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Article ; Online: Hormone Therapy for Transgender Men.

Narasimhan, Supraja / Safer, Joshua D

2018 Volume 45, Issue 3, Page(s) 319–322

Abstract: This article provides an account of the current understanding of hormone therapy options for transgender men and emphasizes the importance of continued physician-supervised monitoring for long-term care. ...

Abstract	This article provides an account of the current understanding of hormone therapy options for transgender men and emphasizes the importance of continued physician-supervised monitoring for long-term care.
MeSH term(s)	Female ; Gender Dysphoria/drug therapy ; Hormone Replacement Therapy/methods ; Humans ; Male ; Transgender Persons
Language	English
Publishing date	2018-04-26
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	193117-9
ISSN	1558-0504 ; 0094-1298
ISSN (online)	1558-0504
ISSN	0094-1298
DOI	10.1016/j.cps.2018.03.004
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Article: The Boston Medical Center Experience: An Achievable Model for the Delivery of Transgender Medical Care at an Academic Medical Center.

Klein, Pamela / Narasimhan, Supraja / Safer, Joshua D

Transgender health

2018 Volume 3, Issue 1, Page(s) 136–140

Abstract: Despite increasing appreciation for the medical needs of transgender individuals, the organization of transgender medical care remains suboptimal. Transgender individuals report difficulty in finding providers who have adequate expertise in caring for ... ...

Abstract	Despite increasing appreciation for the medical needs of transgender individuals, the organization of transgender medical care remains suboptimal. Transgender individuals report difficulty in finding providers who have adequate expertise in caring for transgender patients, a lack of provider cultural competence, health system barriers, and discrimination in healthcare settings. At Boston Medical Center (BMC), we sought to address these gaps within an existing academic medical center. In February 2016, BMC established a Center for Transgender Medicine and Surgery (CTMS) to provide a single address for patients to obtain transgender-specific services across a spectrum of healthcare needs. With the establishment of a CTMS at BMC, we were able to leverage broad transgender medical coverage across multiple specialties within an existing academic medical framework. Furthermore, the development of the CTMS resulted in our identification of multiple gaps in transgender healthcare which we could target. Large gaps in care for our institution included genital surgery, perisurgical support, adolescent care, and care coordination. Notably, most of our interventions used existing resources. We propose that this is a replicable model that should be adopted by other academic medical institutions.
Language	English
Publishing date	2018-07-01
Publishing country	United States
Document type	Journal Article
ISSN	2380-193X
ISSN	2380-193X
DOI	10.1089/trgh.2017.0054
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Article: A Large-Scale Proteomics Resource of Circulating Extracellular Vesicles for Biomarker Discovery in Pancreatic Cancer.

Bockorny, Bruno / Muthuswamy, Lakshmi / Huang, Ling / Hadisurya, Marco / Lim, Christine Maria / Tsai, Leo L / Gill, Ritu R / Wei, Jesse L / Bullock, Andrea J / Grossman, Joseph E / Besaw, Robert J / Narasimhan, Supraja / Tao, W Andy / Perea, Sofia / Sawhney, Mandeep S / Freedman, Steven D / Hidalgo, Manuel / Iliuk, Anton / Muthuswamy, Senthil K

medRxiv : the preprint server for health sciences

2023

Abstract: Pancreatic cancer has the worst prognosis of all common tumors. Earlier cancer diagnosis could increase survival rates and better assessment of metastatic disease could improve patient care. As such, there is an urgent need to develop biomarkers to ... ...

