Andrew D Luster

Harvard Medical School, Boston, Massachusetts, United States

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Publications (330)3212.17 Total impact

  • Yoshishige Miyabe · Nancy D. Kim · Chie Miyabe · Andrew D. Luster
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    ABSTRACT: Chemokines regulate the migration of cells in vivo and dysregulated expression of chemokines and their receptors are implicated in autoimmune and inflammatory diseases. Inflammatory arthritides, such as rheumatoid arthritis (RA), are characterized by the recruitment of inflammatory cells into joints. The K/BxN serum transfer mouse model of inflammatory arthritis shares many similar features with RA. In this autoantibody-induced model of arthritis, neutrophils are the critical immune cells necessary for the development of joint inflammation and damage. In this review, we describe the use of several methods to study the role of chemoattractant receptors, including chemokine receptors, on the recruitment of neutrophils into the joint in the K/BxN model of inflammatory arthritis. This includes both traditional methods, such as flow cytometry, immunohistochemistry, and enzyme assays, as well as multiphoton in vivo microscopy that we have adapted to study the role of immune cell trafficking in and around the joint in live mice.
    No preview · Article · Jan 2016
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    ABSTRACT: The number of humanized mouse models for the human immunodeficiency virus (HIV)/Acquired Immunodeficiency Syndrome (AIDS) and other infectious diseases has expanded rapidly over the past eight years. Highly immunodeficient mouse strains, such as NOD/SCID/gamma chainnull (NSG, NOG), support better human hematopoietic cell engraftment. Another improvement is the derivation of highly immunodeficient mice, transgenic with human leukocyte antigens (HLA) and cytokines that supports development of HLA restricted human T cells and heightened human myeloid cell engraftment. Humanized mice are also used to study the HIV reservoir using new imaging techniques. In spite of these advances, there are still limitations in HIV immune responses and deficits in lymphoid structures in these models in addition to xenogeneic graft-versus-host responses. To understand and disseminate the improvements and limitations of humanized mouse models to the scientific community, the NIH sponsored and convened a meeting on April 15, 2015 to discuss the state of knowledge concerning these questions and best practices for selecting a humanized mouse model for a particular scientific investigation. This report summarizes the findings of the NIH meeting.
    Full-text · Article · Dec 2015 · AIDS research and human retroviruses
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    ABSTRACT: Background: Allergic non-asthmatic (ANA) adults experience upper airway symptoms of allergic disease such as rhinorrhea, congestion and sneezing without symptoms of asthma. The aim of this study was to utilize PET-CT functional imaging to determine whether allergen challenge elicits a pulmonary response in ANA subjects or whether their allergic disease is truly isolated to the upper airways. Methods: In 6 ANA subjects, bronchoalveolar lavages (BAL) were performed at baseline and 24h after instillation of an allergen and a diluent in separate lung lobes. After instillation (10h), functional imaging was performed to quantify and compare regional perfusion, ventilation, fractional gas content (Fgas), and glucose uptake rate (Ki) between the baseline, diluent and allergen lobes. BAL cell counts were also compared. Results: In ANA subjects, compared to the baseline and diluent lobes, perfusion and ventilation were significantly lower in the allergen lobe (median [inter-quartile range], baseline vs. diluent vs. allergen: Mean-normalized perfusion; 0.87 [0.85-0.97] vs. 0.90 [0.86-0.98] vs. 0.59 [0.55-0.67]; p<0.05. Mean-normalized ventilation 0.89 [0.88-0.98] vs. 0.95 [0.89-1.02] vs. 0.63 [0.52-0.67], p<0.05). In contrast, no significant differences were found in Fgas between baseline, diluent and allergen lobes or in Ki. Total cell counts, eosinophil and neutrophil cell counts (cells/ml BAL) were significantly greater in the allergen lobe compared to the baseline lobe (all P<0.05). Conclusions: Despite having no clinical symptoms of a lower airway allergic response (cough and wheeze) allergic non-asthmatic subjects have a pulmonary response to allergen exposure which manifests as reduced ventilation and perfusion.
