DR22 DataRelease
Release Date: 06/16/2017
| SDY625: Anti-CD20 in SLE | |||||||
| Status: | New | ||||||
| Description: | B cells clearly play an essential role in the pathogenesis of SLE since they produce autoantibodies. Clinical observations support the contention that intervening in the production of autoantibodies by the B lymphocyte will be effective therapy. Current approved therapy for B-cell non-Hodgkin's lymphoma includes anti-CD20. The results of anti-CD20 administration in SLE are anticipated to be similar to those in lymphoma patients. The current proposal explores the mechanisms and applicability of B-cell depletion as a potential treatment for SLE. | ||||||
| Program/Contract: |
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| DOI: | 10.21430/M3M92Y22FG | ||||||
| Subjects: | 24 | ||||||
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| Assays: | None | ||||||
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| SDY655: Use of Infliximab for the Treatment of Pemphigus Vulgaris | |||||
| Status: | New | ||||
| Description: | PV involves blistering of the outer layer of skin and mucous membranes, causing a separation of epidermal cells. The disease occurs when the immune system produces antibodies to specific proteins in the skin and mucous membranes; the cause for production of these autoantibodies is unknown. Infliximab is a genetically engineered monoclonal antibody directed against tumor necrosis factor (TNF)-alpha, a chemical messenger that activates an immune response. Infliximab has been used to treat other autoimmune disorders, including rheumatoid arthritis, ankylosing spondylitis, and Crohn's disease. This study will evaluate the safety and efficacy of infliximab given in combination with prednisone for the treatment of adults with PV. | ||||
| Program/Contract: |
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| DOI: | 10.21430/M3ZTR9VQ2U | ||||
| Subjects: | 20 | ||||
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| SDY824: Anti-TNF Agents in RA | |||||||
| Status: | New | ||||||
| Description: | This is a Phase IV, investigator-initiated, partially blinded, randomized, multi-center clinical trial designed to evaluate the mechanistic effects of TNF-a inhibition on clinical and mechanistic measures in RA patients. Subjects will be randomized to one of two active treatment arms, etanercept or adalimumab, and will receive treatment using standard dosing regimens for 24 weeks. Subjects will be randomized in a 2:1 ratio until 40 and 20 subjects are treated with etanercept and adalimumab, respectively. Clinical responses and serologic changes will be monitored throughout the study in all participants. Study visits are scheduled for Screening, Baseline/Treatment-Initiation, and at Weeks 12 and 24. In addition, to assess safety, blood draws are scheduled for Weeks 8 and16, and phone calls are scheduled for Weeks 4, 8, 16, and 20. In order to assess peripheral blood B and T cell changes after treatment initiation, all participating subjects will have a blood sample analyzed by flow cytometry for B and T cell subsets at Baseline/Treatment Initiation and Weeks 12 and 24. Etanercept drug levels will be assessed from samples drawn at Weeks 12 and 24 as study drug levels may impact clinical response. | ||||||
| Program/Contract: |
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| DOI: | 10.21430/M3LU5YSBYO | ||||||
| Subjects: | 63 | ||||||
| Study PI, contact: |
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| Publications: | None | ||||||
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| SDY961: Use of Rituximab for Sjogren's Syndrome | ||||||||||
| Status: | New | |||||||||
| Description: | This study is an open-label, one arm, Phase I study. The study intends to accrue 12 subjects with primary Sjogren's syndrome as defined by the revised European criteria proposed by the American-European Consensus Group over the course of 12 months. Eligible subjects will receive 2 infusions of rituximab at a dose of 1000 mg. The second treatment visit will be scheduled 14 days from the first infusion, within a window of 3 days. Following the treatment phase, subjects will enter a 50-week post-infusion follow-up period and receive no study medication. The sample size was chosen based on prior studies of rituximab treatment of SLE. This research protocol allows for 2 infusions of rituximab. Even if the treatment is shown to be of benefit, additional infusions of rituximab may not be given while the patient is participating in this study. | |||||||||
| Program/Contract: |
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| DOI: | 10.21430/M3G6VGUDEH | |||||||||
| Subjects: | 12 | |||||||||
