Group Leader

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Edward Pearce, PhD
Senior Group Leader (MPI-IE/Uni)
Phone:+49 761 5108 476

Lab Edward Pearce

Selected Publications

1.
O’Neill LA, Pearce EJ (2016)
Immunometabolism governs dendritic cell and macrophage function
2.
Everts B, Tussiwand R, Dreesen L, Fairfax KC, Ching-Cheng Huang S, Smith AM, O’Neill CM, Lam WY, Edelson BT, Urban JF, Murphy KM, Pearce EJ (2016)
Migratory CD103+ Dendritic Cells suppress Helminth-driven Type 2 Immunity through Constitutive Expression of IL-12
3.
Jha AK, Huang SC, Sergushichev A, Lampropoulo V, Ivanova Y, Loginicheva E, Chielewski K, Stewart KM, Ashall J, Everts B, Pearce EJ*, Driggers* EM, Artyomov A* (2015)
Network integration of parallel metabolomics and transcriptional data reveals metabolic modules that regulate macrophage polarization
4.
Huang SC, Everts B, Ivanova Y, O'Sullivan D, Nascimento M, Smith AM, Beatty W, Love-Gregory L, Lam WY, O'Neill CM, Yan C, Du H, Abumrad NA, Urban JF Jr, Artyomov MN, Pearce EL, Pearce EJ (2014)
Cell-intrinsic lysosomal lipolysis is essential for alternative activation of macrophages
5.
Everts B, Amiel E, Huang SC, Smith AM, Chang CH, Lam WY, Redmann V, Freitas TC, Blagih J, van der Windt GJ, Artyomov MN, Jones RG, Pearce EL, Pearce EJ (2014)
TLR-driven early glycolytic reprogramming via the kinases TBK1-IKKɛ supports the anabolic demands of dendritic cell activation

Find more publications of Edward Pearce on PubMed

Laboratory Edward Pearce

Laboratory Edward Pearce

The laboratory emphasizes two overlapping areas of research:

 

Cells of the innate immune system play important roles in tissue hemostasis and in defense against infection. To a great extent the ability of these cells to serve multiple functions reflects their ability to enact different gene expression programs in response to distinct extra- and intra-cellular activating signals.  Recent work has revealed that innate cell activation is highly dependent on metabolic reprogramming.  The laboratory is focused on elucidating the mechanisms involved in innate immune cell metabolic reprogramming and the underlying reasons why different types of metabolism are essential to support different activation states in these cells.

<strong>Anabolic metabolism vs catabolic metabolism and the control of dendritic cell immunogenicity vs. tolerogenicity.</strong>  PRR agonists, cytokines and nutrient and O2 levels can influence the balance of anabolic to catabolic metabolism, as shown.  mTOR and AMPK are important regulators of this metabolic balance and their activation states are highly responsive to a broad array of intracelllar and extracellular signals. Glycolysis coupled to the TCA cycle and citrate export from mitochondria supports an array of biosynthetic processes that are critical for DC activation. In contrast, autophagy and the oxidation of fatty acids and glutamine can create a state in which DCs are tolerogenic. Zoom Image
Anabolic metabolism vs catabolic metabolism and the control of dendritic cell immunogenicity vs. tolerogenicity.  PRR agonists, cytokines and nutrient and O2 levels can influence the balance of anabolic to catabolic metabolism, as shown.  mTOR and AMPK are important regulators of this metabolic balance and their activation states are highly responsive to a broad array of intracelllar and extracellular signals. Glycolysis coupled to the TCA cycle and citrate export from mitochondria supports an array of biosynthetic processes that are critical for DC activation. In contrast, autophagy and the oxidation of fatty acids and glutamine can create a state in which DCs are tolerogenic. [less]

Different types of infection stimulate distinct types of immune responses.  The laboratory is particularly interested in the responses induced by helminth parasites. These multicellular pathogens, which cause disease primarily in developing countries, induce type 2 immunity, which shares features in common with the responses which cause allergy/asthma. Moreover, facets of type 2 immunity are implicated in wound healing, tumor progression and adipose tissue homeostasis.  Research in the laboratory asks how type 2 immunity is initiated and maintained, and examines mechanisms that mediate downstream sequelae of these types of immune responses, both beneficial, such as immunity to helminth parasites, and detrimental, such as tissue fibrosis and cancer progression.  Many of the effects of type 2 immunity are mediated by the effects of cytokines made by CD4+ Th2 lymphocytes and type 2 innate lymphoid cells on macrophages, and the laboratory focuses on the biology of macrophages in these settings, especially from an immunometabolic perspective.

 
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