Germinal Centers
By D. Calado. 2017
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- Christophe Dessimoz
- C. E. Wogsland
- A. Greenplate
- A. Kolstad
- D. Klopfenstein
- J. Myklebust
- K. Huse
- Liangsheng Zhang
Citations in the corpus
- GOATOOLS: A Python library for Gene Ontology analyses (2018, background): “Germinal centers are a developmental process because they are transient structures that develop in the sites of secondary lymphatic organs, such as lymph nodes, during an immune response 26 .”
- Mosaic nanoparticle display of diverse influenza virus hemagglutinins elicits broad B cell responses (2019, unknown): “the affinity and specificity of their B cell receptors (BCRs) through germinal center (GC) reactions 28 .”
- Efficient evolution of human antibodies from general protein language models (2023, unknown): “…line is also plotted at 100. based on the number of B cells contained within a germinal center (about 10 3 to 10 4 ) 76,77 , the mutation rate of somatic hypermutation (about 1 mutation per kb per division) 13 , the doubling time of B cells (about 10 hours) 76 , and a timescale of a few weeks 13 .”
- GERMINAL CENTER B CELL DYNAMICS (2016, unknown): “…upregulated in LZ B cells could be linked to B cell activation by antigen or T cells (Victora et al., 2010, 2012) led us to speculate that, rather than being cell intrinsic, much of the LZ phenotype was a consequence of exposure to the signals present in the LZ (Victora and Nussenzweig, 2012).”
- Immunological Principles Guiding the Rational Design of Particles for Vaccine Delivery. (2017, unknown): “Antigens are captured by SCS macrophages and imported from the SCS into the B cell folllicle.44,45 Here, antigen can either be recognised by cognate B cells, or relayed by non-cognate B cells to FDCs via a mechanism dependent upon complement and complement receptor 2 (CD21).46 Alternatively, protein”
- Mass cytometry of follicular lymphoma tumors reveals intrinsic heterogeneity in proteins including HLA-DR and a deficit in non-malignant plasmablast and germinal center B cell populations (2017, background): “Furthermore, high BCR expression, potentially followed by BCR-induced activation, aligns with the observed skewing of the nonmalignant B-cell populations and suggests that the malignant B cells outcompete the nonmalignant B cells that are most dependent on support from the microenvironment for survi”