Abstract	Pancreatic cancer has the worst prognosis of all common tumors. Earlier cancer diagnosis could increase survival rates and better assessment of metastatic disease could improve patient care. As such, there is an urgent need to develop biomarkers to diagnose this deadly malignancy earlier. Analyzing circulating extracellular vesicles (cEVs) using 'liquid biopsies' offers an attractive approach to diagnose and monitor disease status. However, it is important to differentiate EV-associated proteins enriched in patients with pancreatic ductal adenocarcinoma (PDAC) from those with benign pancreatic diseases such as chronic pancreatitis and intraductal papillary mucinous neoplasm (IPMN). To meet this need, we combined the novel EVtrap method for highly efficient isolation of EVs from plasma and conducted proteomics analysis of samples from 124 individuals, including patients with PDAC, benign pancreatic diseases and controls. On average, 912 EV proteins were identified per 100μL of plasma. EVs containing high levels of PDCD6IP, SERPINA12 and RUVBL2 were associated with PDAC compared to the benign diseases in both discovery and validation cohorts. EVs with PSMB4, RUVBL2 and ANKAR were associated with metastasis, and those with CRP, RALB and CD55 correlated with poor clinical prognosis. Finally, we validated a 7-EV protein PDAC signature against a background of benign pancreatic diseases that yielded an 89% prediction accuracy for the diagnosis of PDAC. To our knowledge, our study represents the largest proteomics profiling of circulating EVs ever conducted in pancreatic cancer and provides a valuable open-source atlas to the scientific community with a comprehensive catalogue of novel cEVs that may assist in the development of biomarkers and improve the outcomes of patients with PDAC.
Language	English
Publishing date	2023-03-20
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.03.13.23287216
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Article ; Online: Organoid Sensitivity Correlates with Therapeutic Response in Patients with Pancreatic Cancer.

Grossman, Joseph E / Muthuswamy, Lakshmi / Huang, Ling / Akshinthala, Dipikaa / Perea, Sofia / Gonzalez, Raul S / Tsai, Leo L / Cohen, Jonah / Bockorny, Bruno / Bullock, Andrea J / Schlechter, Benjamin / Peters, Mary Linton B / Conahan, Catherine / Narasimhan, Supraja / Lim, Christine / Davis, Roger B / Besaw, Robert / Sawhney, Mandeep S / Pleskow, Douglas /

Berzin, Tyler M / Smith, Martin / Kent, Tara S / Callery, Mark / Muthuswamy, Senthil K / Hidalgo, Manuel

Clinical cancer research : an official journal of the American Association for Cancer Research

2021 Volume 28, Issue 4, Page(s) 708–718

Abstract: Purpose: Pancreatic ductal adenocarcinoma (PDAC) remains a significant health issue. For most patients, there are no options for targeted therapy, and existing treatments are limited by toxicity. The HOPE trial (Harnessing Organoids for PErsonalized ... ...

Abstract	Purpose: Pancreatic ductal adenocarcinoma (PDAC) remains a significant health issue. For most patients, there are no options for targeted therapy, and existing treatments are limited by toxicity. The HOPE trial (Harnessing Organoids for PErsonalized Therapy) was a pilot feasibility trial aiming to prospectively generate patient-derived organoids (PDO) from patients with PDAC and test their drug sensitivity and correlation with clinical outcomes. Experimental design: PDOs were established from a heterogeneous population of patients with PDAC including both basal and classical PDAC subtypes. Results: A method for classifying PDOs as sensitive or resistant to chemotherapy regimens was developed to predict the clinical outcome of patients. Drug sensitivity testing on PDOs correlated with clinical responses to treatment in individual patients. Conclusions: These data support the investigation of PDOs to guide treatment in prospective interventional trials in PDAC.
MeSH term(s)	Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/pathology ; Humans ; Organoids/pathology ; Pancreatic Neoplasms/pathology ; Prospective Studies
Language	English
Publishing date	2021-11-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-20-4116
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Article ; Online: Towards Resolving the Pro- and Anti-Tumor Effects of the Aryl Hydrocarbon Receptor.

Narasimhan, Supraja / Stanford Zulick, Elizabeth / Novikov, Olga / Parks, Ashley J / Schlezinger, Jennifer J / Wang, Zhongyan / Laroche, Fabrice / Feng, Hui / Mulas, Francesca / Monti, Stefano / Sherr, David H

International journal of molecular sciences

2018 Volume 19, Issue 5

Abstract: We have postulated that the aryl hydrocarbon receptor (AHR) drives the later, more lethal stages of some cancers when chronically activated by endogenous ligands. However, other studies have suggested that, under some circumstances, the AHR can oppose ... ...

