U.S. Department of Health and Human Services
Autoantigens Discovery and Characterization in Type 1 Diabetes

Autoantigens Discovery and Characterization in Type 1 Diabetes

10/31/2017 5:30 PM
11/1/2017 6:30 PM
(800) 228-9290
​​Program Content
Salvatore Sechi, Ph.D.
T: 301-594-8814
E: sechi@nih.gov

Meeting Logistics

John Hare
The Scientific Consulting Group, Inc.
T: 301-670-4990
E: jhare@scgcorp.com
North Bethesda
Bethesda North Marriott Hotel & Conference Center

Event Details


Type 1 diabetes (T1D) is an autoimmune disease that is thought to be caused, in part, by a T-cell-mediated destruction of insulin-producing β cells. High risk for disease, in those with genetic susceptibility, is predicted by the presence of two or more autoantibodies with different specificities. Autoantibodies against insulin—GAD65, IA-2, and ZnT8—are commonly known as the major specificities in T1D. Despite this knowledge, we still do not know what leads to the breakdown of tolerance, and we have a poor understanding of T1D etiology and pathophysiology. Several new autoantibodies recently have been discovered using innovative technologies, but neither their potential utility in monitoring disease development and treatment nor their role in the pathophysiology and etiology of T1D has been explored.

The occurrence of post-translationally modified proteins (neoantigens) in such autoimmune diseases as rheumatoid arthritis and celiac disease is well documented. It recently was discovered that some T-cells in mouse models, as well as in people with T1D, recognize neoantigens. If these altered self-proteins do not occur in the thymus or are in other ways shielded from normal processes of peripheral self-tolerance, autoreactive T-cells that recognize these peptides could be important for pathogenesis in T1D. In addition, the endocrine function of the β cell and all its attendant processes, together with the pancreatic milieu, are increasingly thought to be associated with mechanisms of post-translational modification (for example, endoplasmic reticulum [ER] stress and microbiome interactions). Thus, continued identification and characterization of T1D-relevant antigen epitopes for both autoantibodies and T-cells is critically important for understanding the etiology and pathophysiology of T1D. Characterization of these autoantigens also could bring new insights into the role of the islet autoimmunity in type 2 diabetes. Powerful new technologies provide opportunities to facilitate a more complete discovery and characterization of autoantigens, including hybrid peptides and post-translational modifications, and the immune response to them.

Meeting Objectives

One of the goals of this workshop is to bring together investigators that use new methods and technologies to identify autoantigens and responses to them (antibodies or T-cells). Researchers with diverse expertise will share ideas and identify resources. This could help them uncover opportunities to work together to accelerate the progress of antigen/antigen response discovery and detection. The workshop also could bring in experts to advise on next steps and help discoveries transition to utility as biomarkers of disease progression, treatment response, and ultimately new antigen-specific therapeutics.

Another goal of the workshop is to have a discussion on the progress and potential future development for (1) the identification of new autoantigens and epitopes in T1D; (2) the characterization of the response to new and previously known antigens (T-cell or humoral); and (3) the use of these antigens/epitopes and their response for identifying disease triggers and mechanisms, monitoring disease progression, and developing new treatments or preventative vaccines.

Registration Deadline

October 15, 2017

This meeting is being held in conjunction with the Workshop on Immune System Engineering for Targeted Tolerance in Type 1 Diabetes (T1D).​​​​


A more detailed agenda will soon be made available.


10/31/2017 5:30 – 6:30 p.m.

11/1/2017 8:25 a.m. – 5:40 p.m.


Teresa DiLorenzo, Albert Einstein College of Medicine

Anthony Purcell, Monash University, Australia

Confirmed Speakers

Thomas DeLong, University of California, San Francisco

Teresa DiLorenzo, Albert Einstein College of Medicine

Sine Reker Hadrup, Technical University of Denmark

Kate Haskins, University of Colorado

Eddie James, Benaroya Research Institute

Sally Kent, University of Massachusetts Medical School

Thomas Kodadek, The Scripps Research Institute

Åke Lernmark, Lund University, Sweden

Aaron Michels, Barbara Davis Center, University of Colorado

Michele Mishto, Berlin Institute of Health, Germany

Jerry Palmer, University of Washington

Marc Peakman, King’s College

Bjoern Peters, La Jolla Institute for Allergy and Immunology

Anthony Purcell, Monash University, Australia

Bart Roep, Beckman Research Institute of City of Hope

Matthew Spitzer, University of California, San Francisco

Larry Stern, University of Massachusetts, Worcester

Rene Toes, Leiden University Medical Center

James Yang, National Cancer Institute​

This meeting is being held in conjunction with the Workshop on Immune System Engineering for Targeted Tolerance in Type 1 Diabetes (T1D).​​​​​​​


Hotel Accommodations

Bethesda North Marriott Hotel & Conference Center
5701 Marinelli Road
North Bethesda, MD 20852
Phone:  (301) 822-9200 or (800) 228-9290

Website:  www.marriott.com/hotels/travel/wasbn-bethesda-north-marriott-hotel-and-conference-center
(More hotel information can be obtained from this website.)


A block of sleeping rooms has been reserved at the Bethesda North Marriott Hotel & Conference Center in Bethesda, MD. The group rate is the prevailing government rate, currently $231 per night, for single occupancy, plus tax (currently 13%). Participants may make reservations by calling the hotel directly or online at https://aws.passkey.com/e/49189239. The room block will be in effect at the group rate until Tuesday, October 3, 2017, only or until full, whichever comes first. Any room reservations received after that date will be accepted on a space- and rate-availability basis. Check-in time is 4:00 p.m., and checkout time is 12:00 p.m. Any reservation cancellations must be made prior to 4:00 p.m. the day before the scheduled arrival date, or charges will apply.

NIH Visitor Information 

Information on visiting the NIH, campus maps, shuttle schedules, driving directions, security, and more can be found on the NIH Visitor Information page.

Driving Directions

Use the following address for your GPS [5701 Marinelli Road, Rockville, MD]



Minutes are currently unavailable.


Attendees are currently unavailable.


Submission Deadline: TBA

All abstracts must be submitted via email to Ms. LaKia Thomas, thomaslac@mail.nih.gov, with “AutoAntigens” in the subject line. Abstract submissions should be no longer than 250 words (not including name and affiliation). Attach the abstract as a Microsoft Word document, and make any relevant comments in the text of the email.

Please follow the instructions below to format an abstract. (Note: Submissions will not be edited for spelling or grammar and will be accepted “as is.”)

  1. The abstract title should be typed in bold font, Title Case Letters (i.e., first letter of each main word capitalized).
  2. List the names, degrees, and institutional affiliations of all authors, and underline the name of the presenting author.
  3. Use 1” margins.
  4. The abstract should not exceed one page.
  5. Simple tables or graphs may be included; however, they must fit within the designated abstract space.
  6. Please use a common font, such as Calibri, Times New Roman, or Arial.
  7. Save the abstract file as: primary authors’ last name_first word in the title (e.g., Smith_AutoAntigens).


  • 5701 Marinelli Road
  • MD 20852


Line ​​Program Content
Salvatore Sechi, Ph.D.
T: 301-594-8814
E: sechi@nih.gov

Meeting Logistics

John Hare
The Scientific Consulting Group, Inc.
T: 301-670-4990
E: jhare@scgcorp.com