Department of Immunology

Jessica Hamerman, Ph.D.

ASSOCIATE MEMBER, BENAROYA RESEARCH INSTITUTE AND AFFILIATE ASSOCIATE PROFESSOR, IMMUNOLOGY

Jessica Hamerman received her B.S. in Biological Sciences from Stanford University and her Ph.D. in Immunology from the University of Washington. She then pursued postdoctoral studies at the University of California San Francisco before joining the Benaroya Research Institute Immunology Program.

CONTACT

Benaroya Research Institute
at Virginia Mason
1201 Ninth Avenue
Seattle, WA 98101-2795
Phone: 206-287-1077
Fax: 206-233-7543

RESEARCH AREAS

Tolerance & Autoimmunity
Innate Immunity

LAB MEMBERS

Graduate Students
Talyn Chu, talyn2@uw.edu
Hayley Waterman, hayleyw@uw.edu

Postdoctoral Fellows
Holly Akilesh, hakilesh@benaroyaresearch.org
Cierra Casson, ccasson@benaroyaresearch.org

Laboratory Staff
Griff Gessay – Research Associate, ggessay@benaroyaresearch.org
Minjian Ni – Staff Scientist, mni@benaroyaresearch.org

LAB

Benaroya Research

PUBMED

Jessica Hamerman on PubMed

 

RESEARCH

Research in our laboratory focuses on the regulation of the innate immune response to pathogens with an emphasis on macrophages and dendritic cells. Macrophages and dendritic cells are distributed throughout the body where they are poised to detect pathogens and to subsequently alert the immune system to the presence of infection through the production of inflammatory mediators. The production of inflammatory mediators, such as tumor necrosis factor (TNF) and other pro-inflammatory cytokines, is tightly regulated. Although these important cytokines are beneficial to the host for pathogen clearance, they can be detrimental if unchecked. This can be seen in septic shock as well as in autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus.

Macrophages and dendritic cells recognize pathogens by a variety of cell surface and intracellular receptors including the family of Toll-like receptors (TLR). We study how signaling through pattern recognition receptors results in the appropriate inflammatory response by macrophages and dendritic cells. We are particularly interested in proteins that inhibit signaling through pattern recognition receptors, providing an essential brake to the inflammatory response.  We study a variety of cell surface receptors and signaling molecules that regulate TLR responses.  Our studies span signal transduction and functional assays of macrophages and dendritic cells in vitro to in vivo infection models and models of autoimmunity.  We also are investigating the effect of human autoimmunity susceptibility alleles on macrophage function to test the hypothesis that increased innate immune responses can participate in the predisposition to autoimmune disease.  Overall, our goal is to understand how the appropriate inflammatory response is determined to fight against infections, yet protect against autoimmunity.

PUBLICATIONS

  1. Sun X, Wiedeman A, Agrawal N, Teal TH, Tanaka L, Hudkins KL, Alpers CE, Bolland S, Buechler MB, Hamerman JA, Ledbetter JA, Liggitt D, and Elkon KB (2013) Increased RNase Expression Reduces Inflammation and Prolongs Survival in TLR7 Transgenic Mice. Journal of Immunology. 2013 Mar 15;190(6):2536-43. PMID: 23382559.
  2. Yee NK, Hamerman JA (2013). β(2) integrins inhibit TLR responses by regulating NF-κB pathway and p38 MAPK activation. European Journal of Immunology. 2013 Mar;43(3):779-92 PMID: 23310953.
  3. Buechler MB, Teal TH, Elkon KB, Hamerman JA (2013) Cutting Edge: Type I IFN Drives Emergency Myelopoiesis and Peripheral Myeloid Expansion during Chronic TLR7 Signaling. Journal of Immunology. 2013 Feb1;190(3):886-91 PMID: 23303674.
  4. Jhingran A, Mar KB, Kumasaka DK, Knoblaugh SE, Ngo LY, Segal BH, Iwakura Y, Lowell CA, Hamerman JA, Lin X, Hohl TM (2012) Tracing conidial fate and measuring host cell antifungal activity using a reporter of microbial viability in the lung. Cell Reports 2012 Dec 27;2(6):1762-73.
  5. Ni M, MacFarlane AW, Toft M, Lowell CA, Campbell KS, Hamerman JA (2012) BCAP negatively regulates Toll-like receptor signaling through activation of PI3-Kinase. Proceedings of the National Academy of Sciences USA 2012 Jan 3;109(1):267-72. PMCID: PMC3252908
  6. Ito H and Hamerman JA (2012) TREM-2, triggering receptor expressed on myeloid cell-2, negatively regulates TLR responses in dendritic cells. European Journal of Immunology 2012 Jan;42(1)176-85. PMCID: PMC3444819
  7. Hamerman JA, Ni M, Killebrew JR, Chu C-L, Lowell CA (2009) The expanding roles of ITAM adapters FcRγ and DAP12 in myeloid cells. Immunological Reviews Nov;232(1):42-58.  PMCID: PMC3248395
  8. N’Diaye EN, Branda CS, Branda SS, Nevarez L, Colonna M, Lowell C, Hamerman JA, Seaman WE (2009) TREM-2 (triggering receptor expressed on myeloid cells 2) is a phagocytic receptor for bacteria. Journal of Cell Biology, Jan 26;184(2):215-23.
  9. Chu CL, Yu YL, Shen KY, Lowell CA, Lanier LL, Hamerman JA (2008) Increased TLR responses in dendritic cells lacking the ITAM-containing adapters DAP12 and FcRγ, European Journal of Immunology, 38 (1), 166-73.  PMCID: PMC2587008
  10. Hamerman JA, Jarjoura JR, Humphrey MB, Nakamura MC, Seaman WE, Lanier LL (2006) Cutting edge: inhibition of TLR and FcR responses in macrophages by triggering receptor expressed on myeloid cells (TREM)-2 and DAP12., Journal of Immunology, 177 (4), 2051-5.
  11. Hamerman JA, Tchao NK, Lowell CA, Lanier LL (2005) Enhanced Toll-like receptor responses in the absence of signaling adaptor DAP12., Nature Immunology, 6 (6), 579-86.