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| Assays: | None | |||||||||
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| SDY1041: CMV CD8 T Cells | |||||||
| Status: | New | ||||||
| Description: | We present human T cell responses in multiple sites including blood, lymphoid, mucosal and secretory tissues of 20 CMV seropositive donors. Overall, CMV-specific T cells were maintained in distinct distribution patterns, either predominant in blood, bone marrow (BM) and lung, or lymph nodes (LN) with the frequency and function in blood distinct from tissues. Together, our results reveal tissue T cell reservoirs for CMV control, with global effects on T cell homeostasis over the human lifespan. | ||||||
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| DOI: | 10.21430/M3MIPLU7ZU | ||||||
| Subjects: | 20 | ||||||
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| Clinical Assessments: | None | ||||||
| SDY1043: A Haystack Heuristic for Autoimmune Disease Biomarker Discovery Using Next-Gen Immune Repertoire Sequencing Data | |||||||
| Status: | New | ||||||
| Description: | In this work, we present a new algorithm that employs local search techniques to discover statistically significant patient-specific motifs in large-scale immune-repertoire datasets. We apply our methodology successfully to our multi-million-sequence immune repertoire dataset to discover a statistically significant MS-specific motif. The discovered sequence motif could potentially serve as biomarker for the clinical diagnosis of Multiple Sclerosis. The presented methodology is efficient and generalizable to other high throughput sequencing datasets. | ||||||
| Program/Contract: |
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| DOI: | 10.21430/M3HUHJSPBP | ||||||
| Subjects: | 97 | ||||||
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| Publications: | None | ||||||
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| Clinical Assessments: | None | ||||||
| SDY1064: An Arntl2-Driven Secretome Enables Lung Adenocarcinoma Metastatic Self-Sufficiency | |||||||
| Status: | New | ||||||
| Description: | The ability of cancer cells to establish lethal metastatic lesions requires the survival and expansion of single cancer cells at distant sites. The factors controlling the clonal growth ability of individual cancer cells remain poorly understood. Here, we show that high expression of the transcription factor ARNTL2 predicts poor lung adenocarcinoma patient outcome. Arntl2 is required for metastatic ability in vivo and clonal growth in cell culture. Arntl2 drives metastatic self-sufficiency by orchestrating the expression of a complex pro-metastatic secretome. We identify Clock as an Arntl2 partner and functionally validate the matricellular protein Smoc2 as a pro-metastatic secreted factor. These findings shed light on the molecular mechanisms that enable single cancer cells to form allochthonous tumors in foreign tissue environments | ||||||
| Program/Contract: |
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| DOI: | 10.21430/M3LJ1COIXP | ||||||
| Subjects: | 2 | ||||||
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| Clinical Assessments: | None | ||||||
| SDY1079: A targetable CD109-Janus kinase-Stat axis in metastatic lung cancer. | |||||||
| Status: | New | ||||||
| Description: | The molecular mechanism of lung cancer metastatic remains incompletely understood. We combined tumor barcoding in a mouse model of human lung adenocarcinoma with unbiased genomic approaches to identify a transcriptional program that confers metastatic ability and predicts patient survival. Small-scale in vivo screening identified several genes, including Cd109, that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 as a critical, pharmacologically targetable effector of CD109-driven lung cancer metastasis. In summary, by coupling the systematic genomic analysis of purified cancer cells in distinct malignant states from mouse models with extensive human validation, we uncovered several key regulators of metastatic ability, including an actionable pro-metastatic CD109?Jak?Stat3 axis | ||||||
| Program/Contract: |
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| DOI: | 10.21430/M3HC3F4A8X | ||||||
| Subjects: | 2 | ||||||
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| Clinical Assessments: | None | ||||||
| SDY1085: RNAseq of Tumor-Associated Microglia Reveals Ccl5 as a Stromal Chemokine Critical for NF1 Glioma Growth | |||||||
| Status: | New | ||||||
