Kathleen E Sullivan

The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States

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Publications (185)774.86 Total impact

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    ABSTRACT: BACKGROUND: Dedicator of cytokinesis 8 (DOCK8) mutations are responsible for a rare primary combined immunodeficiency syndrome associated with severe cutaneous viral infections, increased IgE levels, autoimmunity, and malignancy. Natural killer (NK) cells are essential for tumor surveillance and defense against virally infected cells. NK cell function relies on Wiskott-Aldrich syndrome protein for filamentous actin (F-actin) accumulation at the lytic NK cell immunologic synapse. DOCK8 activates cell division cycle 42, which, together with Wiskott-Aldrich syndrome protein, coordinates F-actin reorganization. Although abnormalities in T- and B-cell function have been described in DOCK8-deficient patients, the role of NK cells in this disease is unclear. OBJECTIVES: We sought to understand the role of DOCK8 in NK cell function to determine whether NK cell abnormalities explain the pathogenesis of the clinical syndrome of DOCK8 deficiency. METHODS: A cohort of DOCK8-deficient patients was assembled, and patients' NK cells, as well as NK cell lines with stably reduced DOCK8 expression, were studied. NK cell cytotoxicity, F-actin content, and lytic immunologic synapse formation were measured. RESULTS: DOCK8-deficient patients' NK cells and DOCK8 knockdown cell lines all had decreased NK cell cytotoxicity, which could not be restored after IL-2 stimulation. Importantly, DOCK8 deficiency impaired F-actin accumulation at the lytic immunologic synapse without affecting overall NK cell F-actin content. CONCLUSIONS: DOCK8 deficiency results in severely impaired NK cell function because of an inability to form a mature lytic immunologic synapse through targeted synaptic F-actin accumulation. This defect might underlie and explain important attributes of the DOCK8 deficiency clinical syndrome, including the unusual susceptibility to viral infection and malignancy.
    The Journal of allergy and clinical immunology 02/2013; · 12.05 Impact Factor
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    ABSTRACT: Influenza is a common respiratory pathogen. Its severity can be unpredictable, but people with chronic illness are at increased risk of severe infection, complications, and death from influenza. This review examines evidence to support various strategies to protect pediatric oncology patients from influenza-related morbidity. Influenza vaccination should be considered standard. Additional evidence-supported measures include antiviral treatment, antiviral prophylaxis, cohorting of patients, and hospital infection control measures. Data from other high-risk populations support the vaccination of family members, double-dose or high-dose vaccination, and the use of barrier methods. These measures have the potential to optimize patient outcomes because there will be fewer treatment interruptions for acute illness. These strategies can also protect patients from prolonged hospitalizations and morbidity related to influenza.
    The Oncologist 01/2013; · 4.10 Impact Factor
  • Revue du Rhumatisme. 01/2013;
  • Solrun Melkorka Maggadottir, Kathleen E. Sullivan
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    ABSTRACT: A 2-year-old boy with chromosome 22q11.2 deletion syndrome was referred for recurrent sinopulmonary infections. He was diagnosed shortly after birth by a fluorescence in situ hybridization test that was performed due to interrupted aortic arch type B. He had no hypocalcemia, and his recovery from cardiac repair was uneventful. He had difficulty feeding and gained weight slowly, but, otherwise, there were no concerns during his first year of life. At 15 months of age, he began to develop significant otitis media and bronchitis. He was hospitalized once for pneumonia at 18 months of age and has never been off antibiotics for more than 1 week since then. He has not had any previous immunologic evaluation. Recurrent sinopulmonary infections in a child with chromosome 22q11.2 deletion syndrome can have the same etiologies as in any other child. Atopy, anatomic issues, cystic fibrosis, and new environmental exposures could be considered in this setting. Early childhood can be problematic for patients with chromosome 22q11.2 deletion syndrome due to unfavorable drainage of the middle ear and sinuses. Atopy occurs at a higher frequency in 22q11.2 deletion syndrome, and these children also have a higher rate of gastroesophageal reflux and aspiration than the general population. As would be appropriate for any child who presents with recurrent infections at 2 years of age, an immunologic evaluation should be performed. In this review, we will highlight recent findings and new data on the management of children and adults with chromosome 22q11.2 deletion syndrome.
