The following are ongoing research studies related to Type 1 Diabetes, in which individuals or families can participate. All studies conducted through the Max McGee Center are also listed on the ClinicalTrials.gov website.
Type 1 diabetes is a disease that happens when the pancreas (a gland behind the stomach) makes little or no insulin. Insulin is a hormone (chemical) released by a pancreatic beta cell which is needed for uptake of sugars (e.g. glucose, the main type of sugar in the blood) into body tissues for energy production. This energy fuels the body’s functions. Without insulin, too much glucose stays in the blood. Over time, increased glucose in the blood can lead to serious problems with the heart, kidneys, nerves, and eyes.
The purpose of this study is to gain more information about the step-by-step process that causes someone to develop type 1 diabetes. Scientists think that a person’s own immune system, directed by genetic and environmental factors play a major role in its development. The Max McGee National Research Center for Juvenile Diabetes, affiliated with the Medical College of Wisconsin and Children’s Wisconsin, is using a genetic approach to try to better understand the step-by-step mechanisms that cause the destruction of the beta cells of the pancreas leading to diabetes. The more information scientists have, the better they can design studies to find possible treatment and prevention options for type 1 diabetes. But first, this study, Genetics of Autoimmunity in Type 1 Diabetes Mellitus may help us find more information about the disease.
Does someone in your family have type 1 diabetes?
If so, your family may be eligible to participate in our study to help us learn more about the causes of type 1 diabetes. If you would like to help, here’s how to get started:
We are looking for families which include a child with type 1 diabetes, brothers, sisters and parents. Adults with type 1 diabetes, their children and spouses are also needed.
If your family fits either description, you may complete our screening questionnaire. You can download, print and complete the paper copy. Type 1 Diabetes Family Study Screening Questionnaire (PDF)
Return completed form by mail or fax to:
Family Study Coordinator
Max McGee Diabetes Research Center
Medical College of Wisconsin
8701 Watertown Plank Rd.
Milwaukee, WI 53226
(414) 955-6663 (fax)
Once we receive your completed form, a study coordinator will contact you and provide more information about study participation OR you may contact study coordinator at (414) 955-4903 or T1dinfo@mcw.edu
- A visit to Children’s Wisconsin by immediate family members to donate a blood sample for genetic analysis and measurement of immune system responses associated with type 1 diabetes
- Completion of a family medical history questionnaire
- Measurement of height and weight
- Possible follow-up: "at-risk" family members may be asked to give an additional blood sample once or twice a year for up to 10 years
If you don’t have type 1 diabetes in your family, you can still help.
We need healthy kids and adults to participate as “control subjects” or a comparison group. Control subjects provide an essential comparative sample to diabetic subjects. Answer the following questions to find out if you are eligible to participate:
- Are you older than age 39?
- Have you ever been told that you have diabetes of any kind?
- Do you have any close relatives (parents, brothers/sisters, aunts/uncles, nieces/nephews or grandparents) with type 1 diabetes?
- Do you have any other known autoimmune diseases or conditions?
(Includes: Addison’s Disease, Ankylosing Spondylitis (Marie-Strümpell Disease), Anterior Uveitis (Iritis), Autoimmune Polyendocrine Syndrome (APS), Autoimmune Thyroid Disease (such as Graves’ Disease or Hashimoto’s), Celiac Disease (gluten intolerance), Inflammatory Bowel Disease (Crohn’s Disease or Ulcerative Colitis), JRA (Juvenile Rheumatoid Arthritis), Multiple Sclerosis (MS), Myasthenia Gravis, Psoriasis, Rheumatoid Arthritis, Systemic Lupus.)
If you answered No to all of these questions, you may be eligible to participate.
Participation involves a visit to Children’s Wisconsin, answering some medical and family history questions and giving a blood sample of 50 ml (about 3 Tablespoons + 1 teaspoon). You will receive a gift certificate for your time and travel.
Please contact a study coordinator at (414) 955-8486 or email@example.com to participate.
Participation in Collaborative Studies
Evidence supports that most subjects who develop Type 1 diabetes (T1D) possess autoimmunity towards β-cells for years prior to clinical onset. Presently, it is impossible to precisely predict who will develop T1D or when they will clinically present. Siblings of T1D probands have an approximately 6% probability of progression to T1D. Therefore, the temporal analyses of samples from siblings of T1D probands is crucial for gaining an understanding of disease initiation and progression. The study of this population is also crucial to understanding mechanisms that prevent T1D progression within the context of high genetic risk. The Max McGee Research Center for Juvenile Diabetes Family Genetics Study is a longitudinal study aimed at gaining new insight into the mechanisms that govern progression to and protection from T1D progression. Subjects are enrolled through Children’s Wisconsin and return for yearly visits. The Children's Wisconsin Diabetes Clinic is a large program that cares for >1,600 pediatric diabetes patients on an annual basis; the majority of these (>91%) are T1D patients.