| Description: | Solid cancers develop within a supportive microenvironment that promotes tumor formation and growth through the elaboration of mitogens and chemokines. Within these tumors, monocytes (macrophages and microglia) represent rich sources of these stromal factors. Leveraging a genetically engineered mouse model of neurofibromatosis type 1 (NF1) low-grade brain tumor (optic glioma), we have previously demonstrated that microglia are essential for glioma formation and maintenance. To identify potential tumor-associated microglial factors that support glioma growth (gliomagens), we initiated a comprehensive large-scale discovery effort using optimized RNA-sequencing methods focused specifically on glioma-associated microglia. Candidate microglial gliomagens were prioritized to identify potential secreted or membrane-bound proteins, which were next validated by quantitative real-time polymerase chain reaction as well as by RNA fluorescence in situ hybridization following minocycline-mediated microglial inactivation in vivo. Using these selection criteria, chemokine (C-C motif) ligand 5 (Ccl5) was identified as a chemokine highly expressed in genetically engineered Nf1 mouse optic gliomas relative to nonneoplastic optic nerves. As a candidate gliomagen, recombinant Ccl5 increased Nf1-deficient optic nerve astrocyte growth in vitro. Importantly, consistent with its critical role in maintaining tumor growth, treatment with Ccl5 neutralizing antibodies reduced Nf1 mouse optic glioma growth and improved retinal dysfunction in vivo. Collectively, these findings establish Ccl5 as an important microglial growth factor for low-grade glioma maintenance relevant to the development of future stroma-targeted brain tumor therapies | ||||||
| Program/Contract: |
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| DOI: | 10.21430/M3AZ2NQ0XP | ||||||
| Subjects: | 6 | ||||||
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| Clinical Assessments: | None | ||||||
| SDY1093: Apc Restoration in Colorectal Cancer | |||||||
| Status: | New | ||||||
| Description: | The Adenomatous Polyposis Coli (APC) tumor suppressor is mutated in the vast majority of human colorectal cancers (CRC) and leads to deregulated Wnt signaling. To determine whether Apc disruption is required for tumor maintenance, we developed a mouse model of CRC whereby Apc can be conditionally suppressed using a doxycycline-regulated shRNA. Apc suppression produces adenomas in both the small intestine and colon that, in the presence of Kras and p53 mutations, can progress to invasive carcinoma. In established tumors, Apc restoration drives rapid and widespread tumor-cell differentiation and sustained regression without relapse. Tumor regression is accompanied by the re-establishment of normal crypt-villus homeostasis, such that once aberrantly proliferating cells reacquire self-renewal and multi-lineage differentiation capability. Our study reveals that CRC cells can revert to functioning normal cells given appropriate signals, and provide compelling in vivo validation of the Wnt pathway as a therapeutic target for treatment of CRC | ||||||
| Program/Contract: |
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| DOI: | 10.21430/M3PC2VFTG8 | ||||||
| Subjects: | 20 | ||||||
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| Clinical Assessments: | None | ||||||
| SDY1097: Early-life compartmentalization of human T cells | |||||||
| Status: | New | ||||||
| Description: | Knowledge of human immune responses during early life remains sparse, owing to the difficulty and impracticality of obtaining blood and tissue samples from infants. Our current view of normal infant immune responses, including T cell differentiation and function, is based mainly on the sampling of umbilical cord blood or fetal tissue, which reflect immune responses in utero but not responses to the diverse antigens encountered in early life. Fundamental information about the establishment of adaptive immunity during infancy, including how T cells respond, differentiate and populate tissue sites, remains undefined. Through collaboration with organ procurement agencies, we have established protocols for obtaining lymphoid and mucosal tissues from individual organ donors for whom consent has been given for the use of tissues for research. | ||||||
| Program/Contract: |
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| DOI: | 10.21430/M35HJN0H16 | ||||||
| Subjects: | 43 | ||||||
| Study PI, contact: |
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| Clinical Assessments: | None | ||||||
| SDY1099: DNMT3A Haploinsufficiency Transforms FLT3 ITD Myeloproliferative Disease into AML | |||||||
| Status: | New | ||||||
