Jennifer Müller

ORCID: 0000-0001-6497-4320
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About
Contact & Profiles
Research Areas
  • T-cell and B-cell Immunology
  • Glycosylation and Glycoproteins Research
  • Immune Cell Function and Interaction
  • Immunotherapy and Immune Responses
  • Monoclonal and Polyclonal Antibodies Research
  • Immune Response and Inflammation
  • NF-κB Signaling Pathways
  • Down syndrome and intellectual disability research
  • Genomics and Rare Diseases
  • Mycobacterium research and diagnosis
  • Cell Adhesion Molecules Research
  • Genetics and Neurodevelopmental Disorders
  • RNA modifications and cancer
  • Ubiquitin and proteasome pathways
  • Advanced Fluorescence Microscopy Techniques
  • Pneumonia and Respiratory Infections
  • Neuroblastoma Research and Treatments
  • Cancer-related molecular mechanisms research
  • Immunodeficiency and Autoimmune Disorders
  • Galectins and Cancer Biology

The Francis Crick Institute
2016-2022

Friedrich-Alexander-Universität Erlangen-Nürnberg
2013-2020

University at Buffalo, State University of New York
2014

Essen University Hospital
2013

Temple Street Children's University Hospital
2013

A high proportion of human B cells carry B-cell receptors (BCRs) that are autoreactive. Inhibitory such as CD22 can downmodulate autoreactive BCR responses. With its extracellular domain, binds to sialic acids in α2,6 linkages cis , on the surface same cell or trans other cells. Sialic self ligands, they abundant vertebrates, but usually not expressed by pathogens. We show cis- ligand binding is crucial for regulation Ca 2+ signaling controlling association BCR. Mice with a mutated...

10.1073/pnas.1304888110 article EN Proceedings of the National Academy of Sciences 2013-07-08

Abstract Infection or vaccination leads to the development of germinal centers (GC) where B cells evolve high affinity antigen receptors, eventually producing antibody-forming plasma memory cells. Here we follow migratory pathways emerging from (B EM ) and find that many migrate into lymph node subcapsular sinus (SCS) guided by sphingosine-1-phosphate (S1P). From SCS, may exit enter distant tissues, while some interact with take up SCS macrophages, followed CCL21-guided return towards GC....

10.1038/s41467-022-29978-y article EN cc-by Nature Communications 2022-05-05

Memory B cells (MBCs) are long-lived that form a critical part of immunological memory, providing rapid antibody responses to recurring infections. However, very little is known about signals controlling MBC survival. Previous work has shown antigen not required for survival, but requirement the cell receptor (BCR) been tested. Other studies have that, unlike naive cells, MBCs do express BAFFR and their survival independent BAFF, ligand BAFFR. Here, using inducible genetic ablation, we show...

10.1084/jem.20191393 article EN cc-by The Journal of Experimental Medicine 2020-10-29

Signaling through the BCR can drive B cell activation and contribute to differentiation into Ab-secreting plasma cells. The positive signal is counterbalanced by a number of membrane-localized inhibitory receptors that limit differentiation. Deficiencies in these negative signaling pathways may cause autoantibody generation autoimmune disease both animal models human patients. We have previously shown transcription factor Ets1 restrain In this study, we tested roles controlling expression...

10.4049/jimmunol.1400666 article EN The Journal of Immunology 2014-06-16

Abstract Siglec-G, a member of the sialic acid–binding Ig-like lectin (Siglec) family, is expressed on B cell and dendritic surfaces. It acts as an inhibitory coreceptor modulates activation, especially B1 cells, Siglec-G–deficient mice show mainly cell–restricted phenotype resulting in increased numbers. Although higher numbers are discussed to be associated with autoimmunity, loss Siglec-G does not result autoimmune disease BALB/c mice. However, there evidence from × CD22 double-deficient...

10.4049/jimmunol.1403139 article EN The Journal of Immunology 2015-05-19

ABSTRACT Down syndrome (DS), trisomy 21, results in many complex phenotypes including cognitive deficits, heart defects and craniofacial alterations. Phenotypes arise from an extra copy of human chromosome 21 (Hsa21) genes. However, these dosage-sensitive causative genes remain unknown. Animal models enable identification pathological mechanisms. The Dp1Tyb mouse model DS has 63% Hsa21-orthologous In order to establish whether this recapitulates phenotypes, we comprehensively phenotyped mice...

10.1242/dmm.049157 article EN cc-by Disease Models & Mechanisms 2021-09-06

Streptococcus pneumoniae is a major human pathogen, causing pneumonia and sepsis. Genetic components strongly influence host responses to pneumococcal infections, but the responsible loci are unknown. We have previously identified locus on mouse chromosome 7 from susceptible strain, CBA/Ca, be crucial for infection. Here we identify gene, Cd22, which carries point mutation in CBA/Ca leading loss of CD22 B cells. mice gene-targeted CD22-deficient C57BL/6 background both similarly infection,...

10.1371/journal.ppat.1008464 article EN cc-by PLoS Pathogens 2020-04-23

Abstract Down syndrome (DS), trisomy 21, results in many complex phenotypes including cognitive deficits, heart defects and craniofacial alterations. Phenotypes arise from an extra copy of human chromosome 21 (Hsa21) genes. However, causative genes remain mostly unknown. Animal models enable identification these pathological mechanisms. The Dp1Tyb mouse model DS has 63% Hsa21-orthologous Here, we comprehensively phenotype mice find wide-ranging DS-like aberrant megakaryopoiesis, reduced bone...

10.1101/2021.02.11.430828 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2021-02-11

Abstract Signaling through the B cell receptor (BCR) can drive activation and contribute to differentiation into antibody-secreting plasma cells. The positive BCR signal is counterbalanced by a number of membrane-localized inhibitory receptors that limit differentiation. Deficiencies in these negative signaling pathways may cause autoantibody generation autoimmune disease both animal models human patients. We have previously shown transcription factor Ets1 restrain Here, we tested roles...

10.4049/jimmunol.192.supp.45.7 article EN The Journal of Immunology 2014-05-01

Introduction: High expression of GD2 on neuroblastoma cells renders this disialoganglioside an attractive target for novel therapeutic and diagnostic approaches. Anti-GD2 antibodies have already entered the clinical stage, but GD2-based markers could also serve in diagnostics imaging purposes.

10.1055/s-0033-1343661 article EN Klinische Pädiatrie 2013-05-22

Infection or vaccination leads to the development of germinal centers (GCs) where B cells evolve high affinity antigen receptors, eventually producing antibody-forming plasma memory cells. We followed migratory pathways emerging from (B EM ) and found that many migrated into lymph node subcapsular sinus (SCS) guided by sphingosine-1-phosphate (S1P). From there, may exit enter distant tissues. Some interacted with took up SCS macrophages, CCL21-guided return towards GC. Disruption local CCL21...

10.1101/2020.12.08.415828 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2020-12-09
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