DR25 DataRelease

SDY1039: Scleroderma: Cyclophosphamide or Transplantation (SCOT)
Status: New
Description: This prospective, randomized, open-label, multi-center, 2-arm, Phase II clinical trial will randomize approximately 114 subjects with severe SSc in the United States and Canada. Subjects will be randomly assigned in a 1:1 ratio to a treatment of high-dose immunosuppressive therapy with autologous stem cell rescue (HDIT transplantation) or to treatment of monthly pulse IV cyclophosphamide. Subjects will be stratified by treatment center. The initial treatment period will be approximately 3 months for the HDIT transplantation arm (from the time of initiation of mobilization until the day of transplant) and 12 months for the cyclophosphamide arm. Subjects will be followed for up to 72 months after randomization. The study will continue for 54 months after the last subject is randomized.
Program/Contract:
ProgramContract
Autoimmunity Centers of Excellence (ACE) SCLERODERMA CYCLOPHOSPHAMIDE OR TRANSPLANTION STUDY (SCOT)
DOI: 10.21430/M3SM4YLTLH
Subjects: 75
Study PI, contact:
NameOrganizationSite
Publications:
Gastric antral vascular ectasia and its clinical correlates in patients with early diffuse systemic sclerosis in the SCOT trial.. J Rheumatol. Apr 2013. doi: 10.3899/jrheum.121087. Epub 2013 Feb 15. [Pubmed: 23418384]
Review: Hematopoietic Stem Cell Transplantation for Scleroderma: Effective Immunomodulatory Therapy for Patients With Pulmonary Involvement.. Arthritis Rheumatol. Oct 2016. doi: 10.1002/art.39748. [Pubmed: 27213276]
Myeloablative Autologous Stem-Cell Transplantation for Severe Scleroderma.. N Engl J Med. Jan 2018. doi: - [Pubmed: 29298160]
Resources:
ClinicalTrials.gov https://clinicaltrials.gov/ct2/show/NCT00114530]
Assays:None
Clinical Assessments:None
SDY1045: KIR and HLA in MS
Status: New
Description: The association of specific alleles and haplotypes at the HLA class I and class II loci with a variety of autoimmune diseases is well established. Recently, polymorphisms in the Killer Immunoglobulin-like Receptors (KIR) genes that encode the stimulatory and inhibitory receptors on NK cells have been reported to be associated with a few of the same HLA-associated diseases, (e.g. psoriatic arthritis, scleroderma, and T1D). The ligands recognized by many of these receptors are epitopes on HLA class I molecules. In this study, we examine the role of HLA and KIR alleles, haplotypes, and KIR gene-HLA ligand pairs with a clinically well-defined Multiple Sclerosis cohort and ethnically matched controls using our Roche 454 GS FLX sequencing system for allelic resolution typing of HLA and our high-throughput MALDI-TOF KIR genotyping assay.
Program/Contract:
ProgramContract
HLA Region Genetics in Immune-mediated Diseases I The Role of HLA and KIR in Rheumatoid Arthritis and Crohn's Disease
DOI: 10.21430/M3QW34U2SG
Subjects: 831
Study PI, contact:
NameOrganizationSite
Elizabeth Trachtenberg Children's Hospital & Research Center Oakland Children's Hospital & Research Center Oakland
Publications:
High resolution HLA analysis reveals independent class I haplotypes and amino-acid motifs protective for multiple sclerosis. Genes and Immunity Jan 2018. doi: 10.1038/s41435-017-0006-8 [Pubmed: 29307888]
Resources:
Assays:
Assay TypeNumber of Exp. Samples
HLA Typing 1662
KIR Typing 831
Clinical Assessments:None
SDY1171: Antibody-dependent enhancement of severe dengue disease in humans
Status: New
Description: For dengue viruses (DENV1-4), a specific range of antibody titer has been shown to enhance viral replication in vitro and severe disease in animal models. Although suspected, such antibody-dependent enhancement (ADE) of severe disease has not been shown to occur in humans. Using multiple statistical approaches to study a long-term pediatric cohort in Nicaragua, we show that risk of severe dengue disease is highest within a narrow range of pre-existing anti-DENV antibody titers. By contrast, we observe protection from all symptomatic dengue disease at high antibody titers. Thus, immune correlates of severe dengue must be evaluated separately from correlates of protection against symptomatic disease. These results have implications for studies of dengue pathogenesis and for vaccine development, because enhancement, not just lack of protection, is of concern.