| Description: | Cytogenetically normal acute myeloid leukemia (CN-AML) represents nearly 50% of human AML. Co-occurring mutations in the de novo DNA methyltransferase DNMT3A and the FMS related tyrosine kinase 3 (FLT3) are common in CN-AML and confer a poorer prognosis, but the molecular mechnism of the double-mutant is unknown. By using a rapid mouse model of FLT3/DNMT3A-Mutant AML and advanced global scRNAseq and methylation profiling techniques, the study demonstrates that DNMT3A haploinsufficiency results in reversible epigenetic alterations that transform FLT3 ITD -mutant myeloproliferative neoplasm into AML. | ||||||
| Program/Contract: |
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| DOI: | 10.21430/M3NA6MQNX3 | ||||||
| Subjects: | 8 | ||||||
| Study PI, contact: |
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| Clinical Assessments: | None | ||||||
| SDY196: Responses to Influenza Vaccination in Systemic Lupus Year 1 2005-2006 | |||||||||||||
| Status: | Updated | ||||||||||||
| Description: | Influenza is an important pathogen in the United States, with approximately 20,000 deaths per year, mainly among elderly people or those with underlying medical conditions that increase susceptibility to complications from the disease. In addition, considerable morbidity is associated with influenza with a significant impact in productivity in the workplace and home. Influenza has the potential for much more serious consequences as demonstrated by the appearance of four world-wide pandemics in the last century. In principle, serious influenza outbreaks can be prevented by vaccination. However, vaccination is complicated by two features: First, the influenza virus undergoes frequent mutations in the genes encoding the surface proteins hemagglutinin (HA) and neuraminidase (NA), leading to the need to reformulate the vaccine every year. Second, the appearance of the rapidity with which influenza infections can spread. Thus, influenza holds significant potential as a bioterrorism agent. Lupus patients have an increased risk of infection and mount lower responses to vaccinations. The objectives of this study will use genetic, cellular and humoral techniques to identify and explain abnormalities in the immune response to influenza vaccination in lupus patients. The results will clarify vaccine effectiveness among affected patients, increase the understanding of immune dysregulation in lupus, and aid in establishing guidelines for the effective vaccination of lupus patients. The benefits to the subjects are not direct; however, information gained may improve responses of reducing or preventing influenza among the affected population. Additionally, with an increased understanding of the processes of lupus, targets for disease intervention or strategies for treatment may appear. | ||||||||||||
| Program/Contract: |
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| DOI: | 10.21430/M3ABJS44K6 | ||||||||||||
| Subjects: | 62 | ||||||||||||
| Study PI, contact: |
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| SDY197: Responses to Influenza Vaccination in Systemic Lupus Year 2 2006-2007 | |||||||||||||
| Status: | Updated | ||||||||||||
| Description: | Influenza is an important pathogen in the United States, with approximately 20,000 deaths per year, mainly among elderly people or those with underlying medical conditions that increase susceptibility to complications from the disease. In addition, considerable morbidity is associated with influenza with a significant impact in productivity in the workplace and home. Influenza has the potential for much more serious consequences as demonstrated by the appearance of four world-wide pandemics in the last century. In principle, serious influenza outbreaks can be prevented by vaccination. However, vaccination is complicated by two features: First, the influenza virus undergoes frequent mutations in the genes encoding the surface proteins hemagglutinin (HA) and neuraminidase (NA), leading to the need to reformulate the vaccine every year. Second, the appearance of the rapidity with which influenza infections can spread. Thus, influenza holds significant potential as a bioterrorism agent. Lupus patients have an increased risk of infection and mount lower responses to vaccinations. The objectives of this study will use genetic, cellular and humoral techniques to identify and explain abnormalities in the immune response to influenza vaccination in lupus patients. The results will clarify vaccine effectiveness among affected patients, increase the understanding of immune dysregulation in lupus, and aid in establishing guidelines for the effective vaccination of lupus patients. The benefits to the subjects are not direct; however, information gained may improve responses of reducing or preventing influenza among the affected population. Additionally, with an increased understanding of the processes of lupus, targets for disease intervention or strategies for treatment may appear. | ||||||||||||
