Joshua Boyce


Affiliation: Harvard University
Country: USA


  1. Liu T, Barrett N, Kanaoka Y, Buchheit K, Laidlaw T, Garofalo D, et al. Cysteinyl leukotriene receptor 2 drives lung immunopathology through a platelet and high mobility box 1-dependent mechanism. Mucosal Immunol. 2019;: pubmed publisher
    ..Antagonists of HMGB1 or RAGE may be useful to treat AERD and other disorders associated with type 2 immunopathology. ..
  2. Boyce J, Austen K. No audible wheezing: nuggets and conundrums from mouse asthma models. J Exp Med. 2005;201:1869-73 pubmed
    ..We suggest that these discordances, reflecting methodological and genetic differences, may be informative for understanding heterogeneity of human asthma. ..
  3. Pan D, Buchheit K, Samuchiwal S, Liu T, Cirka H, Raff H, et al. COX-1 mediates IL-33-induced extracellular signal-regulated kinase activation in mast cells: Implications for aspirin sensitivity. J Allergy Clin Immunol. 2018;: pubmed publisher
    ..MC-intrinsic COX-1 amplifies IL-33-induced activation in the setting of innate type 2 immunity and might help explain the phenomenon of therapeutic desensitization to aspirin by nonselective COX inhibitors in patients with AERD. ..
  4. request reprint
    Boyce J. Eicosanoid mediators of mast cells: receptors, regulation of synthesis, and pathobiologic implications. Chem Immunol Allergy. 2005;87:59-79 pubmed
  5. Laidlaw T, Cutler A, Kidder M, Liu T, Cardet J, Chhay H, et al. Prostaglandin E2 resistance in granulocytes from patients with aspirin-exacerbated respiratory disease. J Allergy Clin Immunol. 2014;133:1692-701.e3 pubmed publisher
  6. Liu T, Garofalo D, Feng C, Lai J, Katz H, Laidlaw T, et al. Platelet-driven leukotriene C4-mediated airway inflammation in mice is aspirin-sensitive and depends on T prostanoid receptors. J Immunol. 2015;194:5061-8 pubmed publisher
    ..The findings suggest applications for TP receptor antagonists in cases of asthma with high levels of cysLT production. ..
  7. Liu T, Kanaoka Y, Barrett N, Feng C, Garofalo D, Lai J, et al. Aspirin-Exacerbated Respiratory Disease Involves a Cysteinyl Leukotriene-Driven IL-33-Mediated Mast Cell Activation Pathway. J Immunol. 2015;195:3537-45 pubmed publisher
    ..Thus, IL-33 is a component of a cysLT-driven innate type 2 immune response that drives pathogenic MC activation and contributes substantially to AERD pathogenesis. ..
  8. Liu T, Barrett N, Kanaoka Y, Yoshimoto E, Garofalo D, Cirka H, et al. Type 2 Cysteinyl Leukotriene Receptors Drive IL-33-Dependent Type 2 Immunopathology and Aspirin Sensitivity. J Immunol. 2018;200:915-927 pubmed publisher
    ..CysLT2R-targeted drugs may interrupt these processes. ..
  9. Samuchiwal S, Boyce J. Role of lipid mediators and control of lymphocyte responses in type 2 immunopathology. J Allergy Clin Immunol. 2018;141:1182-1190 pubmed publisher

More Information


  1. request reprint
    Boyce J. The role of mast cells in asthma. Prostaglandins Leukot Essent Fatty Acids. 2003;69:195-205 pubmed
  2. Samuchiwal S, Balestrieri B, Raff H, Boyce J. Endogenous prostaglandin E2 amplifies IL-33 production by macrophages through an E prostanoid (EP)2/EP4-cAMP-EPAC-dependent pathway. J Biol Chem. 2017;292:8195-8206 pubmed publisher
    ..The ubiquitous induction of mPGES-1-dependent PGE2 may be crucial for innate immune system activation during various IL-33 driven pathologic disorders. ..