Data are available upon request (eharris@berkeley.edu), as is required by the IRB-approved protocol for the Pediatric Dengue Cohort Study. The materials and data used in this study are covered by standard material transfer agreements.
Program/Contract:
ProgramContract
Protective Immunity Following Dengue Virus Natural Infections and Vaccination Protective Immunity Following Dengue Virus Natural Infections and Vaccination
DOI: 10.21430/M3NEL3QH3Q
Subjects: 0
Study PI, contact:
NameOrganizationSite
Eva Harris University of California, Berkeley University of California, Berkeley
Publications:
Antibody-dependent enhancement of severe dengue disease in humans. Science November 2017. doi: 10.1126/science.aan6836 [Pubmed: 29097492]
Resources:
Assays:None
Clinical Assessments:None
SDY1172: Systems Immunology of Malaria
Status: New
Description: Immunity to malaria can be acquired through natural exposure to Plasmodium falciparum (Pf), but only after years of repeated infections. Typically, this immunity is acquired by adolescence and confers protection against disease, but Pf infection per se. Efforts to understand the mechanisms of this immunity are integral to the development of a vaccine that would mimic the induction of adult immunity in children. The current study applies systems biology approaches to a cohort from the rural village of Kalifabougou, Mali, where Pf transmission is intense and seasonal. Signatures that correlate with protection from malaria may yield new hypotheses regarding the biological mechanisms through which malaria immunity is induced by natural Pf infection. The resulting datasets will be of considerable value in the urgent worldwide effort to develop a malaria vaccine that could prevent more than a million deaths annually.
Program/Contract:
ProgramContract
NIAID Laboratory of Immunogenetics NIAID Laboratory of Immunogenetics
DOI: 10.21430/M3CFFNO2V3
Subjects: 80
Study PI, contact:
NameOrganizationSite
Peter Crompton NIH / NIAID / LIG NIH / NIAID / LIG
Publications:
An intensive longitudinal cohort study of Malian children and adults reveals no evidence of acquired immunity to Plasmodium falciparum infection. Clinical Infectious Diseases July 2013. doi: 10.1093/cid/cit174 [Pubmed: 23487390]
Naturally acquired antibodies specific for Plasmodium falciparum reticulocyte-binding protein homologue 5 inhibit parasite growth and predict protection from malaria.. Journal of Infectious Diseases March 2014. doi: 10.1093/infdis/jit553 [Pubmed: 24133188]
Co-infection of long-term carriers of Plasmodium falciparum with Schistosoma haematobium enhances protection from febrile malaria: a prospective cohort study in Mali.. PLoS Neglected Tropical Diseases September 2014. doi: 10.1371/journal.pntd.0003154 [Pubmed: 25210876]
A nested real-time PCR assay for the quantification of Plasmodium falciparum DNA extracted from dried blood spots. Malaria Journal October 2014. doi: 10.1186/1475-2875-13-393 [Pubmed: 25282516]
Gut microbiota elicits a protective immune response against malaria transmission. Cell December 2014. doi: 10.1016/j.cell.2014.10.053 [Pubmed: 25480293]
Impact of acute malaria on pre-existing antibodies to viral and vaccine antigens in mice and humans. PLoS One April 2015. doi: 10.1371/journal.pone.0125090 [Pubmed: 25919588]
Stool microbiota composition is associated with the prospective risk of Plasmodium falciparum infection. BMC Genomics August 2015. doi: 10.1186/s12864-015-1819-3 [Pubmed: 26296559]
Circulating Th1-Cell-type Tfh cells that exhibit impaired B cell help are preferentially activated during acute malaria in children. Cell Reports October 2015. doi: 10.1016/j.celrep.2015.09.004 [Pubmed: 26440897]
Transcriptome evidence for modulation of host inflammatory response during febrile P. falciparum malaria. Scientific Reports August 2016. doi: 10.1038/srep31291 [Pubmed: 27506615]
Treatment of chronic asymptomatic Plasmodium falciparum infection does not increase the risk of clinical malaria upon reinfection. Clinical Infectious Diseases March 2017. doi: 10.1093/cid/ciw849 [Pubmed: 28362910]
Public antibodies to malaria antigens generated by two LAIR1 insertion modalities. Nature August 2017. doi: 10.1038/nature23670 [Pubmed: 28847005]
Resources:
