Keywords
Last Name

Hans Dooms, PhD

TitleAssistant Professor
InstitutionBoston University School of Medicine
DepartmentMedicine
DivisionRheumatology (Arthritis)
Address72 E. Concord St Evans Building
Boston MA 02118
Phone(617) 414-2506
ORCID ORCID Icon0000-0001-7964-0876
Other Positions
TitleAssistant Professor
InstitutionBoston University School of Medicine
DepartmentMicrobiology

TitleCenter Faculty Member
InstitutionBoston University School of Medicine
DepartmentArthritis Center

TitleGraduate Faculty (Primary Mentor of Grad Students)
InstitutionBoston University School of Medicine, Division of Graduate Medical Sciences

 Research Expertise & Professional Interests
The broad goal of my research is to understand the role of T cells in the pathogenesis of autoimmune diseases and to apply this knowledge for the development of new therapeutic interventions. My laboratory uses in vivo models of autoimmune diseases to follow T cell responses against tissues (e.g. pancreatic islets) and to identify molecules (e.g. cytokines) that orchestrate the autoimmune attack. In addition, we are developing novel gene-deficient and transgenic models to obtain mechanistic insights into the cytokine signaling pathways and transcription factors that drive autoreactive T cells.

To combine the capacity for potent protective responses against pathogens with the prevention of autoimmunity and tissue damage, the immune system works with “checks and balances” to generate the appropriate cellular response to foreign antigens while maintaining tolerance to self. Autoimmune diseases result from breakdowns of these control mechanisms, either due to defects in tolerance-inducing pathways or because autoreactive lymphocytes acquire resistance to proper regulation. I am particularly interested in the contribution of one type of lymphocytes, memory T cells, to the autoimmune process. Memory T cells possess superior effector capacity and long-term viability to fulfill their physiologic function of protecting the host against recurring infections and tumors. However, memory T cells that develop against self-antigens are, precisely due to these characteristics, a significant clinical problem and a major obstacle to restoring tolerance for the therapy of autoimmune diseases and the protection of transplants.

We are currently studying type 1 diabetes as a model of autoimmunity. Islet-specific memory T cells are present in animal models as well as patients with type 1 diabetes and perpetuate anti-islet immune responses, ultimately leading to the onset of hyperglycemia. We recently found that blocking the cytokine Interleukin-7 (IL-7) inhibits these pathogenic memory cells and stops further destruction of the insulin-producing cells in the pancreas. Cytokines such as IL-7 and IL-2 are important regulators for the differentiation, programming and maintenance of memory T cells and modulating their function is a promising approach for controlling memory responses. Ongoing projects in the lab focus on (1) elucidating the molecular and cellular mechanisms underlying IL-7’s role in type 1 diabetes, (2) understanding the dual function of IL-2 in immunity and tolerance and (3) identifying transcriptional programs in CD4+ memory T cells.

