenges in mouse models.
Expertise in signal transduction techniques, including cell culture, biochemical assays, and molecular biology, is strongly preferred; experience in rodent studies is an advantage. Applicants should possess a Ph.D. degree in Immunology, Molecular Biology, Biochemistry, Pharmacology, or a related field, and have no more than five years of previous postdoctoral experience.
For additional information about this position, contact Dr. Michael B. Fessler at email below. For prompt consideration, please email a cover letter including a brief summary of relevant experience, a C.V. including list of publications in peer-reviewed journals, and the names and contact information of 3 people who could provide letters of reference to: fesslermniehs.nih.gov
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