Alix Berglund, Assistant Professor
2018-2022: Postdoctoral scholar, North Carolina State University, Raleigh, NC
2018: Ph. D., Comparative Biomedical Sciences, North Carolina State University, Raleigh, NC
2014: D.V.M., Washington State University, Pullman, WA
2010: B.S., Zoology, Washington State University, Pullman, WA
Mesenchymal stem cells (MSCs) are multipotent cells that can be isolated from numerous tissues including bone marrow, adipose tissue, and blood. In the body, MSCs home to injured tissue where they secrete anti-inflammatory mediators that prevent further damage to the tissue by the immune system and pro-regeneration factors that help the tissue to heal. Due to their strong immunomodulatory and regenerative capabilities, MSCs are of interest for treating inflammatory, immune-mediated, and degenerative diseases. Understanding how MSCs suppress immune responses and promote tissue healing is important for improving the safety and efficacy of MSC therapy.
The Berglund laboratory is focused on reducing the immunogenicity of allogeneic MSCs and enhancing the therapeutic properties of MSCs using transforming growth factor-b (TGF-β). Treating allogeneic MSCs withTGF-β downregulates antigen processing and presentation, which reduces activation of T cells, and increases the expression of certain immunomodulatory cytokines, growth factors, and extracellular matrix molecules. Understanding the mechanism by which TGF-b downregulates antigen processing and presentation is also a goal of the lab.
We are looking for a qualified and independent postdoctoral fellow to investigate interactions of TGF-β-treated MSCs with macrophages or TGF-β signaling pathways involved in regulation of antigen processing and presentation. If interested, please send your CV and a list of three recommenders to email@example.com. A one-page career statement is encouraged as well.
Full list at https://scholar.google.com/citations?user=4GDHFHkAAAAJ&hl=en
Berglund AK, Hinson AL, Schnabel LV. TGF-b downregulates genes associated with antigen processing and presentation and MHC I surface expression through a Smad3-dependent mechanism. Preprint. BioRXiv. 2023 Feb. doi: https://doi.org/10.1101/2023.01.30.526196
Koch DW, Schnabel LV, Ellis IM, Bates RE, Berglund AK. TGF-b2 enhances tendon healing-associated paracrine factors in equine bone marrow-derived mesenchymal stem cells. Stem Cell Res Ther. 2022 Sept;13:477. PubMed PMID: 36114555; PubMed Central PMCID: PMC9482193.
Koch DW, Berglund AK, Messenger KM, Gilbertie JM, Ellis IM, Schnabel LV. Interleukin-1b in tendon injury enhances reparative gene and protein expression in mesenchymal stem cells. Frontiers Vet Sci. 2022 Aug;9:963759. PubMed PMID: 36032300; PubMed Central PMCID: PMC9410625.
Berglund AK, Long JM, Robertson JB, Schnabel LV. TGF-2 reduces the cell-mediated cytotoxicity of MHC-mismatched equine bone marrow-derived mesenchymal stem cells without altering immunomodulatory properties. Front Cell Dev Biol. 2021 Feb 4; 9:628382. PubMed PMID: 33614658; PubMed Central PMCID: PMC7889809.
Rowland AL, Miller D, Berglund AK, Schnabel LV, Levine GJ, Antczak DF, Watts AE. Cross-matching of allogeneic mesenchymal stromal cells eliminates recipient immune targeting. Stem Cells Transl Med. 2021 May;10(5):694-710. PubMed PMID:33369287; PubMed Central PMCID: PMC8046071.
Berglund AK, Fortier LA, Antczak DF, Schnabel LV. Immune privileged no more: measuring the immunogenicity of allogeneic adult mesenchymal stem cells. Stem Cell Res Ther. 2017 Dec 22;8(1):288. PubMed PMID: 29273086; PubMed Central PMCID: PMC5741939.
Berglund AK, Fisher MB, Cameron KA, Poole EJ, Schnabel LV. TGF-β2 downregulates MHC I and MHC II surface expression on equine bone marrow-derived mesenchymal stem cells without altering phenotype. Front Vet Sci. 2017 Jun 12.4:84. PubMed PMID:28660198; PubMed Central PMCID: PMC5466990.
Sherman AB, Gilger BC, Berglund AK, Schnabel LV. Effect of bone marrow-derived mesenchymal stem cells and stem cell supernatant on equine corneal wound healing in vitro. Stem Cell Res Ther. 2017 May 25;8(1):120. PubMed PMID: 28545510; PubMed Central PMCID: PMC5445363.