    The Journal of Allergy and Clinical Immunology: In Practice. 01/2013; 1(6):589–594.
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    ABSTRACT: BACKGROUND: 22q11.2 deletion syndrome (22q11.2DS) is the most common microdeletion disorder, affecting an estimated 1 : 2000-4000 live births. Patients with 22q11.2DS have a broad spectrum of phenotypic abnormalities which generally includes congenital cardiac abnormalities, palatal anomalies, and immunodeficiency. Additional findings, such as skeletal anomalies and autoimmune disorders, can confer significant morbidity in a subset of patients. 22q11.2DS is a contiguous gene DS and over 40 genes are deleted in patients; thus deletion of several genes within this region contributes to the clinical features. Mutations outside or on the remaining 22q11.2 allele are also known to modify the phenotype. METHODS: We utilised whole exome, targeted exome and/or Sanger sequencing to examine the genome of 17 patients with 22q11.2 deletions and phenotypic features found in <10% of affected individuals. RESULTS AND CONCLUSIONS: In four unrelated patients, we identified three novel mutations in SNAP29, the gene implicated in the autosomal recessive condition cerebral dysgenesis, neuropathy, ichthyosis and keratoderma (CEDNIK). SNAP29 maps to 22q11.2 and encodes a soluble SNARE protein that is predicted to mediate vesicle fusion at the endoplasmic reticulum or Golgi membranes. This work confirms that the phenotypic variability observed in a subset of patients with 22q11.2DS is due to mutations on the non-deleted chromosome, which leads to unmasking of autosomal recessive conditions such as CEDNIK, Kousseff, and a potentially autosomal recessive form of Opitz G/BBB syndrome. Furthermore, our work implicates SNAP29 as a major modifier of variable expressivity in 22q11.2 DS patients.
    Journal of Medical Genetics 12/2012; · 5.70 Impact Factor
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    ABSTRACT: Please cite this paper as: Kersun et al. (2012) A prospective study of chemotherapy immunologic effects and predictors of humoral influenza vaccine responses in a pediatric oncology cohort. Influenza and Other Respiratory Viruses DOI: 10.1111/irv.12058. Background:  Pediatric oncology patients represent a cohort of individuals uniquely at risk of complications from influenza, yet less likely to respond to the vaccine. It is not yet clear how to best protect this vulnerable population. Methods:  We performed a prospective analysis of 177 pediatric oncology patients to define the predictors of influenza vaccine responses. Each variable was examined over three time points and a repeated measure analysis was performed. Results:  Patients with ALL vaccinated during induction phase had superior influenza vaccine responses than those subjects vaccinated during post-induction or maintenance phases (P = 0·0237). Higher aggregate HAI titer responses were associated with a higher baseline B-cell count (P = 0·0240), and higher CD4 and CD8 influenza-specific T-cell responses, suggesting prior antigen exposure is a significant contributor. The solid tumor cohort had equivalent responses during all time frames of chemotherapy. Discussion:  The optimal protection from influenza of pediatric patients on chemotherapy should include vaccination, but it is clear that not all patients produce high titers of antibodies after vaccination. This study identified biomarkers that could be used to individualize vaccine approaches. Immunologic predictors might have a role in targeting resources, as B-cell counts predicted of vaccine responses among the patients with ALL.