Trials.gov https://clinicaltrials.gov/ct2/show/study/NCT01322581]
RNA-seq GEO https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52166]
Assays:
Assay TypeNumber of Exp. Samples
RNA sequencing 151
Clinical Assessments:
Febrile Mal
Protection Status
Temperature
SDY1185: Dog Sarcoma Therapy
Status: New
Description: The drug eBAT is a bispecific angiotoxin targeted to both tumor and tumor neovasculature for sarcomas. It has been shown effectively kills canine hemangiosarcoma and human sarcoma cells in vitro. The paper studied the drug in an in vivo ?ontarget? companion dog trial. Splenectomized dogs with minimal residual disease were given one cycle of eBAT followed by adjuvant doxorubicin in an adaptive dose-finding, phase I?II study of 23 dogs with spontaneous, stage I?II, splenic hemangiosarcoma. eBAT improved 6-month survival from <40% in a comparison population to approximately 70% in dogs treated at a biologically active dose (50 ?g/kg). Six dogs were long-term survivors, living >450 days. The expected targeted markers, uPAR and EGFR, are validated in both human and canine sarcoma samples. The results support further translation of eBAT for human patients with sarcomas and perhaps other EGFR-expressing malignancies.
Program/Contract:
ProgramContract
Research Projects to Enhance Applicability of Mammalian Models for Translational Research Preclinical Evaluation And Clinical Translation Of Novel Bispecific Toxins
Research Projects to Enhance Applicability of Mammalian Models for Translational Research Preclinical Evaluation and Clinical Translation of Novel Bispecific Targeted Toxins for the Treatment of Sarcomas
DOI: 10.21430/M3F266SILJ
Subjects: 114
Study PI, contact:
NameOrganizationSite
Antonella Borgatti University of Minnesota Masonic Cancer Center
Publications:
Safe and Effective Sarcoma Therapy through Bispecific Targeting of EGFR and uPAR.. Mol Cancer Ther. May 2017. doi: 10.1158/1535-7163.MCT-16-0637. Epub 2017 Feb 13. [Pubmed: 28193671]
Resources:
PRJNA345482 https://www.ncbi.nlm.nih.gov/bioproject/PRJNA345482]
PRJNA376380 https://www.ncbi.nlm.nih.gov/bioproject/PRJNA376380]
PRJNA376379 https://www.ncbi.nlm.nih.gov/bioproject/PRJNA376379]
Assays:
Assay TypeNumber of Exp. Samples
RNA sequencing 146
Clinical Assessments:None
SDY1205: PTB-associated ancestry variants identification through genome-wide analysis
Status: New
Description: Preterm birth (PTB), the delivery of an infant prior to 37 weeks of gestation, is a significant determinant of infant morbidity and mortality. The vast majority of PTBs are spontaneous, caused by either preterm labor or preterm premature rupture of membranes (PPROM). The exact mechanism of spontaneous PTB is unknown, though a multitude of social, environmental, and maternal factors have been implicated. Various observations, such as the tendency for recurrent PTBs and the increased risk of preterm delivery for women who themselves were born preterm, suggest a heritable component to the risk of PTB. Twin studies estimate that maternal genetic variants account for approximately 27% to 36% of the incidence of PTB. A recent study estimated that 11% of variation is due to fetal genetic effects, and a follow up study found a significant effect in individuals with European ancestry, but not African Americans. PTB rates vary among races and ethnicities, with significantly higher rates observed in African Americans, though it is currently unclear how the genetics of PTB differ across groups. This study is a cross-ethnic, ancestry-informed GWAS analysis of 1,349 infants born prematurely. A large cohort of over 12,000 individuals obtained by leveraging publicly available data served as a control cohort. Using this approach, after extensive filtering and quality control, two intergenic variants, statistically significantly associated with PTB were identified. Several existing replication cohorts were queried and no support of these associations were found. The authors concludes that the fetal genetic contribution to PTB is unlikely due to single common genetic variant, but could be explained by interactions of multiple common variants, or of rare variants affected by environmental influences, all not detectable using a GWAS alone.
