Jennifer Fransson

ORCID: 0000-0003-4762-901X
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About
Contact & Profiles
Research Areas
  • Gene Regulatory Network Analysis
  • Bioinformatics and Genomic Networks
  • Multiple Sclerosis Research Studies
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Immune cells in cancer
  • Immune responses and vaccinations
  • Immune Cell Function and Interaction
  • Computational Drug Discovery Methods
  • Inflammasome and immune disorders
  • Immunotherapy and Immune Responses
  • T-cell and B-cell Immunology
  • Sphingolipid Metabolism and Signaling
  • Single-cell and spatial transcriptomics
  • Food Allergy and Anaphylaxis Research
  • Cancer Cells and Metastasis
  • Neurogenesis and neuroplasticity mechanisms
  • interferon and immune responses
  • IL-33, ST2, and ILC Pathways
  • Molecular Biology Techniques and Applications
  • Cytokine Signaling Pathways and Interactions
  • Epigenetics and DNA Methylation
  • Contact Dermatitis and Allergies
  • Phagocytosis and Immune Regulation
  • Allergic Rhinitis and Sensitization
  • Gene expression and cancer classification

Science for Life Laboratory
2025

Uppsala University
2025

Institut du Cerveau
2018-2024

Inserm
2017-2024

Sorbonne Université
2017-2024

Centre National de la Recherche Scientifique
2017-2024

CentraleSupélec
2024

Université Paris-Saclay
2024

Karolinska Institutet
2024

Karolinska University Hospital
2024

One major challenge in multiple sclerosis is to understand the cellular and molecular mechanisms leading disease severity progression. The recently demonstrated correlation between remyelination emphasizes importance of identifying factors a favourable outcome. Why fails or succeeds patients remains largely unknown, mainly because has never been studied within humanized pathological context that would recapitulate events plaque formation such as infiltration inflammatory cells. Therefore, we...

10.1093/brain/awx008 article EN cc-by-nc Brain 2017-01-30

Abstract Uncontrolled regeneration leads to neoplastic transformation 1–3 . The intestinal epithelium requires precise regulation during continuous homeostatic and damage-induced tissue renewal prevent transformation, suggesting that pathways unlinking tumour growth from regenerative processes must exist. Here, by mining RNA-sequencing datasets two damage models 4,5 using pharmacological, transcriptomics genetic tools, we identified liver X receptor (LXR) pathway activation as a adaptation...

10.1038/s41586-024-08247-6 article EN cc-by Nature 2024-11-20

Background Tumour-infiltrating T cells can mediate both antitumour immunity and promote tumour progression by creating an immunosuppressive environment. This dual role is especially relevant in hepatocellular carcinoma (HCC), characterised a unique microenvironment limited success with current immunotherapy. Objective We evaluated cell responses patients advanced HCC analysing tumours, liver flushes liver-draining lymph nodes, to understand whether reactive populations could be identified...

10.1136/gutjnl-2024-334148 article EN cc-by-nc Gut 2025-01-19

Forty-three nickel-allergic patients (40 females and 3 males) participated in this study which was designed to elucidate the correlation between quantitative vivo vitro responses. All were patch-tested with various concentrations of nickel-sulphate serial-diluted water. The lowest concentration eliciting a cutaneous reaction (indicating severity allergy) recorded for each individual compared lymphocyte response, using transformation test. best coefficients obtained 0.42 0.46, tested linear...

10.2340/0001555565385389 article EN cc-by-nc Acta Dermato Venereologica 1985-09-01

Abstract The polygenic and multi-cellular nature of multiple sclerosis (MS) immunopathology necessitates cell-type-specific molecular studies in order to improve our understanding the diverse mechanisms underlying immune cell dysfunction MS. Here, by generating a dataset 1,075 transcriptomes from 209 participants (167 MS 42 healthy), we assessed MS-associated transcriptional changes six implicated cell-type-states: naïve memory helper T cells classical monocytes purified peripheral blood,...

10.1101/2022.06.29.498195 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-07-02

In multiple sclerosis (MS), immune cells invade the CNS and destroy myelin. Macrophages contribute to demyelination myelin repair, their role in each process depends on ability acquire specific phenotypes response external signals. this article, we assess whether defects MS patient macrophage responses may lead increased inflammation or lack of neuroregenerative effects.

10.1212/nxi.0000000000200312 article EN cc-by-nc-nd Neurology Neuroimmunology & Neuroinflammation 2024-10-28

Identifying the nodes able to drive state of a network is crucial understand, and eventually control, biological systems. Despite recent advances, such identification remains difficult because huge number equivalent controllable configurations, even in relatively simple networks. Based on evidence that many applications it essential test ability individual control specific target subset, we develop fast principled method identify driver-target configurations sparse directed We demonstrate...

10.1162/netn_a_00180 article EN cc-by Network Neuroscience 2020-12-22

Abstract Multiple sclerosis (MS) is a neuro-inflammatory disease for which the pathogenesis remains largely unclear. Lysophosphatidic acid (LPA) an endogenous phospholipid that involved in multiple immune cell functions and dysregulated MS. Its receptor LPA 1 expressed macrophages regulates their activation, of interest due to role macrophage activation MS both destruction repair. In this study, we studied viable Malaga variant -null mutation as well pharmaceutical inhibition mice with...

10.1101/870980 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2019-12-11

Abstract In multiple sclerosis (MS), immune cells invade the central nervous system and destroy myelin. Macrophages contribute to demyelination myelin repair, their role in each process depends on ability acquire specific phenotypes response external signals. Here, we assess whether defects MS patient macrophage responses may lead increased inflammation or lack of neuro-regenerative effects. To test this hypothesis, CD14 + CD16 - monocytes from patients healthy controls were activated vitro...

10.1101/2021.01.13.426327 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2021-01-14

Identifying the nodes that have potential to influence state of a network is relevant question for many complex systems. In applications it often essential test ability an individual node control specific target subset network. biological networks, this might provide precious information on how single genes regulate expression groups molecules in cell. Taking into account these constraints, we propose optimized heuristic based Kalman rank condition quantify centrality as number can control....

10.48550/arxiv.2003.08913 preprint EN other-oa arXiv (Cornell University) 2020-01-01

The polygenic and multi-cellular nature of multiple sclerosis (MS) immunopathology necessitates cell-type-specific molecular studies in order to improve our understanding the diverse mechanisms underlying immune cell dysfunction MS. Here, by generating a dataset 1,075 transcriptomes from 209 participants (167 MS 42 healthy), we assessed MS-associated transcriptional changes six implicated cell-type-states: naïve memory helper T cells classical monocytes purified peripheral blood, each their...

10.2139/ssrn.4267402 article EN SSRN Electronic Journal 2022-01-01
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