Abstract	We have postulated that the aryl hydrocarbon receptor (AHR) drives the later, more lethal stages of some cancers when chronically activated by endogenous ligands. However, other studies have suggested that, under some circumstances, the AHR can oppose tumor aggression. Resolving this apparent contradiction is critical to the design of AHR-targeted cancer therapeutics. Molecular (siRNA, shRNA, AHR repressor, CRISPR-Cas9) and pharmacological (AHR inhibitors) approaches were used to confirm the hypothesis that AHR inhibition reduces human cancer cell invasion (irregular colony growth in 3D Matrigel cultures and Boyden chambers), migration (scratch wound assay) and metastasis (human cancer cell xenografts in zebrafish). Furthermore, these assays were used for a head-to-head comparison between AHR antagonists and agonists. AHR inhibition or knockdown/knockout consistently reduced human ER
MeSH term(s)	Animals ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Movement/drug effects ; Female ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Humans ; Neoplasm Invasiveness/genetics ; Neoplasm Invasiveness/pathology ; Neoplasm Invasiveness/prevention & control ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Receptors, Aryl Hydrocarbon/agonists ; Receptors, Aryl Hydrocarbon/antagonists & inhibitors ; Receptors, Aryl Hydrocarbon/genetics ; Zebrafish
Chemical Substances	Receptors, Aryl Hydrocarbon
Language	English
Publishing date	2018-05-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19051388
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Article ; Online: Determination of quantitative and site-specific DNA methylation of perforin by pyrosequencing.

Narasimhan, Supraja / Falkenberg, Virginia R / Khin, Maung M / Rajeevan, Mangalathu S

BMC research notes

2009 Volume 2, Page(s) 104

Abstract: Background: Differential expression of perforin (PRF1), a gene with a pivotal role in immune surveillance, can be attributed to differential methylation of CpG sites in its promoter region. A reproducible method for quantitative and CpG site-specific ... ...

Abstract	Background: Differential expression of perforin (PRF1), a gene with a pivotal role in immune surveillance, can be attributed to differential methylation of CpG sites in its promoter region. A reproducible method for quantitative and CpG site-specific determination of perforin methylation is required for molecular epidemiologic studies of chronic diseases with immune dysfunction. Findings: We developed a pyrosequencing based method to quantify site-specific methylation levels in 32 out of 34 CpG sites in the PRF1 promoter, and also compared methylation pattern in DNAs extracted from whole blood drawn into PAXgene blood DNA tubes (whole blood DNA) or DNA extracted from peripheral blood mononuclear cells (PBMC DNA) from the same normal subjects. Sodium bisulfite treatment of DNA and touchdown PCR were highly reproducible (coefficient of variation 1.63 to 2.18%) to preserve methylation information. Application of optimized pyrosequencing protocol to whole blood DNA revealed that methylation level varied along the promoter in normal subjects with extremely high methylation (mean 86%; range 82-92%) in the distal enhancer region (CpG sites 1-10), a variable methylation (range 49%-83%) in the methylation sensitive region (CpG sites 11-17), and a progressively declining methylation level (range 12%-80%) in the proximal promoter region (CpG sites 18-32) of PRF1. This pattern of methylation remained the same between whole blood and PBMC DNAs, but the absolute values of methylation in 30 out of 32 CpG sites differed significantly, with higher values for all CpG sites in the whole blood DNA. Conclusion: This reproducible, site-specific and quantitative method for methylation determination of PRF1 based on pyrosequencing without cloning is well suited for large-scale molecular epidemiologic studies of diseases with immune dysfunction. PBMC DNA may be better suited than whole blood DNA for examining methylation levels in genes associated with immune function.
Language	English
Publishing date	2009-06-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2413336-X
ISSN	1756-0500 ; 1756-0500
ISSN (online)	1756-0500
ISSN	1756-0500
DOI	10.1186/1756-0500-2-104
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Article ; Online: Determination of quantitative and site-specific DNA methylation of perforin by pyrosequencing

Rajeevan Mangalathu S / Khin Maung M / Falkenberg Virginia R / Narasimhan Supraja

BMC Research Notes, Vol 2, Iss 1, p

2009 Volume 104

Abstract: Abstract Background Differential expression of perforin ( PRF1 ), a gene with a pivotal role in immune surveillance, can be attributed to differential methylation of CpG sites in its promoter region. A reproducible method for quantitative and CpG site- ... ...