Program/Contract:
ProgramContract
March of Dimes March of Dimes Human Microbiome
DOI: 10.21430/M37N6PJEQT
Subjects: 0
Study PI, contact:
NameOrganizationSite
Marina Sirota University of California, San Fransisco University of California, San Fransisco
Atul Butte University of California, San Fransisco University of California, San Fransisco
Publications:
A genome-wide association study identifies only two ancestry specific variants associated with spontaneous preterm birth.. Sci Rep. Jan 2018. doi: 10.1038/s41598-017-18246-5. [Pubmed: 29317701]
Resources:
University of Michigan HRS ? Control Cohort http://hrsonline.isr.umich.edu/gwas]
dbGAP ? Control Cohort data https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000428.v2.p2]
1000 Genomes Project http://www.internationalgenome.org/]
GWAS Data Visualization http://comphealth.ucsf.edu/ptb_gwas/]
Assays:None
Clinical Assessments:None
SDY1206: Early pregnancy vaginal microbiome trends and preterm birth (see companion study SDY1341)
Status: New
Description: Previous studies have shown that vaginal microbiota of asymptomatic, nonpregnant, reproductive age women cluster into 5 distinct ?community-state types?, which differ both by dominant Lactobacillus species as well as overall community composition. A much greater proportion of African-American and Hispanic women harbored a non-Lactobacillus-dominant community, suggesting that in some women a non-Lactobacillus-based vaginal community may be a normal variant. A recent study examined vaginal microbial composition and the risk for preterm birth but had very few African-American subjects and few preterm births. This study characterizes vaginal microbial community characteristics over time in a large predominantly African-American cohort of pregnant women and test whether particular community characteristics are associated with the risk for subsequent preterm birth.
Program/Contract:
ProgramContract
March of Dimes March of Dimes Human Microbiome
DOI: 10.21430/M3H1U3KJMZ
Subjects: 77
Study PI, contact:
NameOrganizationSite
Methodius Tuuli Washington University in St Louis School of Medicine, St. Louis, MO Washington University in St Louis School of Medicine, St. Louis, MO
Molly Stout Washington University in St Louis School of Medicine, St. Louis, MO Washington University in St Louis School of Medicine, St. Louis, MO
Publications:
Early pregnancy vaginal microbiome trends and preterm birth.. Am J Obstet Gynecol. Sep 2017. doi: 10.1016/j.ajog.2017.05.030. Epub 2017 May 23. [Pubmed: 28549981]
Resources:
SRA ? Microbiome Data https://www.ncbi.nlm.nih.gov/bioproject/PRJNA294119/]
Assays:
Assay TypeNumber of Exp. Samples
16S rRNA gene sequencing 149
Clinical Assessments:
Pregnancy History
SDY1215: Mitochondrial and Nuclear Ancestry Association to PTB
Status: New
Description: The risk of preterm birth is unequally distributed between different ethnic groups. African American women are at increased risk for delivering preterm compared with the population as a whole. Determining the etiologies responsible for this heightened risk is complex, because it can be difficult to distinguish environmental and genetic influences. Attempts to elucidate such influences have evaluated carefully controlled populations, such as members of the military, to conclude that African ancestry is an independent risk factor. Specifying genetic risk factors in a related group is greatly complicated by false attribution, but a possible link between Americans of African descent is that African haplogroup mitochondrial DNA (mtDNA) is highly prevalent in this group. Matrilineal pedigree and mitochondrial ancestry are both consistent with a mitochondria-inherited risk factor. There is also evidence that mitochondrial function is important for the maintenance of pregnancy. However, attempts to link preterm birth to specific polymorphisms in mtDNA in case-control studies failed to identify polymorphisms associated with preterm birth. Thus, it remains unclear how a mtDNA-specific inheritance pattern could be associated with a common outcome like preterm birth. Mitochondrial haplogroup and nuclear ancestry for individuals were determined and used to develop a scoring for the degree to which mitochondrial ancestry is divergent from nuclear ancestry. Infants with higher degrees of divergent mitochondrial ancestry were at increased risk for preterm birth (0.124 for preterm vs 0.105 for term infants; P < .05). This finding was validated in 1 of 2 replication cohorts. Greater degrees of divergent ancestry correlating with earlier delivery within the primary study population was observed, but this finding was not replicated in secondary cohorts born preterm. Individuals with divergent patterns of mitochondrial and nuclear ancestry are at increased risk for preterm birth. These findings may in part explain the higher rates of preterm birth in African Americans and in individuals with a matrilineal family history of preterm birth.