    Influenza and Other Respiratory Viruses 11/2012; · 1.47 Impact Factor
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    ABSTRACT: PURPOSE: Children with high-risk neuroblastoma have a poor prognosis with chemotherapy alone and hematopoietic stem cell transplantation offers improved survival. As a dose escalation strategy, tandem transplants have been utilized, but are associated with persistent immune compromise. This study evaluated the provision of an autologous co-stimulated, activated T cell product to support immunologic function. EXPERIMENTAL DESIGN: Nineteen subjects with high risk neuroblastoma were enrolled in a pilot phase and twenty three subjects were entered in to the randomized study. Immunologic reconstitution was defined by flow cytometry and functional assays. Next generation sequencing was performed to identify changes to the T cell repertoire. Twenty-two patients were vaccinated to define effects on antibody responses. RESULTS: Subjects who received their autologous co-stimulated T cell product on Day 2 had significantly superior T cell counts and T cell proliferation compared to those who received T cells on Day 90. Early administration of autologous T cells suppressed oligoclonality and enhanced repertoire diversity. The subjects who received the Day 2 T cell product also had better responses to the pneumococcal vaccine. CONCLUSIONS: The infusion of activated T cells can improve immunologic function especially when given early after transplant. This study demonstrated the benefit of providing cell therapies during periods of maximum lymphopenia.
    Clinical Cancer Research 10/2012; · 7.84 Impact Factor
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    ABSTRACT: The efficacy of influenza vaccination in patients treated with rituximab is a clinically important question. Rheumatology clinics are populated with patients receiving rituximab for a broad array of disorders. Although several studies have explored the efficacy of other vaccines in rituximab-treated populations, results have been conflicting. We wished to define influenza vaccine efficacy in a rituximab-treated cohort. We examined 17 evaluable subjects treated with rituximab for rheumatologic conditions. T cell subsets, B cells subsets, T cell function, and B cell function were evaluated at specific time points along with hemagglutinination inhibition titers after receiving the standard inactivated influenza vaccine. T cell subset counts were significantly different than controls but did not change with rituximab. B cells depleted in all patients but were in various stages of recovery at the time of vaccination. Influenza vaccine responsiveness was poor overall, with only 16 % of subjects having a four-fold increase in titer. Pre-existing titers were retained throughout the study, however. The ability to respond to the influenza vaccine appeared to be related to the degree of B cell recovery at the time of vaccination. This study emphasizes that antibody responses to vaccine are impaired in subjects treated with rituximab and supports the concept that B cell recovery influences influenza vaccine responsiveness.
    Journal of Clinical Immunology 10/2012; · 3.38 Impact Factor
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    ABSTRACT: There are few data characterizing the immunologic consequences of chemotherapy for acute myeloid leukemia (AML) and almost nothing is known about the effects of chemotherapy in a pediatric AML cohort. We identified T-cell subsets, B-cell subsets, and used Enzyme-linked immunosorbent spot analyses to define the function of T cells and B cells in 7 pediatric patients with AML on chemotherapy. The data show that the effects of chemotherapy disproportionately target the B cell and depletion of B cells is associated with impaired responses to the inactivated influenza vaccine. Diminished T-cell numbers were also observed although the magnitude of the effect was less than what was seen for B cells. Furthermore, measures of T-cell function were largely intact. We conclude that humoral immunity is significantly affected by chemotherapy for AML.
    Journal of Pediatric Hematology/Oncology 09/2012; · 0.97 Impact Factor
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    ABSTRACT: DiGeorge syndrome is associated with a T-lymphocyte immunodeficiency. The prevalence of hypogammaglobulinemia has not been reported. We found that 3% of patients with DiGeorge syndrome were receiving immunoglobulin replacement therapy and 6% of patients over the age of 3 years had hypogammaglobulinemia. We conclude that DiGeorge syndrome is associated with significant humoral immune deficiency.
    The Journal of pediatrics 07/2012; 161(5):950-953.e1. · 4.02 Impact Factor
  • Samuel Goldfarb, Kathleen E Sullivan, Soma Jyonouchi
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    ABSTRACT: Dyskeratosis congenita (DKC) is a syndrome characterized by immunodeficiency, bone marrow (BM) failure, somatic abnormalities, and predisposition to malignancy, resulting from mutations in proteins involved in maintenance of telomeres. Pulmonary fibrosis resulting in respiratory failure is a serious complication affecting approximately 20% of DKC patients. Pediatric pulmonologists should consider this diagnosis in patients with lung fibrosis and concurrent immunodeficiency or BM failure. Pediatr Pulmonol. © 2012 Wiley Periodicals, Inc.