 Self-Described Keywords
  • autoimmune diseases
  • immune regulation
  • immunologic memory
  • interleukin-2
  • interleukin-7
  • T cells
  • tolerance
  • type 1 diabetes
 Publications
Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
List All   |   Timeline
  1. Vazquez-Mateo C, Collins J, Fleury M, Dooms H. Broad induction of immunoregulatory mechanisms after a short course of anti-IL-7Ra antibodies in NOD mice. BMC Immunol. 2017 Mar 29; 18(1):18. PMID: 28356069.
    View in: PubMed
  2. Nicholas D, Proctor EA, Raval FM, Ip BC, Habib C, Ritou E, Grammatopoulos TN, Steenkamp D, Dooms H, Apovian CM, Lauffenburger DA, Nikolajczyk BS. Advances in the quantification of mitochondrial function in primary human immune cells through extracellular flux analysis. PLoS One. 2017; 12(2):e0170975. PMID: 28178278.
    View in: PubMed
  3. Dooms H. Interleukin-7: Fuel for the autoimmune attack. J Autoimmun. 2013 Sep; 45:40-8. PMID: 23831438.
    View in: PubMed
  4. Schoenbrunn A, Frentsch M, Kohler S, Keye J, Dooms H, Moewes B, Dong J, Loddenkemper C, Sieper J, Wu P, Romagnani C, Matzmohr N, Thiel A. A converse 4-1BB and CD40 ligand expression pattern delineates activated regulatory T cells (Treg) and conventional T cells enabling direct isolation of alloantigen-reactive natural Foxp3+ Treg. J Immunol. 2012 Dec 15; 189(12):5985-94. PMID: 23162126.
    View in: PubMed
  5. Van Belle TL, Dooms H, Boonefaes T, Wei XQ, Leclercq G, Grooten J. IL-15 augments TCR-induced CD4+ T cell expansion in vitro by inhibiting the suppressive function of CD25 High CD4+ T cells. PLoS One. 2012; 7(9):e45299. PMID: 23028916.
    View in: PubMed
  6. Penaranda C, Kuswanto W, Hofmann J, Kenefeck R, Narendran P, Walker LS, Bluestone JA, Abbas AK, Dooms H. IL-7 receptor blockade reverses autoimmune diabetes by promoting inhibition of effector/memory T cells. Proc Natl Acad Sci U S A. 2012 Jul 31; 109(31):12668-73. PMID: 22733744.
    View in: PubMed
  7. Katzman SD, Hoyer KK, Dooms H, Gratz IK, Rosenblum MD, Paw JS, Isakson SH, Abbas AK. Opposing functions of IL-2 and IL-7 in the regulation of immune responses. Cytokine. 2011 Oct; 56(1):116-21. PMID: 21807532.
    View in: PubMed
  8. Barron L, Dooms H, Hoyer KK, Kuswanto W, Hofmann J, O'Gorman WE, Abbas AK. Cutting edge: mechanisms of IL-2-dependent maintenance of functional regulatory T cells. J Immunol. 2010 Dec 1; 185(11):6426-30. PMID: 21037099.
    View in: PubMed
  9. Dooms H, Abbas AK. Revisiting the role of IL-2 in autoimmunity. Eur J Immunol. 2010 Jun; 40(6):1538-40. PMID: 20458706.
    View in: PubMed
  10. O'Gorman WE, Dooms H, Thorne SH, Kuswanto WF, Simonds EF, Krutzik PO, Nolan GP, Abbas AK. The initial phase of an immune response functions to activate regulatory T cells. J Immunol. 2009 Jul 1; 183(1):332-9. PMID: 19542444.
    View in: PubMed
  11. Hoyer KK, Dooms H, Barron L, Abbas AK. Interleukin-2 in the development and control of inflammatory disease. Immunol Rev. 2008 Dec; 226:19-28. PMID: 19161413.
    View in: PubMed
  12. Hoyer KK, Wolslegel K, Dooms H, Abbas AK. Targeting T cell-specific costimulators and growth factors in a model of autoimmune hemolytic anemia. J Immunol. 2007 Sep 1; 179(5):2844-50. PMID: 17709498.
    View in: PubMed
  13. Dooms H, Wolslegel K, Lin P, Abbas AK. Interleukin-2 enhances CD4+ T cell memory by promoting the generation of IL-7R alpha-expressing cells. J Exp Med. 2007 Mar 19; 204(3):547-57. PMID: 17312008.
    View in: PubMed
  14. Dooms H, Abbas AK. Control of CD4+ T-cell memory by cytokines and costimulators. Immunol Rev. 2006 Jun; 211:23-38. PMID: 16824114.
    View in: PubMed
  15. Dooms H, Kahn E, Knoechel B, Abbas AK. IL-2 induces a competitive survival advantage in T lymphocytes. J Immunol. 2004 May 15; 172(10):5973-9. PMID: 15128779.
    View in: PubMed
  16. Walker LS, Chodos A, Eggena M, Dooms H, Abbas AK. Antigen-dependent proliferation of CD4+ CD25+ regulatory T cells in vivo. J Exp Med. 2003 Jul 21; 198(2):249-58. PMID: 12874258.
    View in: PubMed
  17. Matthys P, Dooms H, Rottiers P, Mitera T, Overgergh L, Leclercq G, Billiau A, Grooten J. Induction of IL-15 by TCR/CD3 aggregation depends on IFN-gamma and protects against apoptosis of immature thymocytes in vivo. Clin Exp Immunol. 2002 Dec; 130(3):379-85. PMID: 12452826.
    View in: PubMed
  18. Dooms H, Abbas AK. Life and death in effector T cells. Nat Immunol. 2002 Sep; 3(9):797-8. PMID: 12205464.
    View in: PubMed
  19. Dooms H, Van Belle T, Desmedt M, Rottiers P, Grooten J. Interleukin-15 redirects the outcome of a tolerizing T-cell stimulus from apoptosis to anergy. Blood. 2000 Aug 1; 96(3):1006-12. PMID: 10910916.
    View in: PubMed
  20. Denecker G, Dooms H, Van Loo G, Vercammen D, Grooten J, Fiers W, Declercq W, Vandenabeele P. Phosphatidyl serine exposure during apoptosis precedes release of cytochrome c and decrease in mitochondrial transmembrane potential. FEBS Lett. 2000 Jan 7; 465(1):47-52. PMID: 10620704.
    View in: PubMed
  21. Rottiers P, Desmedt M, Dooms H, Contreras R, Grooten J. Tumoral environment triggers transcript anomalies in established tumors: induction of altered gene expression and of aberrant, truncated and B2 repeat-containing gene transcripts. Neoplasia. 1999 Dec; 1(6):557-67. PMID: 10935503.
    View in: PubMed
  22. Rottiers P, Verfaillie T, Contreras R, Revets H, Desmedt M, Dooms H, Fiers W, Grooten J. Differentiation of EL4 lymphoma cells by tumoral environment is associated with inappropriate expression of the large chondroitin sulfate proteoglycan PG-M and the tumor-associated antigen HTgp-175. Int J Cancer. 1998 Nov 9; 78(4):503-10. PMID: 9797141.
    View in: PubMed
  23. Dooms H, Desmedt M, Vancaeneghem S, Rottiers P, Goossens V, Fiers W, Grooten J. Quiescence-inducing and antiapoptotic activities of IL-15 enhance secondary CD4+ T cell responsiveness to antigen. J Immunol. 1998 Sep 1; 161(5):2141-50. PMID: 9725205.
    View in: PubMed
  24. Desmedt M, Rottiers P, Dooms H, Fiers W, Grooten J. Macrophages induce cellular immunity by activating Th1 cell responses and suppressing Th2 cell responses. J Immunol. 1998 Jun 1; 160(11):5300-8. PMID: 9605128.
    View in: PubMed
Hans's Networks
Click the "See All" links for more information and interactive visualizations!
Concepts
_
BU Co-Authors
_
Similar BU People
_
Same Department