Maria Bettini

Associate Professor of Microbiology and Immunology

David Blair

B.S. East Tennessee State University

Ph.D. Emory University

Research

References

Maria.Bettini@path.utah.edu

Maria Bettini's Lab Page

Maria Bettini's PubMed Literature Search

Molecular Biology Program

T cell autoimmunity and metabolism

Research

The ultimate goal of the research in our laboratory is to understand the immunological mechanisms of autoimmunity. We are primarily interested in T cell mediated autoimmunity and mechanisms of T cell function in health and disease. The majority of our work is focused on type 1 autoimmune diabetes, which results from T cell mediated destruction of insulin producing beta cells in the pancreas.  Loss of beta cells leads to dysregulation of glucose metabolism and a life-long dependency on insulin injections. There is no cure for type 1 diabetes, and we still have limited understanding of the immunologic and metabolic dysfunction that ultimately leads to beta cell loss. Members of the laboratory utilize genetically modified mouse models, flow cytometry, transcriptional analysis and metabolic assays to study the interactions between the immune system and metabolism. Our goal is to understand why self-tolerance mechanisms fail in autoimmunity, and whether we can identify immunologic or metabolic pathways that can be manipulated to reverse this process. We are particularly interested in a special population of T cells that can suppress autoimmunity – Foxp3+ regulatory T cells. Regulatory T cells employ multiple mechanisms to maintain immune and metabolic homeostasis, suppress autoimmunity, and aid in tissue repair. Our laboratory has shown that T cell receptor signaling can modulate the type and amplitude of regulatory T cell suppressive mechanisms, which suggests that there are sub-populations of cells with specialized functions. Current work in the lab is focused on further understanding of T cell receptor signaling and downstream suppressive functions in regulatory T cell populations. Additional projects are focused on transcriptional and epigenetic mechanisms associated with chronic T cell activation and inflammation in autoimmunity.

References

  1. Kong Y, Jing Y, Bettini M (2019). Generation of T cell receptor retrogenic mice. Curr Protoc Immunol.
  2. Scavuzzo MA, Hill MC, Chmielowiec J, Yang D, Teaw J, Sheng K, Kong Y, Bettini M, Zong C, Martin JF, Borowiak M (2018). Endocrine lineage biases arise in temporally distinct endocrine progenitors during pancreatic morphogenesis. Nat Commun.
  3. Sprouse ML, Scavuzzo MA, Blum S, Shevchenko I, Lee T, Makedonas G, Borowiak M, Bettini ML, Bettini M (2018). High self-reactivity drives T-bet and potentiates Treg function in tissue- specific autoimmunity. JCI Insight.
  4. Sprouse ML, Shevchenko I, Scavuzzo MA, Joseph F, Lee T, Blum S, Borowiak M, Bettini ML, Bettini M (2018). Cutting Edge: Low-Affinity TCRs Support Regulatory T Cell Function in Autoimmunity. J Immunol.
  5. Bettini ML, Bettini M (2017). Understanding Autoimmune Diabetes through the Prism of the Tri-Molecular Complex. Front Endocrinol, 8, 351.
  6.  Zhang Q, Chikina M, Szymczak-Workman AL, Horne W, Kolls JK, Vignali KM, Normolle D, Bettini M, Workman CJ, Vignali DAA (2017). LAG3 limits regulatory T cell proliferation and function in autoimmune diabetes. Sci Immunol, 2(9).
  7. Bettini M, Blanchfield L, Castellaw A, Zhang Q, Nakayama M, Smeltzer MP, Zhang H, Hogquist KA, Evavold BD, Vignali DA (2014). TCR affinity and tolerance mechanisms converge to shape T cell diabetogenic potential. J Immunol, 193(2), 571-9.
  8. Bettini ML, Bettini M, Nakayama M, Guy CS, Vignali DA (2013 Oct). Generation of T cell receptor-retrogenic mice: improved retroviral-mediated stem cell gene transfer. Nat Protoc, 8 (10), 1837-40.
  9. Bettini M, Castellaw AH, Lennon GP, Burton AR, Vignali DA (2012). Prevention of autoimmune diabetes by ectopic pancreatic beta-cell expression of interleukin-35. Diabetes, 61(6), 1519-26.
  10. Lennon GP, Bettini M, Burton AR, Vincent E, Arnold PY, Santamaria P, Vignali DA (2009 Oct 16). T cell islet accumulation in type 1 diabetes is a tightly regulated, cell-autonomous event. Immunity, 31(4), 643-53.

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Last Updated: 11/18/19