Program/Contract:
ProgramContract
March of Dimes March of Dimes Human Microbiome
DOI: 10.21430/M3VCNPMD4B
Subjects: 0
Study PI, contact:
NameOrganizationSite
Neal Sondheimer Department of Pediatrics, The University of Toronto, Toronto, Ontario, Canada Department of Pediatrics, The University of Toronto, Toronto, Ontario, Canada
Publications:
Divergent Patterns of Mitochondrial and Nuclear Ancestry Are Associated with the Risk for Preterm Birth.. J Pediatr. Dec 2017. doi: 10.1016/j.jpeds.2017.10.052 [Pubmed: 29249523]
Resources:
Eunice Kennedy Shriver Institute of Child Health and Human Development Genomic and Proteomic Network for Preterm Birth Research (GPN) cohort https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000714.v1.p1]
Boston Birth Cohort (BBC) https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000332.v3.p2]
Danish National Birth Cohort Study (DNBC) https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000103.v1.p1]
Genetics Resource with the Health and Retirement Study (HRS) https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000428.v2.p2]
Genome-Wide Association Studies of Prematurity and Its Complications (GENEVA-AA) https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000353.v1.p1]
Assays:None
Clinical Assessments:None
SDY997: AMP Lupus Network Project: Molecular Characterization of Lupus Nephritis and Correlation with Response to Therapy
Status: Updated
Description: Phase I will be devoted to the study of at least 45 subjects with lupus nephritis and 25 controls with the intent of achieving the following goals: (i) to assess feasibility of obtaining a sufficient yield of high quality data based on current and refined AMP SOPs, (ii) to assess recruitment rates and the number of sites necessary to effectively recruit for Phase II, (iii) to ensure that the technologies developed in Phase 0 are working well, especially with regard to transport and scaling up to handle specimens from multiple sites; (iv) to demonstrate that the selected technologies can be used for the purpose of reliably differentiating lupus nephritis kidneys from kidney tissue without lupus nephritis, (v) where necessary, to further refine the technologies before embarking on a large-scale project; and most importantly (vi) to provide critical data upon which to make rational decisions about key elements of the Phase II study design (e.g., eligibility criteria, estimates of variation for power calculations, and site-specific capability regarding patient recruitment, specimen handling, etc.).
Program/Contract:
ProgramContract
Accelerating Medicines Partnership (AMP) Accelerating Medicines Partnership (AMP)
DOI: 10.21430/M35FLWNXH1
Subjects: 105
Study PI, contact:
NameOrganizationSite
PJ Utz Stanford PEARL
Michael Holers Colorado PEARL
Publications:None
Resources:
NIH AMP RA/SLE Program https://www.niams.nih.gov/Funding/Funded_Research/AMP_RA_Lupus/default.asp]
Assays:
Assay TypeNumber of Exp. Samples
CyTOF 259
Flow Cytometry 171
RNA sequencing 13415
Clinical Assessments:
SLE Assessments
SDY998: AMP Rheumatoid Arthritis Arthroplasty Phase 1
Status: Updated
Description: The primary goal for RA arthroplasty P1 studies are: To establish if molecular signatures and pathways identified using core AMP technologies differ between OA and RA in 20 RA surgical samples and 10 OA arthroplasty samples.
Program/Contract:
ProgramContract
Accelerating Medicines Partnership (AMP) Accelerating Medicines Partnership (AMP)
DOI: 10.21430/M3KXJHSP4T
Subjects: 40
Study PI, contact:
NameOrganizationSite
Jennifer Anolik Rochester Rochester
Vivian Bykerk HSS HSS
Larry Moreland Pittsburg Pittsburg
Michael Holers Colorado Colorado
Peter Gregersen Northwell Northwell
Gary Firestein UCSD UCSD
PJ Utz Stanford Stanford
Michael Weisman Cedars Sinai Cedars Sinai
Publications:None
Resources:
NIH AMP RA/SLE Program https://www.niams.nih.gov/Funding/Funded_Research/AMP_RA_Lupus/default.asp]
Assays:
Assay TypeNumber of Exp. Samples
CyTOF 105
Flow Cytometry 136
Microscopy 192
RNA sequencing 3856
Clinical Assessments:
Medical History
SDY999: AMP Rheumatoid Arthritis Synovial Phase 1
Status: Updated
Description: The primary goal for RA synovial P1 studies are: To establish feasibility of obtaining ultrasound-guided synovial biopsies in the United States (U.S.) by comparing to frozen synovial biopsies obtained in the United Kingdom (U.K.)