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| DOI: | 10.21430/M3FD1QTLQQ | ||||||||||||
| Subjects: | 63 | ||||||||||||
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| SDY198: Responses to Influenza Vaccination in Systemic Lupus Year 3 2007-2008 | |||||||||||||
| Status: | Updated | ||||||||||||
| Description: | Influenza is an important pathogen in the United States, with approximately 20,000 deaths per year, mainly among elderly people or those with underlying medical conditions that increase susceptibility to complications from the disease. In addition, considerable morbidity is associated with influenza with a significant impact in productivity in the workplace and home. Influenza has the potential for much more serious consequences as demonstrated by the appearance of four world-wide pandemics in the last century. In principle, serious influenza outbreaks can be prevented by vaccination. However, vaccination is complicated by two features: First, the influenza virus undergoes frequent mutations in the genes encoding the surface proteins hemagglutinin (HA) and neuraminidase (NA), leading to the need to reformulate the vaccine every year. Second, the appearance of the rapidity with which influenza infections can spread. Thus, influenza holds significant potential as a bioterrorism agent. Lupus patients have an increased risk of infection and mount lower responses to vaccinations. The objectives of this study will use genetic, cellular and humoral techniques to identify and explain abnormalities in the immune response to influenza vaccination in lupus patients. The results will clarify vaccine effectiveness among affected patients, increase the understanding of immune dysregulation in lupus, and aid in establishing guidelines for the effective vaccination of lupus patients. The benefits to the subjects are not direct; however, information gained may improve responses of reducing or preventing influenza among the affected population. Additionally, with an increased understanding of the processes of lupus, targets for disease intervention or strategies for treatment may appear. | ||||||||||||
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| DOI: | 10.21430/M3D393V41D | ||||||||||||
| Subjects: | 74 | ||||||||||||
| Study PI, contact: |
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| SDY199: Responses to Influenza Vaccination in Systemic Lupus Year 4 2008-2009 | |||||||||||||
| Status: | Updated | ||||||||||||
| Description: | Influenza is an important pathogen in the United States, with approximately 20,000 deaths per year, mainly among elderly people or those with underlying medical conditions that increase susceptibility to complications from the disease. In addition, considerable morbidity is associated with influenza with a significant impact in productivity in the workplace and home. Influenza has the potential for much more serious consequences as demonstrated by the appearance of four world-wide pandemics in the last century. In principle, serious influenza outbreaks can be prevented by vaccination. However, vaccination is complicated by two features: First, the influenza virus undergoes frequent mutations in the genes encoding the surface proteins hemagglutinin (HA) and neuraminidase (NA), leading to the need to reformulate the vaccine every year. Second, the appearance of the rapidity with which influenza infections can spread. Thus, influenza holds significant potential as a bioterrorism agent. Lupus patients have an increased risk of infection and mount lower responses to vaccinations. The objectives of this study will use genetic, cellular and humoral techniques to identify and explain abnormalities in the immune response to influenza vaccination in lupus patients. The results will clarify vaccine effectiveness among affected patients, increase the understanding of immune dysregulation in lupus, and aid in establishing guidelines for the effective vaccination of lupus patients. The benefits to the subjects are not direct; however, information gained may improve responses of reducing or preventing influenza among the affected population. Additionally, with an increased understanding of the processes of lupus, targets for disease intervention or strategies for treatment may appear. | ||||||||||||
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| DOI: | 10.21430/M39YLN3479 | ||||||||||||
| Subjects: | 69 | ||||||||||||
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| SDY200: Responses to Influenza Vaccination in Systemic Lupus Year 5 2009-2010 | |||||||||||