Abstract	Abstract Background Differential expression of perforin ( PRF1 ), a gene with a pivotal role in immune surveillance, can be attributed to differential methylation of CpG sites in its promoter region. A reproducible method for quantitative and CpG site-specific determination of perforin methylation is required for molecular epidemiologic studies of chronic diseases with immune dysfunction. Findings We developed a pyrosequencing based method to quantify site-specific methylation levels in 32 out of 34 CpG sites in the PRF1 promoter, and also compared methylation pattern in DNAs extracted from whole blood drawn into PAXgene blood DNA tubes (whole blood DNA) or DNA extracted from peripheral blood mononuclear cells (PBMC DNA) from the same normal subjects. Sodium bisulfite treatment of DNA and touchdown PCR were highly reproducible (coefficient of variation 1.63 to 2.18%) to preserve methylation information. Application of optimized pyrosequencing protocol to whole blood DNA revealed that methylation level varied along the promoter in normal subjects with extremely high methylation (mean 86%; range 82–92%) in the distal enhancer region (CpG sites 1–10), a variable methylation (range 49%–83%) in the methylation sensitive region (CpG sites 11–17), and a progressively declining methylation level (range 12%–80%) in the proximal promoter region (CpG sites 18–32) of PRF1 . This pattern of methylation remained the same between whole blood and PBMC DNAs, but the absolute values of methylation in 30 out of 32 CpG sites differed significantly, with higher values for all CpG sites in the whole blood DNA. Conclusion This reproducible, site-specific and quantitative method for methylation determination of PRF1 based on pyrosequencing without cloning is well suited for large-scale molecular epidemiologic studies of diseases with immune dysfunction. PBMC DNA may be better suited than whole blood DNA for examining methylation levels in genes associated with immune function.
Keywords	Medicine ; R ; Biology (General) ; QH301-705.5 ; Science (General) ; Q1-390
Subject code	570
Language	English
Publishing date	2009-06-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article: Genetic evaluation of the serotonergic system in chronic fatigue syndrome.

Smith, Alicia K / Dimulescu, Irina / Falkenberg, Virginia R / Narasimhan, Supraja / Heim, Christine / Vernon, Suzanne D / Rajeevan, Mangalathu S

Psychoneuroendocrinology

2008 Volume 33, Issue 2, Page(s) 188–197

Abstract: Chronic fatigue syndrome (CFS) is a debilitating disorder of unknown etiology with no known lesions, diagnostic markers or therapeutic intervention. The pathophysiology of CFS remains elusive, although abnormalities in the central nervous system (CNS) ... ...

