Jennifer Martinez, Ph.D.
Immunity, Inflammation, and Disease Laboratory / Inflammation and Autoimmunity Group
D248A Rall Building
111 T W Alexander Dr
Research Triangle Park, NC 27709
Phagocytes of the innate immune system are critical sentinels of their environment, patrolling the body for unwanted components and eliminating them. While clearance of invasive pathogens is a necessary function of phagocytes, the sensing, recognition, and removal of cellular corpses, a process termed efferocytosis, is also a critical role that phagocytes play during times of development, cellular homeostasis, and stress. Considering the average 50 billion adult human cells that undergo apoptosis daily and the rarity of observing an uncleared apoptotic cell under normal physiological conditions, one must truly appreciate the efficiency with which phagocytes perform their duties. Moreover, as this is a normal, reoccurring event in the lifespan of an organism, efferocytosis must occur in an â€œimmunologically silentâ€ manner, so as to not inappropriately alert the immune system. Therefore, the response of a phagocyte must be tailored to both the cargo and the preferred outcome. The effective clearance of extracellular components (be it pathogens or dying cells) requires that phagocytes first recognize and engulf them using surface receptors, followed by processing of the cargo and orchestration of the appropriate local and systemic immune responses. While much work has been accomplished to characterize the molecules responsible for attracting the phagocyte and facilitating engulfment, the mechanisms by which a phagocyte handles the ingested corpse in terms of its processing, degradation, and subsequent influence on the pursuant immune response is an area of growing interest.
Dr. Jennifer Martinez heads the Inflammation and Autoimmunity Group within the Immunity, Inflammation, and Disease Laboratory at NIEHS. Dr. Martinez earned her B.S. in Cellular and Molecular Biology from Tulane University in 2001 and her Ph.D. in immunology from Duke University in 2010. She began her work on the autophagy machinery and its role in inflammation and host defense as a postdoctoral fellow in the laboratory of Douglas R. Green, Ph.D., at the St. Jude Children's Research Hospital in Memphis, Tennessee. After completing her fellowship, she joined the NIEHS Immunity, Inflammation, and Disease Laboratory as a Tenure-track Investigator in 2015.
Liu L, Lu Y, Martinez J, Bi Y, Lian G, Wang T, Milasta S, Wang J, Yang M, Liu G, Green DR, Wang R. Proinflammatory signal suppresses proliferation and shifts macrophage metabolism from Myc-dependent to HIF1α-dependent. Proc Natl Acad Sci U S A. 2016;113(6):1564-9.
Daniels BP, Snyder AG, Olsen TM, Orozco S, Oguin TH 3rd, Tait SW, Martinez J, Gale M Jr, Loo YM, Oberst A. RIPK3 Restricts Viral Pathogenesis via Cell Death-Independent Neuroinflammation. Cell. 2017;169(2):301-313.e11.
Martinez J, Cunha LD, Park S, Yang M, Lu Q, Orchard R, Li QZ, Yan M, Janke L, Guy C, Linkermann A, Virgin HW, Green DR. Noncanonical autophagy inhibits the autoinflammatory, lupus-like response to dying cells. Nature. 2016;533(7601):115-9.
Ravindran R, Loebbermann J, Nakaya HI, Khan N, Ma H, Gama L, Machiah DK, Lawson B, Hakimpour P, Wang YC, Li S, Sharma P, Kaufman RJ, Martinez J, Pulendran B. The amino acid sensor GCN2 controls gut inflammation by inhibiting inflammasome activation. Nature. 2016;531(7595):523-527.
Martinez J, Malireddi RK, Lu Q, Cunha LD, Pelletier S, Gingras S, Orchard R, Guan JL, Tan H, Peng J, Kanneganti TD, Virgin HW, Green DR. Molecular characterization of LC3-associated phagocytosis reveals distinct roles for Rubicon, NOX2 and autophagy proteins. Nat Cell Biol. 2015;17(7):893-906.
Related Scientific Focus Areas
Microbiology and Infectious Diseases
Molecular Biology and Biochemistry
Genetics and Genomics
This page was last updated on February 19th, 2016