Hans Dooms, PhD
Assistant Professor
Boston University School of Medicine
Dept of Medicine
Rheumatology (Arthritis)

PhD, Universiteit Gent
MSc, Universiteit Gent



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.

Assistant Professor
Boston University School of Medicine
Microbiology


Center Faculty Member
Boston University School of Medicine
Arthritis Center


Graduate Faculty (Primary Mentor of Grad Students)
Boston University School of Medicine, Graduate Medical Sciences




MECHANISMS UNDERLYING THE ROLE OF INTERLEUKIN-7 IN TYPE 1 DIABETES
12/01/2015 - 11/30/2020 (PI)
NIH/National Diabetes & Digestive & Kidney Diseases
3R01DK102911-03S1

THE ROLE OF T CELL CO-INHIBITORY RECEPTORS IN SYSTEMIC SCLEROSIS
05/04/2018 - 04/30/2020 (PI)
NIH/National Institute of Arthritis & Musculoskeletal & Skin Diseases
1R21AR071580-01A1

A NOVEL COMBINATORIAL VACCINATION METHOD TO GENERATE ISLET AUTOANTIGEN-SPECIFIC TREGS
07/01/2015 - 03/31/2018 (PI)
Juvenile Diabetes Research Foundation

BADERC: DYSREGULATED CELLULAR METABOLISM PREDISPOSES TO TYPE 1 DIABETES
04/01/2015 - 03/31/2017 (PI)
General Hospital Corp d/b/a Massachusetts General Hospital NIH NIDDK
5P30DK057521-17

INHIBITING AUTOREACTIVE MEMORY T CELLS IN TYPE 1 DIABETES
01/01/2013 - 12/31/2015 (PI)
American Diabetes Association



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.

  1. Fleury M, Belkina AC, Proctor EA, Zammitti C, Simms RW, Lauffenburger DA, Snyder-Cappione JE, Lafyatis R, Dooms H. Increased Expression and Modulated Regulatory Activity of Coinhibitory Receptors PD-1, TIGIT, and TIM-3 in Lymphocytes From Patients With Systemic Sclerosis. Arthritis Rheumatol. 2018 Apr; 70(4):566-577.View Related Profiles. PMID: 29245183.
     
  2. Jones Iv AR, Coleman EL, Husni NR, Deeney JT, Raval F, Steenkamp D, Dooms H, Nikolajczyk BS, Corkey BE. Type 1 diabetes alters lipid handling and metabolism in human fibroblasts and peripheral blood mononuclear cells. PLoS One. 2017; 12(12):e0188474.View Related Profiles. PMID: 29206239; DOI: 10.1371/journal.pone.0188474;.
     
  3. Smith NM, Wasserman GA, Coleman FT, Hilliard KL, Yamamoto K, Lipsitz E, Malley R, Dooms H, Jones MR, Quinton LJ, Mizgerd JP. Regionally compartmentalized resident memory T cells mediate naturally acquired protection against pneumococcal pneumonia. Mucosal Immunol. 2018 Jan; 11(1):220-235.View Related Profiles. PMID: 28513594.
     
  4. 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.View Related Profiles. PMID: 28356069; DOI: 10.1186/s12865-017-0201-4;.
     
  5. 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.View Related Profiles. PMID: 28178278; DOI: 10.1371/journal.pone.0170975;.
     
  6. Dooms H. Interleukin-7: Fuel for the autoimmune attack. J Autoimmun. 2013 Sep; 45:40-8. PMID: 23831438; DOI: 10.1016/j.jaut.2013.06.007;.
     
  7. 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; DOI: 10.4049/jimmunol.1201090;.
     
  8. 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; PMCID: PMC3447928; DOI: 10.1371/journal.pone.0045299;.
     
  9. 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; PMCID: PMC3411948; DOI: 10.1073/pnas.1203692109;.
     
  10. 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; PMCID: PMC3171642; DOI: 10.1016/j.cyto.2011.07.005;.
     
Showing 10 of 27 results. Show More

This graph shows the total number of publications by year, by first, middle/unknown, or last author.

Bar chart showing 27 publications over 16 distinct years, with a maximum of 4 publications in 2017

YearPublications
19983
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In addition to these self-described keywords below, a list of MeSH based concepts is available here.

autoimmune diseases
immune regulation
immunologic memory
interleukin-2
interleukin-7
T cells
tolerance
type 1 diabetes

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72 E. Concord St Evans Building
Boston MA 02118
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