Abstract	Chronic fatigue syndrome (CFS) is a debilitating disorder of unknown etiology with no known lesions, diagnostic markers or therapeutic intervention. The pathophysiology of CFS remains elusive, although abnormalities in the central nervous system (CNS) have been implicated, particularly hyperactivity of the serotonergic (5-hydroxytryptamine; 5-HT) system and hypoactivity of the hypothalamic-pituitary-adrenal (HPA) axis. Since alterations in 5-HT signaling can lead to physiologic and behavioral changes, a genetic evaluation of the 5-HT system was undertaken to identify serotonergic markers associated with CFS and potential mechanisms for CNS abnormality. A total of 77 polymorphisms in genes related to serotonin synthesis (TPH2), signaling (HTR1A, HTR1E, HTR2A, HTR2B, HTR2C, HTR3A, HTR3B, HTR4, HTR5A, HTR6, and HTR7), transport (SLC6A4), and catabolism (MAOA) were examined in 137 clinically evaluated subjects (40 CFS, 55 with insufficient fatigue, and 42 non-fatigued, NF, controls) derived from a population-based CFS surveillance study in Wichita, Kansas. Of the polymorphisms examined, three markers (-1438G/A, C102T, and rs1923884) all located in the 5-HT receptor subtype HTR2A were associated with CFS when compared to NF controls. Additionally, consistent associations were observed between HTR2A variants and quantitative measures of disability and fatigue in all subjects. The most compelling of these associations was with the A allele of -1438G/A (rs6311) which is suggested to have increased promoter activity in functional studies. Further, in silico analysis revealed that the -1438 A allele creates a consensus binding site for Th1/E47, a transcription factor implicated in the development of the nervous system. Electrophoretic mobility shift assay supports allele-specific binding of E47 to the A allele but not the G allele at this locus. These data indicate that sequence variation in HTR2A, potentially resulting in its enhanced activity, may be involved in the pathophysiology of CFS.
MeSH term(s)	Adult ; Case-Control Studies ; Chi-Square Distribution ; Chromosomes, Human, X/genetics ; Disability Evaluation ; Fatigue/diagnosis ; Fatigue/genetics ; Fatigue Syndrome, Chronic/diagnosis ; Fatigue Syndrome, Chronic/genetics ; Female ; Genetic Markers ; Humans ; Linkage Disequilibrium ; Male ; Middle Aged ; Receptor, Serotonin, 5-HT2A/genetics ; Receptors, Serotonin/classification ; Receptors, Serotonin/genetics ; Reference Values ; Serotonin Plasma Membrane Transport Proteins/genetics
Chemical Substances	Genetic Markers ; Receptor, Serotonin, 5-HT2A ; Receptors, Serotonin ; Serotonin Plasma Membrane Transport Proteins
Language	English
Publishing date	2008-02
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	197636-9
ISSN	1873-3360 ; 0306-4530
ISSN (online)	1873-3360
ISSN	0306-4530
DOI	10.1016/j.psyneuen.2007.11.001
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Article ; Online: In silico identification of an aryl hydrocarbon receptor antagonist with biological activity in vitro and in vivo.

Parks, Ashley J / Pollastri, Michael P / Hahn, Mark E / Stanford, Elizabeth A / Novikov, Olga / Franks, Diana G / Haigh, Sarah E / Narasimhan, Supraja / Ashton, Trent D / Hopper, Timothy G / Kozakov, Dmytro / Beglov, Dimitri / Vajda, Sandor / Schlezinger, Jennifer J / Sherr, David H

Molecular pharmacology

2014 Volume 86, Issue 5, Page(s) 593–608

Abstract: The aryl hydrocarbon receptor (AHR) is critically involved in several physiologic processes, including cancer progression and multiple immune system activities. We, and others, have hypothesized that AHR modulators represent an important new class of ... ...

Abstract	The aryl hydrocarbon receptor (AHR) is critically involved in several physiologic processes, including cancer progression and multiple immune system activities. We, and others, have hypothesized that AHR modulators represent an important new class of targeted therapeutics. Here, ligand shape-based virtual modeling techniques were used to identify novel AHR ligands on the basis of previously identified chemotypes. Four structurally unique compounds were identified. One lead compound, 2-((2-(5-bromofuran-2-yl)-4-oxo-4H-chromen-3-yl)oxy)acetamide (CB7993113), was further tested for its ability to block three AHR-dependent biologic activities: triple-negative breast cancer cell invasion or migration in vitro and AHR ligand-induced bone marrow toxicity in vivo. CB7993113 directly bound both murine and human AHR and inhibited polycyclic aromatic hydrocarbon (PAH)- and TCDD-induced reporter activity by 75% and 90% respectively. A novel homology model, comprehensive agonist and inhibitor titration experiments, and AHR localization studies were consistent with competitive antagonism and blockade of nuclear translocation as the primary mechanism of action. CB7993113 (IC50 3.3 × 10(-7) M) effectively reduced invasion of human breast cancer cells in three-dimensional cultures and blocked tumor cell migration in two-dimensional cultures without significantly affecting cell viability or proliferation. Finally, CB7993113 effectively inhibited the bone marrow ablative effects of 7,12-dimethylbenz[a]anthracene in vivo, demonstrating drug absorption and tissue distribution leading to pharmacological efficacy. These experiments suggest that AHR antagonists such as CB7993113 may represent a new class of targeted therapeutics for immunomodulation and/or cancer therapy.
MeSH term(s)	Animals ; Biological Factors/pharmacology ; Bone Marrow Cells/drug effects ; COS Cells ; Cell Line ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Chlorocebus aethiops ; Humans ; Ligands ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Aryl Hydrocarbon/antagonists & inhibitors ; Stromal Cells/drug effects ; Triple Negative Breast Neoplasms/drug therapy
Chemical Substances	Biological Factors ; Ligands ; Receptors, Aryl Hydrocarbon
Language	English
Publishing date	2014-08-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	124034-1
ISSN	1521-0111 ; 0026-895X
ISSN (online)	1521-0111
ISSN	0026-895X
DOI	10.1124/mol.114.093369
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Article: Bordetella pertussis infection of primary human monocytes alters HLA-DR expression.