    Full-text · Article · Dec 2015 · PLoS ONE
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    ABSTRACT: Background: Microvesicles (MVs) (100-1000 nm diameter) are subcellular particles that are enriched in nucleic acid, including microRNA (miR), which may be transferred from cell to cell as a novel form of intercellular communication. In this study, we wished to characterize the microRNA content of microvesicles purified from the synovial fluid of patients with osteoarthritis or rheumatoid arthritis. Furthermore, we wished to determine whether predominant miR species identified in RA SF MVs may be transferred to recipient fibroblast-like synoviocytes (FLS) in vitro. Methods: Discarded synovial fluid (SF) from patients with osteoarthritis (OA) (n=5) or rheumatoid arthritis (RA) (n=5) obtained during routine clinical care was transferred into tubes containing acid-citrate-dextrose and stored at 4°C until further processing. SF was treated with thromboplastin D, centrifuged at 300 g x 10 minutes and 3000 g x 15 minutes to remove cells and cellular debris, respectively, and filtered through a 0.8 m filter. Next, SF was placed into ultracentrifuge tubes diluted with sterile PBS in a 1:8 ratio and ultracentrifuged at 100,000 g x 90 min using a Beckman 70.1Ti rotor. Purified MV pellets were resuspended in sterile PBS at one-fifth the original volume and quantified using a Nanosight LM10 instrument. MicroRNA from purified MV pellets was purified using a miRNeasy Serum/Plasma Kit (Qiagen), reverse transcribed, and subject to miRNA analysis using miScript miRNA PCR Serum/Plasma Arrays. PCR array data were analyzed using the Qiagen GeneGlobe Data Analysis Center online software tool, normalizing to global CT mean of expressed miRNAs, using a cutoff of CT=37. Purified RA SF MVs were incubated with OA FLS for 16 hours, and pri-miR, pre-miR, and mature miR expression by FLS was determined by qPCR. Results: Purified RA SF MVs purified in this manner were significantly greater than OA SF MVs (OA vs. RA 24.95 vs. 53.55 million/l, p=0.0001). A total of 39 miRs showed greater than 2-fold statistically significant differences in expression between groups (p<0.05). Of these miRs, hsa-mir-223-3p expression was significantly upregulated in the RA SF MV group (102.4 fold regulation, p=0.005) when compared with the OA SF MV group. Addition of purified RA SF MVs to cultured human FLS induced expression of mir-223, but not pri-miR-223 or pre-mir-223, indicating that mir-223 in FLS was of exogenous (i.e. microvesicle) origin. Conclusion: Microvesicle numbers in RA synovial fluid are greater than in OA synovial fluid, consistent with other previously published reports. We found significantly increased expression of mir-223-3p in RA SF MV, likely reflecting myeloid cell activation in the inflamed joint, and demonstrated that mir-223 may be transferred to recipient FLS in vitro.
    No preview · Conference Paper · Nov 2015

  • No preview · Article · Oct 2015 · Chest
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    ABSTRACT: Anti-CD3 therapy of type 1 diabetes results in a temporary halt of the pathogenesis but does not constitute a permanent cure. One problem is the re-infiltration of the islets of Langerhans with regenerated, autoaggressive lymphocytes. We aimed at blocking such a re-entry by neutralizing the key chemokine CXCL10. Combination therapy of diabetic RIP-LCMV and NOD mice with anti-CD3 and anti-CXCL10 antibodies caused a substantial remission of diabetes and was superior to monotherapies with anti-CD3 or anti-CXCL10 alone. The combination therapy prevented islet-specific T cells from re-entry of the islets of Langerhans and thereby blocked the autodestructive process. In addition, the local immune balance in the pancreas was shifted towards a regulatory phenotype. A sequential temporal inactivation of T cells and blockade of T cell migration might constitute a novel therapy for patients with type 1 diabetes. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    No preview · Article · Aug 2015 · Diabetes
  • Nancy D Kim · Andrew D Luster
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    ABSTRACT: Neutrophils are first responders of the immune system, rapidly migrating into affected tissues in response to injury or infection. To effectively call in this first line of defense, strategically placed cells within the vasculature and tissue respond to noxious stimuli by sending out coordinated signals that recruit neutrophils. Regulation of organ-specific neutrophil entry occurs at two levels. First, the vasculature supplying the organ provides cues for neutrophil egress out of the bloodstream in a manner dependent upon its unique cellular composition and architectural features. Second, resident immune cells and stromal cells within the organ send coordinated signals that guide neutrophils to their final destination. Here, we review recent findings that highlight the importance of these tissue-specific responses in the regulation of neutrophil recruitment and the initiation and resolution of inflammation. Copyright © 2015 Elsevier Ltd. All rights reserved.