    Pediatric Pulmonology 03/2012; · 2.38 Impact Factor
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    The Journal of allergy and clinical immunology 02/2012; 129(6):1666-8. · 12.05 Impact Factor
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    ABSTRACT: PIDD are rare inherited disorders that can result in life-threatening infections. Allogeneic HSCT is the only cure for many primary immune deficiencies; however, the specific diseases and optimal type(s) of transplants are not clear. This study compares transplant outcomes in a large cohort with a relatively uniform pre- and post-transplant management strategies. We conducted a retrospective analysis of 39 pediatric patients who underwent HSCT for SCID (n = 25) or other immune deficiencies (n = 14) from 1986 to 2010. A structured case report form was used to collect clinical information. The outcomes of survival, immune reconstitution, engraftment, incidence of GvHD and IVIG dependency were tabulated. Overall survival rates were 88% for SCID and 86% for other primary immune deficiencies, which are high compared to other historical series. No single variable was associated with mortality. Immunoglobulin dependence occurred only in patients who had X-linked SCID and a parental donor haploidentical transplant. Because of improved supportive care and use of alternative donors and conditioning regimens, HSCT has become an acceptable option for an increasing number of PIDD subtypes not previously transplanted with high frequency. This study encourages greater use of transplantation.
    Pediatric Transplantation 11/2011; 16(1):63-72. · 1.50 Impact Factor
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    ABSTRACT: Pneumocystis jirovecii is a leading cause of opportunistic infections among the immune compromised. During the 1980s, attention focused on patients with HIV, however, with the advent of anti-retroviral therapy, we wished to revisit the question of underlying diseases associated with Pneumocystis pneumonia in children. We identified 80 cases from 1986 to 2006 and performed a retrospective chart review to identify clinical characteristics for each of the cases. HIV was the single most common associated underlying condition seen in this cohort, accounting for 39% of the cases overall, however, it was seen in just 15% of the cases since 1998. Transplant recipients and oncology patients together comprised another 39% of the cases, with 9% of cases attributed to primary immune deficiency and another 9% of cases associated with less well-recognized causes of susceptibility. This study documents the ongoing need for vigilance to diagnose Pneumocystis pneumonia in less well-recognized clinical scenarios.
    Pediatric Pulmonology 10/2011; 47(5):510-6. · 2.38 Impact Factor
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    ABSTRACT: Prior to the advent of cardiac bypass, most children with congenital cardiac anomalies and chromosome 22q11.2 deletion syndrome died. With improved technology, there is now a wave of young adults with chromosome 22q11.2 deletion syndrome requiring clinical care. Fifteen young children and 20 adults with chromosome 22q11.2 deletion had flow cytometry, functional T cell analyses, and functional B cell analyses to characterize their immune system. Subjects were vaccinated with the annual inactivated influenza vaccine, and responses were evaluated by hemagglutination inhibition titer assessment. The pattern of T cell subset abnormalities was markedly different between pediatric and adult patients. In spite of the cellular deficits observed in adults, titers produced after influenza vaccine administration were largely intact. We conclude that disruption to T cell production appears to have secondary consequences for T cell differentiation and B cell function although the clinical impact remains to be determined.