Program/Contract:
ProgramContract
Accelerating Medicines Partnership (AMP) Accelerating Medicines Partnership (AMP)
DOI: 10.21430/M3XRJHRPBC
Subjects: 22
Study PI, contact:
NameOrganizationSite
Jennifer Anolik Rochester Rochester
Vivian Bykerk HSS HSS
Gary Firestein UCSD UCSD
Peter Gregersen Northwell Northwell
Michael Holers Colorado Colorado
Larry Moreland Pittsburg Pittsburg
PJ Utz Stanford Stanford
Publications:None
Resources:
Assays:
Assay TypeNumber of Exp. Samples
CyTOF 70
Flow Cytometry 173
Microscopy 229
RNA sequencing 6333
Clinical Assessments:
Medical History
SDY1164: Vaginal microbial signature for preterm birth
Status: Updated
Description: Recent studies about association between maternal vaginal microbiota and risks for preterm birth (PTB) conflicted along similar lines: Caucasian and Asian women cohorts showed associations between PTB and low Lactobacillus vaginal communities (BV-like) while no significant association with PTB was detected in cohorts of African-American women. This study compares two new larger cohorts of women at low and high risk for PTB, addressing two challenges: (i) low power resulting from the combination of small study populations (30?91 pregnant women), the many taxa measured by metabarcoding, and the absence of initial hypotheses more specific than some difference between preterm and term gestations; and (ii) insufficient understanding of population-specific factors that might modulate the PTB?microbiota association.
Program/Contract:
ProgramContract
March of Dimes March of Dimes Human Microbiome
DOI: 10.21430/M37W3869AH
Subjects: 136
Study PI, contact:
NameOrganizationSite
David Relman March of Dimes Prematurity Research Center at Stanford University School of Medicine March of Dimes Prematurity Research Center at Stanford University School of Medicine
Publications:
Replication and refinement of a vaginal microbial signature of preterm birth in two racially distinct cohorts of US women.. Proc Natl Acad Sci U S A. Aug 2017. doi: - [Pubmed: 28847941]
Resources:
March of Dimes Prematurity Research Center at Stanford University http://prematurity.stanford.edu/]
SRA ? Raw sequencing data https://www.ncbi.nlm.nih.gov/sra/SRP115697]
Stanford Digital Repository - Sequence table and R scripts for analysis workflow https://purl.stanford.edu/yb681vm1809]
Assays:
Assay TypeNumber of Exp. Samples
16S rRNA gene sequencing 2367
Clinical Assessments:
Pregnancy Delivery
SDY1176: Extensive homeostatic T cell phenotypic variation within the Collaborative Cross
Status: Updated
Description: The Collaborative Cross (CC) is a panel of reproducible recombinant inbred mouse strains with high levels of standing genetic variation, thereby affording unprecedented opportunity to perform experiments in a small animal model containing controlled genetic diversity while allowing for genetic replicates. Here, we advance the utility of this unique mouse resource for immunology research, as it allows for both examination and genetic dissection of mechanisms behind adaptive immune states in mice with distinct and defined genetic makeups. This approach is founded on quantitative trait locus mapping: identifying genetically variant genome regions associated with phenotypic variance in traits-of-interest. Furthermore, the CC can be utilized for mouse model development; distinct strains have unique immunophenotypes and immune properties, making them suitable for research on particular diseases and infections. Here, we describe variation in cellular immune phenotypes across F1 crosses of CC strains, and reveal novel quantitative trait loci responsible for several immune phenotypes.
Program/Contract:
ProgramContract
Systems Approach to Immunity and Inflammation Systems Immunogenetics of Biodefense Pathogens in the Collaborative Cross
DOI: 10.21430/M3RKBKOYKS
Subjects: 476
Study PI, contact:
NameOrganizationSite
Jennifer Lund Fred Hutchinson Cancer Research Center Vaccine and Infectious Disease Division
Publications:None
Resources:
https://research.fhcrc.org/lund/en.html Dr. Jennifer Lund's Lab]
Assays:
Assay TypeNumber of Exp. Samples
Flow Cytometry 822
Clinical Assessments:None
Back to top