    No preview · Article · Aug 2015 · Trends in Immunology
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    ABSTRACT: Initial events after exposure determine HIV-1 disease progression, underscoring a critical need to understand host mechanisms that interfere with initial viral replication. Although associated with chronic HIV-1 control, it is not known whether interleukin-21 (IL-21) contributes to early HIV-1 immunity. Here we take advantage of tractable primary human lymphoid organ aggregate cultures to show that IL-21 directly suppresses HIV-1 replication, and identify microRNA-29 (miR-29) as an antiviral factor induced by IL-21 in CD4 T cells. IL-21 promotes transcription of all miR-29 species through STAT3, whose binding to putative regulatory regions within the MIR29 gene is enriched by IL-21 signalling. Notably, exogenous IL-21 limits early HIV-1 infection in humanized mice, and lower viremia in vivo is associated with higher miR-29 expression. Together, these findings reveal a novel antiviral IL-21-miR-29 axis that promotes CD4 T-cell-intrinsic resistance to HIV-1 infection, and suggest a role for IL-21 in initial HIV-1 control in vivo.
    Full-text · Article · Jun 2015 · Nature Communications
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    ABSTRACT: T-cell trafficking at vascular sites has emerged as a key step in antitumour immunity. Chemokines are credited with guiding the multistep recruitment of CD8(+) T cells across tumour vessels. However, the multiplicity of chemokines within tumours has obscured the contributions of individual chemokine receptor/chemokine pairs to this process. Moreover, recent studies have challenged whether T cells require chemokine receptor signalling at effector sites. Here we investigate the hierarchy of chemokine receptor requirements during T-cell trafficking to murine and human melanoma. These studies reveal a non-redundant role for Gαi-coupled CXCR3 in stabilizing intravascular adhesion and extravasation of adoptively transferred CD8(+) effectors that is indispensable for therapeutic efficacy. In contrast, functional CCR2 and CCR5 on CD8(+) effectors fail to support trafficking despite the presence of intratumoral cognate chemokines. Taken together, these studies identify CXCR3-mediated trafficking at the tumour vascular interface as a critical checkpoint to effective T-cell-based cancer immunotherapy.
    No preview · Article · Jun 2015 · Nature Communications
  • Jeffrey Lian · Andrew D Luster
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    ABSTRACT: The generation of adaptive immune responses occurs in the lymph node (LN) and requires that lymphocytes locate and interact with cognate antigen-bearing dendritic cells. This process requires the coordinated movement of both innate and adaptive immune cells, and is orchestrated by the chemokine family of chemotactic cytokines. Upon initiation of inflammation, the LN undergoes dramatic changes that include the marked induction of specific chemokines in distinct regions of the reactive LN. These chemokine rich domains establish LN niches that facilitate the differentiation of CD4+ T cells into effector cell subsets and the rapid activation of memory CD8+ T cells. This review will focus on recent advances highlighting the importance of LN chemokines for shaping adaptive immune responses by controlling immune cell migration, positioning, and interactions in the reactive LN. Copyright © 2015 Elsevier Ltd. All rights reserved.