    Journal of Clinical Immunology 08/2011; 31(6):927-35. · 3.38 Impact Factor
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    ABSTRACT: IRF1 is a transcription factor that participates in interferon signaling. Previous studies of IRF1 binding have utilized in vitro assays. We used ChIP-seq in human monocytes to better define the recognition motif for IRF1. The newly identified 18bp motif (RAAASNGAAAGTGAAASY) is a refinement of the 13bp IRF1 motif commonly used. We utilized the 18bp consensus motif and identified 345 potential target genes. To compare the 18bp motif with the 13bp motif, we compared putative gene targets. Only 56 potential gene targets were defined by both consensus motifs. To compare biological effects of interferon on the 13bp and the 18bp consensus targets, we mined expression data from cells exposed to interferons or transfected with IRF1. In all cases, the 18bp consensus motif was more strongly associated with transcriptional responses than the 13bp motif. Therefore, the new 18bp consensus motif appears to have a greater association with biological activities of IRF1.
    Gene 07/2011; 487(1):21-8. · 2.20 Impact Factor
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    ABSTRACT: Common variable immunodeficiency (CVID) is a heterogeneous immune defect characterized by hypogammaglobulinemia, failure of specific antibody production, susceptibility to infections, and an array of comorbidities. To address the underlying immunopathogenesis of CVID and comorbidities, we conducted the first genome-wide association and gene copy number variation (CNV) study in patients with CVID. Three hundred sixty-three patients with CVID from 4 study sites were genotyped with 610,000 single nucleotide polymorphisms (SNPs). Patients were divided into a discovery cohort of 179 cases in comparison with 1,917 control subjects and a replication cohort of 109 cases and 1,114 control subjects. Our analyses detected strong association with the MHC region and association with a disintegrin and metalloproteinase (ADAM) genes (P combined = 1.96 × 10(-7)) replicated in the independent cohort. CNV analysis defined 16 disease-associated deletions and duplications, including duplication of origin recognition complex 4L (ORC4L) that was unique to 15 cases (P = 8.66 × 10(-16)), as well as numerous unique rare intraexonic deletions and duplications suggesting multiple novel genetic causes of CVID. Furthermore, the 1,000 most significant SNPs were strongly predictive of the CVID phenotype by using a Support Vector Machine algorithm with positive and negative predictive values of 1.0 and 0.957, respectively. Our integrative genome-wide analysis of SNP genotypes and CNVs has uncovered multiple novel susceptibility loci for CVID, both common and rare, which is consistent with the highly heterogeneous nature of CVID. These results provide new mechanistic insights into immunopathogenesis based on these unique genetic variations and might allow for improved diagnosis of CVID based on accurate prediction of the CVID clinical phenotypes by using our Support Vector Machine model.
    The Journal of allergy and clinical immunology 06/2011; 127(6):1360-7.e6. · 12.05 Impact Factor
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    ABSTRACT: The International 22q11.2 Deletion Syndrome Consortium** A 12-year-old boy currently is followed by multiple sub-specialists for problems caused by the chromosome 22q11.2 deletion syndrome (22q11DS) (Figure). He was born via spontaneous vaginal delivery, weighing 3033 g, to a 31-year-old G3P3 mother after a full-term pregnancy complicated only by mild polyhydramnios. Family history was non-contributory. Apgar scores were 8 at 1 minute and 9 at 5 minutes. With the exception of a weak cry, the results of the infant's initial examination were unremarkable, and he was moved to the well-baby nursery. Shortly thereafter, a cardiac murmur was noted, the cardiology department was consulted, and the child was transferred to a local tertiary care facility with a diagnosis of tetralogy of Fallot. Stable, he was discharged home at 3 days of life. At 5 days of life, he had jerky movements. On presentation to the local emergency department, his total calcium level was 4.7 mg/dL, and later partial hypoparathyroidism was diagnosed. At that time, a consulting geneticist suggested the diagnosis of chromosome 22q11DS. Weeks later, the family received a telephone call confirming the diagnosis