Department of Immunology

Justin Taylor, Ph.D.


Dr. Taylor earned his Ph.D. from the University of Pennsylvania in 2008. He is currently an Assistant Member in the Clinical Research Division of the Program in Immunology at Fred Hutchinson Cancer Research Center. Dr. Taylor joined the University of Washington Department of Immunology as an Affiliate Assistant Professor in 2018.


Phone: 206-667-7794

Mail Stop: E5-110


Adaptive Immune Responses
Antibodies, B cells


Taylor Lab at Fred Hutch


Taylor Lab


Justin Taylor on PubMed


Identification of naive B cells specific for candidate vaccine antigens

The traditional vaccine development process has focused upon designing the pathogen component of the vaccine. This meant either developing ways to weaken or inactivate the pathogen, or developing a process to produce an immunogenic subunit of the pathogen. While these approaches have been incredibly successful for some pathogens, protective vaccines for many infections remain elusive. Recent, evidence suggests that one reason that previous HIV-1 vaccines many have failed is that the HIV-1 antigen included in these vaccines did not stimulate naïve B cells that express antibodies with the ability to protect against HIV-1. If true, this means that vaccine failure could have been predicted if researchers had been able to assess the repertoire of naïve B cells able to bind to the candidate HIV-1 vaccine immunogen prior to vaccination. In light of this, we have begun to utilize our rare antigen-specific enrichment approaches to isolate B cells able to bind to candidate vaccine antigens. These enrichments allow for a robust analysis of the binding abilities of the antibodies expressed by these antigen-specific B cells as well as the phenotype and function of the cells themselves.

Understanding factors limiting B cell activation following vaccination

Protective vaccines rely on the ability of host B cells to recognize foreign antigen and respond, generating effector subsets that can produce antibody and neutralize invading pathogens. However, the critical first step in this process is that the naïve B cell must bind antigen and become activated. Surprisingly, we recently found that in mice 60%-80% of naïve antigen-specific B cells fail to expand in response to vaccination. Current work is aimed at understanding the intrinsic and extrinsic factors that limit the activation of naïve B cells after vaccination. To investigate these questions, we probe the phenotypes and functions of rare antigen-specific human and murine B cells using our antigen-specific enrichment techniques. The goal of this work is to understand the factors that limit naïve B cell activation allowing for activation of all potentially protective naïve B cells after vaccination.

Understanding the differentiation of B cells following vaccination

Naïve B cell activation and proliferation is only the first step in a protective response. Activated B cells must also undergo a complicated process of differentiation in order to produce long-lived antibody-secreting plasma cells and long-lived memory B cells. In previous work we have assessed the number and phenotype of memory B cells generated through the germinal center-dependent and germinal center-independent pathways. Using an in vivo limited dilution approach we have found that a single antigen-specific naïve murine B cell usually does not produce progeny that differentiate down each developmental pathway. Current work is focused upon understanding the B cell intrinsic and extrinsic mechanisms that control differentiation. The ultimate goal of this work is to be able to direct B cell differentiation to ensure that B cells expressing potentially-protective antibodies enter the optimal differentiation pathway to produce long-lived protective progeny.


  1. Spanier J#, Frederick D#, Taylor JJ#, Heffernan J, Kotov D, Matinov T, Osum K, Ruggiero J, Rust B, Landry S, Jenkins M, Mclachlan J, Fife B. Efficient generation of monoclonal antibodies against peptide in the context of MHCII using magnetic enrichment. Nat Commun 7:11804, 2016 [PMCID: PMC4909947]. (#contributed equally)
  2. Taylor JJ, Pape KA, Steach HR, Jenkins MK. Humoral immunity. Apoptosis and antigen affinity limit effector cell differentiation of a single naïve B cell. Science 347(6223):784-87, 2015 [PMCID: PMC4412594].
  3. Taylor JJ, Laudenbach M, Tucker AM, Jenkins MK, Pravetoni M. Hapten-specific naïve B cells are biomarkers of vaccine efficacy against drugs of abuse. J Immunol Methods 405:74-86, 2014 [PMCID: PMC4018303].
  4. Taylor JJ, Pape KA, Jenkins MK. A germinal center-independent pathway generates unswitched memory B cells early in the primary response. J Exp Med 209(3):597-606, 2012 [PMCID: PMC3302224].
  5. Taylor JJ, Martinez RJ, Titcombe PJ, Barsness LO, Thomas SR, Zhang N, Katzman SD, Jenkins MK, Mueller DL. Deletion and anergy of polyclonal B cells specific for ubiquitous membrane bound self antigen. J Exp Med 209(11):2065-2077, 2012 [PMCID: PMC3478923].
  6. Taylor JJ, Krawczyk CM, Mohrs M, Pearce EJ. Th2 hyporesponsiveness during chronic murine schistosomiasis is cell intrinsic and linked to GRAIL expression. J Clin Invest 119(4):1019-1028, 2009 [PMCID: PMC2662551].
  7. Glatman-Zaretsky A#, Taylor JJ#, King IL, Marshall FA, Mohrs M, Pearce EJ. T follicular helper cells differentiate from Th2 cells in response to helminth antigens. J Exp Med 206(5):991-999, 2009 [PMCID: PMC2715032] (#contributed equally).
  8. Taylor JJ, Mohrs M, Pearce EJ. Regulatory T cell responses develop in parallel to Th responses and control the magnitude and phenotype of the Th effector population. J Immunol 176(10):5839-5847, 2006.