    No preview · Article · Jun 2015 · Current opinion in cell biology
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    C. Miyabe · K. Strle · Y. Miyabe · J.H. Stone · A.D. Luster · S. Unizony
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    ABSTRACT: Background Both CD4+ T helper (Th)-type 17 lymphocytes and Th1-type lymphocytes appear to contribute to the pathogenesis of giant cell arteritis (GCA). In addition, regulatory T cell (Treg) responses appear to be suppressed in GCA. Interleukin (IL)-6, highly expressed in GCA patients, is a key mediator in the differentiation of both Th17 and Treg cells. Preliminary experience in GCA with the use of tocilizumab (TCZ), an IL-6 receptor antagonist, has been encouraging. However, it is unknown whether TCZ affects the differentiation and function of these CD4+ T-cell subsets in these patients. Objectives We aimed to characterize the effector and regulatory CD4+ T-cell compartments in the peripheral blood of GCA patients treated with TCZ. Methods We evaluated 38 GCA patients classified into one of three categories: 1) active disease (aGCA, n=9); 2) disease remission on corticosteroid (CS) monotherapy (rGCA-CS, n=18); and 3) disease remission on TCZ therapy (rGCA-TCZ, n=11). Nine healthy controls were also included. Using flow cytometry, we determined the percentages (%) of IFNg+IL-17- (Th1), IL-17+IFNg- (Th17), CD25high (Treg), and CD45RA-Foxp3high (activated Treg, aTreg) cells within the CD4+ lymphocyte population. In addition, we determined the % of Foxp3+ cells expressing Ki67 (proliferating Treg). We assessed Treg function in suppression assays. Serum concentrations of IL-12, IFNg, IL-6, IL-1β, IL-23, IL-21, TNF-α, CCL20, IL-17A, and IL-10 were measured by Luminex. Results The frequencies (mean %) of Th1, Th17, and Treg cells were equivalent across groups. However, the frequency of aTregs was higher in rGCA-TCZ patients (1.3%) compared with rGCA-CS patients (0.6%; p=0.02). Moreover, the number of proliferating Tregs was significantly higher in rGCA-TCZ patients (31.7%) compared to rGCA-CS (16.4%; p=0.003) and aGCA (15.5%; p=0.007) patients. Tregs were functional in all groups. IL-10 levels were significantly increased in the serum of patients with aGCA. There were no significant differences in the serum levels of other cytokines or chemokines measured. Conclusions The therapeutic effects of tocilizumab in GCA could be mediated by increasing the activation and proliferative potential of Tregs. Further studies are needed to expand these preliminary findings. References Disclosure of Interest None declared
    Full-text · Article · Jun 2015 · Annals of the Rheumatic Diseases
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    ABSTRACT: Chronic exposure to crystalline silica (CS) causes silicosis, an irreversible lung inflammatory disease that may eventually lead to lung cancer. In this study, we demonstrate that in K-ras LA1 mice, CS exposure markedly enhances the lung tumour burden and genetic deletion of leukotriene B4 receptor-1 (BLT1 À / À) attenuates this increase. Pulmonary neutrophilic inflammation induced by CS is significantly reduced in BLT1 À / À K-ras LA1 mice. CS exposure induces LTB 4 production by mast cells and macrophages independent of inflammasome activation. In an air-pouch model, CS-induced neutrophil recruitment is dependent on LTB 4 production by mast cells and BLT1 expression on neutrophils. In an implantable lung tumour model, CS exposure results in rapid tumour growth and decreased survival that is attenuated in the absence of BLT1. These results suggest that the LTB 4 /BLT1 axis sets the pace of CS-induced sterile inflammation that promotes lung cancer progression. This knowledge may facilitate development of immunotherapeutic strategies to fight silicosis and lung cancer.
    Full-text · Article · Apr 2015 · Nature Communications
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    ABSTRACT: The molecules and pathways that fine-tune innate inflammatory responses mediated by Toll-like receptor 7 (TLR7) remain to be fully elucidated. Using an unbiased genome-scale screen with short hairpin RNA (shRNA), we identified the receptor TREML4 as an essential positive regulator of TLR7 signaling. Macrophages from Treml4(-/-) mice were hyporesponsive to TLR7 agonists and failed to produce type I interferons due to impaired phosphorylation of the transcription factor STAT1 by the mitogen-activated protein kinase p38 and decreased recruitment of the adaptor MyD88 to TLR7. TREML4 deficiency reduced the production of inflammatory cytokines and autoantibodies in MRL/lpr mice, which are prone to systemic lupus erythematosus (SLE), and inhibited the antiviral immune response to influenza virus. Our data identify TREML4 as a positive regulator of TLR7 signaling and provide insight into the molecular mechanisms that control antiviral immunity and the development of autoimmunity.