with fluorescence in situ hybridization (FISH). No additional information about the diagnosis, prognosis, etiology, or recurrence risk was pro-vided until the child was 5 months of age, when he underwent cardiac repair at a third hospital, where a comprehensive 22q11DS program was in operation. In the interim, the child had feeding difficulties requiring supplemental nasogastric tube feeds, nasal regurgitation, and gastroesophageal reflux, while the parents searched the internet for reliable information about their son's diagnosis. Subsequent notable abnormalities and interventions included: recurrent otitis media with bilateral myringotomy tube placement at 6 months; angioplasty with left pulmonary artery stent placement after the identification of pulmonary artery stenosis with bilateral pleural effusions at age 6 years; chronic upper respiratory infections with significant T cell dysfunction requiring live viral vaccines to be held until age 7 years; velopharyngeal incompetence necessitating posterior pharyngeal flap surgery at 7 years; enamel hypoplasia and numerous caries resulting in 3 separate dental procedures under general cardiac anesthesia beginning at age 7 years; multiple cervical and thoracic vertebral anomalies with tho-racic levoconvex scoliosis and upper lumbar dextroscoliosis requiring growing rod placement at age 11 years with subse-quent rod extension at ages 11.5 and 12 years; postoperative hypocalcemia; short stature; constipation; and persistent idiopathic thrombocytopenia. Pertinent negative test results included normal renal ultrasound scanning and parental 22q11.2 deletion studies. On physical examination, the boy's height and weight have consistently tracked just below the fifth percentile, with no evidence of growth hormone deficiency. His head circumfer-ence is within reference range at the 25th percentile. Dysmor-phic features include: a low anterior hairline; hooded eyelids; malar flatness; normally formed but protuberant ears with attached lobes; a mildly deviated nose with a bulbous nasal tip and hypoplastic alae nasi; asymmetric crying facies with a thin upper lip; mild micrognathia; a sacral dimple; and soft tissue syndactyly of the second and third toes. Developmentally, the boy had mild delays in achieving mo-tor milestones, sitting at 11 months and walking at 18 months. However, he exhibited significant delays in the emergence of language: he never babbled, spoke his first words at age 3 years, and only achieved full conversational speech at 7 years. However, he had relative strengths in receptive language and communicated appropriately by the use of sign language. Now quite conversant, he is mainstreamed in the seventh grade with resource room supports. Moreover, he is affable, but exhibits anxiety and perseverations. Lastly, despite numerous medical, academic, and social challenges, he
    The Journal of pediatrics 05/2011; 159(2):332-9.e1. · 4.02 Impact Factor
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    ABSTRACT: Chronic granulomatous disease (CGD) is an inherited disorder of the nicotinamide adenine dinucleotide phosphate oxidase that leads to defective production of microbicidal superoxide and other oxidative radicals, resulting in increased susceptibility to invasive infections, especially those due to fungi. Geosmithia argillacea was identified from cultured isolates by genomic sequencing of the internal transcribed spacer region. Isolates previously identified as Paecilomyces variotii, a filamentous fungus closely resembling G. argillacea, were also examined. We identified G. argillacea as the cause of invasive mycosis in 7 CGD patients. In 5 cases, the fungus had been previously identified morphologically as P. variotii. All patients had pulmonary lesions; 1 had disseminated lesions following inhalational pneumonia. Infections involved the chest wall and contiguous ribs in 2 patients and disseminated to the brain in 1 patient. Four patients with pneumonia underwent surgical intervention. All patients responded poorly to medical treatment, and 3 died. We report the first cases of invasive mycosis caused by G. argillacea in CGD patients. G. argillacea infections in CGD are often refractory and severe with a high fatality rate. Surgical intervention has been effective in some cases. G. argillacea is a previously underappreciated and frequently misidentified pathogen in CGD that should be excluded when P. variotii is identified morphologically.