Shumilla, Jennifer A / Lacaille, Vashti / Hornell, Tara M C / Huang, Jennifer / Narasimhan, Supraja / Relman, David A / Mellins, Elizabeth D

Infection and immunity

2004 Volume 72, Issue 3, Page(s) 1450–1462

Abstract: Bordetella pertussis is the causative agent of whooping cough, a potentially lethal respiratory disease in children. In immunocompetent individuals, B. pertussis infection elicits an effective adaptive immune response driven by activated CD4(+) T cells. ... ...

Abstract	Bordetella pertussis is the causative agent of whooping cough, a potentially lethal respiratory disease in children. In immunocompetent individuals, B. pertussis infection elicits an effective adaptive immune response driven by activated CD4(+) T cells. However, live B. pertussis persists in the host for 3 to 4 weeks prior to clearance. Thus, B. pertussis appears to have evolved short-term mechanisms for immune system evasion. We investigated the effects of B. pertussis wild-type strain BP338 on antigen presentation in primary human monocytes. BP338 infection reduced cell surface expression of HLA-DR and CD86 but not that of major histocompatibility complex class I proteins. This change in cell surface HLA-DR expression reflected intracellular redistribution of HLA-DR. The proportion of peptide-loaded molecules was unchanged in infected cells, suggesting that intracellular retention occurred after peptide loading. Although B. pertussis infection of monocytes induced rapid and robust expression of interleukin-10 (IL-10), HLA-DR redistribution did not appear to be explained by increased IL-10 levels. BP338-infected monocytes exhibited reduced synthesis of HLA-DR dimers. Interestingly, those HLA-DR proteins that were generated appeared to be longer-lived than HLA-DR in uninfected monocytes. BP338 infection also prevented gamma interferon (IFN-gamma) induction of HLA-DR protein synthesis. Using mutant strains of B. pertussis, we found that reduction in HLA-DR surface expression was due in part to the presence of pertussis toxin whereas the inhibition of IFN-gamma induction of HLA-DR could not be linked to any of the virulence factors tested. These data demonstrate that B. pertussis utilizes several mechanisms to modulate HLA-DR expression.
MeSH term(s)	Antigen Presentation ; Antigens, CD/metabolism ; B7-2 Antigen ; Bordetella pertussis/pathogenicity ; Cell Membrane/immunology ; HLA-DR Antigens/biosynthesis ; HLA-DR Antigens/metabolism ; Humans ; In Vitro Techniques ; Interferon-gamma/pharmacology ; Interleukin-10/biosynthesis ; Interleukin-10/pharmacology ; Membrane Glycoproteins/metabolism ; Monocytes/drug effects ; Monocytes/immunology ; Monocytes/microbiology ; Pertussis Toxin/toxicity ; Recombinant Proteins/pharmacology
Chemical Substances	Antigens, CD ; B7-2 Antigen ; CD86 protein, human ; HLA-DR Antigens ; Membrane Glycoproteins ; Recombinant Proteins ; Interleukin-10 (130068-27-8) ; Interferon-gamma (82115-62-6) ; Pertussis Toxin (EC 2.4.2.31)
Language	English
Publishing date	2004-02-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.72.3.1450-1462.2004
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