    Preview · Article · Apr 2015 · Nature Immunology
  • Maud Deruaz · Andrew D Luster
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    ABSTRACT: The genital tract mucosa is the site where sexually transmitted infections gain entry to the host. The immune response at this site is thus critical to provide innate protection against pathogens that are seen for the very first time as well as provide long-term pathogen-specific immunity, which would be required for an effective vaccine against sexually transmitted infection. A finely regulated immune response is therefore required to provide an effective barrier against pathogens without compromising the capacity of the genital tract to allow for successful conception and fetal development. We review recent developments in our understanding of the immune response in the female genital tract to infectious pathogens, using herpes simplex virus-2, human immunodeficiency virus-1 and Chlamydia trachomatis as examples, with a particular focus on the role of chemokines in orchestrating immune cell migration necessary to achieve effective innate and adaptive immune responses in the female genital tract.Immunology and Cell Biology advance online publication, 17 March 2015; doi:10.1038/icb.2015.20.
    No preview · Article · Mar 2015 · Immunology and Cell Biology
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    Caroline L Sokol · Andrew D Luster
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    ABSTRACT: Chemokines are chemotactic cytokines that control the migration and positioning of immune cells in tissues and are critical for the function of the innate immune system. Chemokines control the release of innate immune cells from the bone marrow during homeostasis as well as in response to infection and inflammation. They also recruit innate immune effectors out of the circulation and into the tissue where, in collaboration with other chemoattractants, they guide these cells to the very sites of tissue injury. Chemokine function is also critical for the positioning of innate immune sentinels in peripheral tissue and then, following innate immune activation, guiding these activated cells to the draining lymph node to initiate and imprint an adaptive immune response. In this review, we will highlight recent advances in understanding how chemokine function regulates the movement and positioning of innate immune cells at homeostasis and in response to acute inflammation, and then we will review how chemokine-mediated innate immune cell trafficking plays an essential role in linking the innate and adaptive immune responses. Copyright © 2015 Cold Spring Harbor Laboratory Press; all rights reserved.
    Preview · Article · Jan 2015 · Cold Spring Harbor perspectives in biology
  • Zamaneh Mikhak · William W. Agace · Andrew D. Luster
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    ABSTRACT: Lymphocytes are the key cells of the adaptive immune system that provide antigen-specific responses tailored to the context of antigen exposure. Through cytokine release and antibody production, lymphocytes orchestrate and amplify the recruitment and function of other immune cells and contribute to host defense against invading pathogens and the pathogenesis of many inflammatory diseases. Lymphocyte function is critically dependent on their ability to traffic into the correct anatomic locations at the appropriate times. This process is highly regulated and requires that lymphocytes interact with various homing molecules and respond to tightly regulated navigational cues.
    No preview · Article · Jan 2015
  • Melvyn T Chow · Andrew D Luster
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    ABSTRACT: Chemokines are chemotactic cytokines that control the migration of cells between tissues and the positioning and interactions of cells within tissue. The chemokine superfamily consists of approximately 50 endogenous chemokine ligands and 20 G protein-coupled seven-transmembrane spanning signaling receptors. Chemokines mediate the host response to cancer by directing the trafficking of leukocytes into the tumor microenvironment. This migratory response is complex and consists of diverse leukocyte subsets with both antitumor and protumor activities. Although chemokines were initially appreciated as important mediators of immune cell migration, we now know that they also play important roles in the biology of nonimmune cells important for tumor growth and progression. Chemokines can directly modulate the growth of tumors by inducing the proliferation of cancer cells and preventing their apoptosis. They also direct tumor cell movement required for metastasis. Chemokines can also indirectly modulate tumor growth through their effects on tumor stromal cells and by inducing the release of growth and angiogenic factors from cells in the tumor microenvironment. In this Masters of Immunology primer, we focus on recent advances in understanding the complex nature of the chemokine system in tumor biology with a focus on how the chemokine system could be used to augment cancer immunotherapeutic strategies to elicit a more robust and long-lasting host antitumor immune response. Cancer Immunol Res; 2(12); 1125-31. ©2014 AACR. ©2014 American Association for Cancer Research.
    No preview · Article · Dec 2014

  • No preview · Conference Paper · Nov 2014
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    ABSTRACT: Dendritic cells (DCs) are well established as potent antigen-presenting cells critical to adaptive immunity. In vaccination approaches, appropriately stimulating lymph node-resident DCs (LNDCs) is highly relevant to effective immunization. Although LNDCs have been implicated in immune response, their ability to directly drive effective immunity to lymph-borne antigen remains unclear. Using an inactive influenza vaccine model and whole node imaging approaches, we observed surprising responsiveness of LNDC populations to vaccine arrival resulting in a transnodal repositioning into specific antigen collection sites within minutes after immunization. Once there, LNDCs acquired viral antigen and initiated activation of viral specific CD4(+) T cells, resulting in germinal center formation and B cell memory in the absence of skin migratory DCs. Together, these results demonstrate an unexpected stimulatory role for LNDCs where they are capable of rapidly locating viral antigen, driving early activation of T cell populations, and independently establishing functional immune response.