    Clinical Infectious Diseases 03/2011; 52(6):e136-43. · 9.37 Impact Factor
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    Z Zhang, L Song, K Maurer, A Bagashev, K E Sullivan
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    ABSTRACT: The character of monocytes is both molded by and contributes to ongoing immune responses. We hypothesized that monocyte polarization could have durable qualities and these would be mediated partly by changes in the chromatin. We defined genome-wide expression and histone H4 acetylation (H4ac) changes after γ-interferon (IFN), α-IFN and interleukin-4 treatment. To identify genes with altered potential for expression, we stimulated polarized monocytes and identified genes up- or downregulated after polarization and stimulation but not either treatment alone. We also defined durability after an 18-h or 3-day washout. Genes uniquely regulated after the combination of polarization and stimulus were durably altered, with 51% of the effects being durable. This gene set was highly enriched for cytokine-induced alterations in H4ac, with P-values ranging from 10(-24) to 10(-37). Certain regulons defined by patterns of expression were also associated with altered H4ac, with P-values ranging from 10(-4) to 10(-29). Networking software revealed a high density of mitogen-activated protein (MAP) kinase nodes in these clusters. Therefore, some changes in monocyte gene expression were sustained over a 3-day period. These durably altered gene sets were enriched for changes in H4ac and were associated with potential MAP kinase effects.
    Genes and immunity 03/2011; 12(6):445-56. · 4.22 Impact Factor

Publication Stats

3k Citations
774.86 Total Impact Points

Institutions

  • 1994–2014
    • The Children's Hospital of Philadelphia
      • • Department of Pediatrics
      • • Division of Oncology
      • • Division of Human Genetics and Molecular Biology
      Philadelphia, Pennsylvania, United States
  • 2013
    • Helsinki University Central Hospital
      • Division of Infectious Diseases
      Helsinki, Southern Finland Province, Finland
  • 2000–2012
    • University of Pennsylvania
      • • Perelman School of Medicine
      • • "Abramson" Cancer Center
      • • Department of Dermatology
      Philadelphia, PA, United States
  • 2010
    • Minneapolis Veterans Affairs Hospital
      Minneapolis, Minnesota, United States
  • 2003–2010
    • Hospital of the University of Pennsylvania
      • • Division of Pulmonary Allergy and Critical Care
      • • Department of Pediatrics
      Philadelphia, Pennsylvania, United States
    • Westat
      Maryland, United States
  • 2008
    • Treatment Research Institute, Philadelphia PA
      Philadelphia, Pennsylvania, United States
    • Boston Children's Hospital
      Boston, Massachusetts, United States
  • 2007
    • University Hospital Motol
      Praha, Praha, Czech Republic
    • Royal Liverpool and Broadgreen University Hospitals NHS Trust
      Liverpool, England, United Kingdom
    • Lund University
      • Department of Paediatrics
      Lund, Skane, Sweden
    • George Washington University
      • School of Medicine and Health Sciences
      Washington, D. C., DC, United States
    • Emory University
      Atlanta, Georgia, United States
  • 2006
    • Ninewells Hospital
      Dundee, Scotland, United Kingdom
    • Martin Luther University of Halle-Wittenberg
      Halle-on-the-Saale, Saxony-Anhalt, Germany
    • University of Strasbourg
      Strasburg, Alsace, France
  • 2005–2006
    • Cincinnati Children's Hospital Medical Center
      Cincinnati, Ohio, United States
    • Universitätsklinikum Schleswig - Holstein
      Kiel, Schleswig-Holstein, Germany
    • University of Chicago
      • Section of Gastroenterology, Hepatology and Nutrition
      Chicago, IL, United States
    • Northwestern University
      • Feinberg School of Medicine
      Evanston, IL, United States
    • University of Milan
      • Department of Internal Medicine
      Milano, Lombardy, Italy
  • 1993–2006
    • Johns Hopkins University
      • Department of Pediatrics
      Baltimore, Maryland, United States
  • 2004
    • BC Children's Hospital
      Vancouver, British Columbia, Canada
  • 1994–2004
    • Johns Hopkins Medicine
      • Department of Pediatrics
      Baltimore, Maryland, United States
  • 2002
    • University of California, Los Angeles
      • Department of Pediatrics
      Los Angeles, CA, United States
  • 1997
    • University of Auckland
      • Department of Molecular Medicine and Pathology
      Auckland, Auckland, New Zealand