Immunology
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Peter F. Weller

Department of Medicine
Harvard Medical School
Beth Israel Deaconess Medical School
Dana Building, Room 617
330 Brookline Avenue
Boston, MA 02215
Tel: 617-667-3307
Fax: 617-667-5541
e-mail: pweller@bidmc.harvard.edu
4 Postdoctoral Fellows

 Peter F. Weller

Research in this laboratory is centered around understanding basic mechanisms of leukocyte functioning in forms of inflammation. The two principal areas of investigation are:

  • the immunobiology of eosinophilic leukocytes
  • the intracellular regulation and compartmentalization of inducible mediators of inflammation in neutrophils and other leukocytes.

Studies of human eosinophils are aimed at defining mechanisms whereby eosinophils may collaboratively interact with other cellular elements of the immune system. These studies include investigations of the mechanisms whereby eosinophils may function as antigen-presenting cells in governing T-lymphocyte dependent immune responses, and include investigations of the in vivo migration and function of eosinophils and of the regulated expression of cell surface proteins involved in collaborative interactions between eosinophils and other cell types. Additional studies are focused on defining the molecular mechanisms governing the synthesis, granule storage and release mechanisms of eosinophil derived cytokines.

The second area of research involves the molecular and cellular biologic bases of inducible responses of leukocytes participating in host defense and other forms of inflammation. These are centered on a unique intracellular compartment, termed the lipid body, whose formation is rapidly inducible in leukocytes. The intracellular signaling mechanisms responsible for lipid body induction and especially the roles of lipid bodies as distinct sites of cytokine and eicosanoid mediator formation are being studied. In addition to investigating previously undefined pathways of leukocyte responses to inflammation, these studies also offer the potential to identify novel anti inflammatory therapeutic targets.

 

Papers & Publications:

  1. Shi HZ, Humbles A, Gerard C, Jin Z, Weller PF. Lymph node trafficking and antigen presentation by endobronchial eosinophils. J Clin Invest 2000; 105:945-953.
  2. Bandeira-Melo C, Sugiyama K, Phoofolo M,Weller PF. Extranuclear lipid bodies, elicited by CCR3-mediated signaling pathways, are the sites of chemokine-enhanced leukotriene C4 production in eosinophils and basophils. J Biol Chem 2001; 276:22779-22787.
  3. Bandeira-Melo C, Woods LJ, Weller PF. Cutting Edge: Eotaxin elicits rapid, vesicular transport-mediated release of preformed IL-4 from human eosinophils. J Immunol. 2001; 166:4813-7.
  4. Bandeira-Melo C, Sugiyama K, Woods LJ, Phoofolo M, Center DM, Cruikshank WW, Weller PF. Interleukin-16 promotes leukotriene C4 and interleukin-4 release from human eosinophils via CD4- and autocrine CCR3-chemokine-mediated signaling. J. Immunol. 2002; 4756-4763
  5. 5.Bandeira-Melo C, Woods LJ, Phoofolo M, Weller PF. Intracrine cysteinyl leukotriene receptor-mediated signaling of eosinophil vesicular transport-mediated interleukin-4 secretion. J Exp Med. 2002; 196: 841-850.