    Full-text · Article · Jul 2014 · Journal of Experimental Medicine
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    ABSTRACT: Obesity associates with increased numbers of inflammatory cells in adipose tissue (AT), including T cells, but the mechanism of T-cell recruitment remains unknown. This study tested the hypothesis that the chemokine receptor CXCR3 participates in T-cell accumulation in AT of obese mice and thus in the regulation of local inflammation and systemic metabolism. Obese wild-type mice exhibited higher mRNA expression of CXCR3 in periepididymal AT-derived stromal vascular cells compared with lean mice. We evaluated the function of CXCR3 in AT inflammation in vivo using CXCR3-deficient and wild-type control mice that consumed a high-fat diet. Periepididymal AT from obese CXCR3-deficient mice contained fewer T cells than obese controls after 8 and 16 weeks on high-fat diet, as assessed by flow cytometry. Obese CXCR3-deficient mice had greater glucose tolerance than obese controls after 8 weeks, but not after 16 weeks. CXCR3-deficient mice fed high-fat diet had reduced mRNA expression of proinflammatory mediators, such as monocyte chemoattractant protein-1 and regulated on activation, normal T cell expressed and secreted, and anti-inflammatory genes, such as Foxp3, IL-10, and arginase-1 in periepididymal AT, compared with obese controls. These results demonstrate that CXCR3 contributes to T-cell accumulation in periepididymal AT of obese mice. Our results also suggest that CXCR3 regulates the accumulation of distinct subsets of T cells and that the ratio between these functional subsets across time likely modulates local inflammation and systemic metabolism.
    Full-text · Article · May 2014 · Arteriosclerosis Thrombosis and Vascular Biology

Publication Stats

32k Citations
3,212.17 Total Impact Points

Institutions

  • 1993-2016
    • Harvard Medical School
      • • Department of Microbiology and Immunobiology
      • • Department of Pathology
      • • Department of Medicine
      • • Department of Genetics
      Boston, Massachusetts, United States
  • 2015
    • Tufts Medical Center
      Boston, Massachusetts, United States
  • 1998-2015
    • Harvard University
      Cambridge, Massachusetts, United States
  • 1995-2015
    • Massachusetts General Hospital
      • • Division of Rheumatology, Allergy and Immunology
      • • Center for Immunology and Inflammatory Diseases
      • • Pediatric Infectious Disease Unit
      • • Allergy and Clinical Immunology Unit
      • • Department of Medicine
      Boston, Massachusetts, United States
  • 2011
    • Chiba University
      • Department of Infection and Host Defense
      Tiba, Chiba, Japan
  • 1997-2011
    • Howard Hughes Medical Institute
      Ashburn, Virginia, United States
  • 2007
    • Medical University of Graz
      Gratz, Styria, Austria
  • 2003
    • Lund University
      Lund, Skåne, Sweden
  • 2002
    • Dana-Farber Cancer Institute
      • Department of Pediatric Oncology
      Boston, Massachusetts, United States
    • Harbor-UCLA Medical Center
      Torrance, California, United States
    • Vanderbilt University
      • Division of Cardiovascular Medicine
      Nashville, MI, United States
  • 1999
    • Metamark Genetics
      Cambridge, Massachusetts, United States
  • 1997-1999
    • McGill University
      • Meakins-Christie Laboratories
      Montréal, Quebec, Canada
  • 1996
    • Beth Israel Deaconess Medical Center
      • Department of Medicine
      Boston, MA, United States
  • 1987-1991
    • The Rockefeller University
      • • Laboratory of Investigative Dermatology
      • • Laboratory of Cellular Physiology and Immunology
      New York, New York, United States
  • 1985-1988
    • Memorial Sloan-Kettering Cancer Center
      • DeWitt Wallace Research Laboratory
      New York, New York, United States