Anna M. Scipioni
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Anna M. Scipioni has a total of 18 co-authors. Here are the top co-authors by number of shared publications:
- Allen R. Kunselman
Department of Public Health Sciences, Penn State College of Medicine, Hershey, PA, USA
1 shared publication Amélie Collins
Department of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, NY 10032; Department of Pediatrics, College of Physicians and Surgeons, Columbia University, New York, NY 10032
1 shared publication- Christy Stetter
Department of Public Health Sciences, Penn State Health Milton S. Hershey Medical Center, Hershey, Pennsylvania
1 shared publication - Eric Vivier
Aix Marseille Université, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d’Immunologie de Marseille-Luminy (CIML), Marseille, France
1 shared publication - Jaimie Maines
Obstetrics and Gynecology Penn State College of Medicine Hershey PA USA
1 shared publication - Jeffrey R. Kaiser
Departments of Pediatrics (Neonatal-Perinatal Medicine) and Obstetrics and Gynecology, Penn State Health Children's Hospital, Penn State College of Medicine, Hershey, Pennsylvania, USA
1 shared publication
Latest Publications
- Open Access
- 14 October 2021
- Published by Wiley in Ultrasound in Obstetrics & Gynecology
- Vol. 58 (S1) , 89-312
VP35.01: Standard Hadlock definition versus percentile change in estimated fetal weight for detection of suboptimal fetal growth: a non‐inferiority study
- 14 October 2021
- Published by Wiley in Ultrasound in Obstetrics & Gynecology
- Vol. 58 (S1) , 89-312
Open AccessVP35.01: Standard Hadlock definition versus percentile change in estimated fetal weight for detection of suboptimal fetal growth: a non‐inferiority study
- Open Access
- 1 February 2019
- Published by Elsevier in Journal of Adolescent Health
- Vol. 64 (2) , S13
24. Differential Expression Of Salivary Microrna In Anorexia Nervosa And Anxiety Disorders
- 1 February 2019
- Published by Elsevier in Journal of Adolescent Health
- Vol. 64 (2) , S13
Open Access24. Differential Expression Of Salivary Microrna In Anorexia Nervosa And Anxiety Disorders
- Open Access
- 15 February 2016
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 196 (4) , 1449-1454
Cutting Edge: Eomesodermin Is Sufficient To Direct Type 1 Innate Lymphocyte Development into the Conventional NK Lineage
Type 1 innate lymphocytes comprise two developmentally divergent lineages, type 1 helper innate lymphoid cells (hILC1s) and conventional NK cells (cNKs). All type 1 innate lymphocytes (ILCs) express the transcription factor T-bet, but cNKs additionally express Eomesodermin (Eomes). We show that deletion of Eomes alleles at the onset of type 1 ILC maturation using NKp46-Cre imposes a substantial block in cNK development. Formation of the entire lymphoid and nonlymphoid type 1 ILC compartment appears to require the semiredundant action of both T-bet and Eomes. To determine if Eomes is sufficient to redirect hILC1 development to a cNK fate, we generated transgenic mice that express Eomes when and where T-bet is expressed using Tbx21 locus control to drive expression of Eomes codons. Ectopic Eomes induces cNK-like properties across the lymphoid and nonlymphoid type 1 ILC compartments. Subsequent to their divergent lineage specification, hILC1s and cNKs thus possess substantial developmental plasticity.
- 15 February 2016
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 196 (4) , 1449-1454
Open AccessCutting Edge: Eomesodermin Is Sufficient To Direct Type 1 Innate Lymphocyte Development into the Conventional NK Lineage
Type 1 innate lymphocytes comprise two developmentally divergent lineages, type 1 helper innate lymphoid cells (hILC1s) and conventional NK cells (cNKs). All type 1 innate lymphocytes (ILCs) express the transcription factor T-bet, but cNKs additionally express Eomesodermin (Eomes). We show that deletion of Eomes alleles at the onset of type 1 ILC maturation using NKp46-Cre imposes a substantial block in cNK development. Formation of the entire lymphoid and nonlymphoid type 1 ILC compartment appears to require the semiredundant action of both T-bet and Eomes. To determine if Eomes is sufficient to redirect hILC1 development to a cNK fate, we generated transgenic mice that express Eomes when and where T-bet is expressed using Tbx21 locus control to drive expression of Eomes codons. Ectopic Eomes induces cNK-like properties across the lymphoid and nonlymphoid type 1 ILC compartments. Subsequent to their divergent lineage specification, hILC1s and cNKs thus possess substantial developmental plasticity.