| Status: | Updated | ||||||||||
| Description: | Influenza is an important pathogen in the United States, with approximately 20,000 deaths per year, mainly among elderly people or those with underlying medical conditions that increase susceptibility to complications from the disease. In addition, considerable morbidity is associated with influenza with a significant impact in productivity in the workplace and home. Influenza has the potential for much more serious consequences as demonstrated by the appearance of four world-wide pandemics in the last century. In principle, serious influenza outbreaks can be prevented by vaccination. However, vaccination is complicated by two features: First, the influenza virus undergoes frequent mutations in the genes encoding the surface proteins hemagglutinin (HA) and neuraminidase (NA), leading to the need to reformulate the vaccine every year. Second, the appearance of the rapidity with which influenza infections can spread. Thus, influenza holds significant potential as a bioterrorism agent. Lupus patients have an increased risk of infection and mount lower responses to vaccinations. The objectives of this study will use genetic, cellular and humoral techniques to identify and explain abnormalities in the immune response to influenza vaccination in lupus patients. The results will clarify vaccine effectiveness among affected patients, increase the understanding of immune dysregulation in lupus, and aid in establishing guidelines for the effective vaccination of lupus patients. The benefits to the subjects are not direct; however, information gained may improve responses of reducing or preventing influenza among the affected population. Additionally, with an increased understanding of the processes of lupus, targets for disease intervention or strategies for treatment may appear. | ||||||||||
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| DOI: | 10.21430/M3ZR6IH181 | ||||||||||
| Subjects: | 73 | ||||||||||
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| SDY201: Responses to Influenza Vaccination in Systemic Lupus Year 6 2010-2011 | |||||||||||
| Status: | Updated | ||||||||||
| Description: | Influenza is an important pathogen in the United States, with approximately 20,000 deaths per year, mainly among elderly people or those with underlying medical conditions that increase susceptibility to complications from the disease. In addition, considerable morbidity is associated with influenza with a significant impact in productivity in the workplace and home. Influenza has the potential for much more serious consequences as demonstrated by the appearance of four world-wide pandemics in the last century. In principle, serious influenza outbreaks can be prevented by vaccination. However, vaccination is complicated by two features: First, the influenza virus undergoes frequent mutations in the genes encoding the surface proteins hemagglutinin (HA) and neuraminidase (NA), leading to the need to reformulate the vaccine every year. Second, the appearance of the rapidity with which influenza infections can spread. Thus, influenza holds significant potential as a bioterrorism agent. Lupus patients have an increased risk of infection and mount lower responses to vaccinations. The objectives of this study will use genetic, cellular and humoral techniques to identify and explain abnormalities in the immune response to influenza vaccination in lupus patients. The results will clarify vaccine effectiveness among affected patients, increase the understanding of immune dysregulation in lupus, and aid in establishing guidelines for the effective vaccination of lupus patients. The benefits to the subjects are not direct; however, information gained may improve responses of reducing or preventing influenza among the affected population. Additionally, with an increased understanding of the processes of lupus, targets for disease intervention or strategies for treatment may appear. | ||||||||||
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| DOI: | 10.21430/M35J0WA7CR | ||||||||||
| Subjects: | 34 | ||||||||||
| Study PI, contact: |
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| SDY691: HLA and KIR Haplotype Sequencing | |||||||
| Status: | Updated | ||||||
| Description: | Assay development for complete HLA and KIR haplotype sequencing from cell lines | ||||||
| Program/Contract: |
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| DOI: | 10.21430/M3RES1FXTG | ||||||
| Subjects: | 97 | ||||||
| Study PI, contact: |
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| Clinical Assessments: | None | ||||||