Presently the study includes approximately 500 families with T1D. In most cases, the parents, the pediatric new onset T1D proband, and the unaffected siblings have been enrolled. Eligible subjects are >2 years of age at the time of enrollment and are followed for a duration of up to 10 years. This study has been ongoing for nearly 15 years and to date we have collected samples and clinical data from >2,200 subjects, with longitudinal analyses of approximately 600 siblings. All subjects have been HLA typed by nucleotide sequencing of the second exons of HLA-DQA1 and HLA-DQB1. At each annual visit, serum, plasma, cryopreserved leukocytes, and DNA, have been collected and antibody titers have been measured (INS, ZnT8, GAD, IA2). Presently, the study encompasses >65 non-diabetic subjects that have seroconverted to autoantibody positivity and >500 persistently autoantibody negative subjects. To date, progression to T1D has been captured in 15 subjects. The study also includes age-, sex- and ethnically-matched unrelated healthy controls, as well as Type 2 diabetes controls.
We recognize that collaboration with investigators at other institutions is essential to our mission of understanding T1D pathogenesis and to our goal of identifying biomarkers of T1D progression or non-progression. As such, we have, and will continue to grant investigators at other institutions access to study samples through collaborative arrangements. Access is predicated on:
1) Scientific merit of the proposed analyses, in particular an assessment of the likelihood of scientific advancement over the risk of using samples that are difficult to replace;
2) sample availability and the ability to address the scientific question with appropriate control and statistical rigor;
3) an agreement that all analyses will be conducted in a blinded manner;
4) an understanding that data generated will be integrated with other analyses conducted on the same subjects with the objective of attaining a deeper understanding of progression/non-progression;
5) compliance with all institutional policies and IRB regulations at the collaborative sites involved.
Inquiries should be made directly with Martin Hessner, PhD (firstname.lastname@example.org). All collaborative arrangements will be reviewed/approved by a panel of McGee Center faculty.
Type 1 Diabetes TrialNet is a global network of researchers and immunology experts dedicated to the study, prevention, and early treatment of type 1 diabetes. It is supported by the Department of Health and Human Services National Institutes of Health, Juvenile Diabetes Research Foundation International, and the American Diabetes Association.
The Max McGee Diabetes Research Center* is an Affiliate Site for the Natural History Study of the Development of Type 1 Diabetes. This study screens relatives of people with type 1 diabetes to find out if family members are at risk for developing diabetes.
The purpose of this study is to gain more information about how type 1 diabetes develops. Then studies can be designed for people who are at risk for developing type 1 diabetes or have just been told they have type 1 diabetes. The more information scientists have, the better they can design studies to find possible treatment and prevention options for type 1 diabetes. But first, the Natural History Study may help find more information about the disease.
TrialNet also has prevention studies and intervention studies. If you are enrolled in the Natural History Study and learn you are at risk for developing type 1 diabetes, you may qualify to be enrolled in a prevention study. If you develop diabetes during the study, you may qualify for an intervention study.
You may be able to take part in this study if you are:
- Between 1 and 45 years old and have a brother, sister, child or parent who has been diagnosed with type 1 diabetes
- or -
- Between 1 and 20 years old and have a cousin, niece, nephew, aunt, uncle, half sibling, or grandparent who has been diagnosed with type 1 diabetes
You may not be able to participate if you:
- Have diabetes already
- Have a previous history of being treated with insulin or oral diabetes medications
- Are currently using systemic immunosuppressive agents (topical or inhaled agents are acceptable
- Have any known serious diseases
You may contact the study coordinator for more information:
(414) 955-4903 | T1dinfo@mcw.edu
TrialNet Study Coordinator
Max McGee Diabetes Research Center
Children’s Wisconsin/ Medical College of Wisconsin
8701 Watertown Plank Rd.
Milwaukee, WI 53226
- A visit to Children’s Wisconsin to donate a blood sample which will be screened for diabetes-related antibodies
- Answering a few medical history questions
- Possible follow-up: individuals with a positive antibody result may be offered further testing to determine their risk of developing diabetes over the next 5 years. You would need to give additional permission to participate in the next stage of testing.
- National Institute of Diabetes & Digestive & Kidney Disease (NIDDK)
- National Institute of Allergy and Infectious Diseases (NIAID)
- National Institute of Child Health and Human Development (NICHD)
- National Center for Research Resources (NCRR)
- Juvenile Diabetes Research Foundation International (JDRF)
- American Diabetes Association (ADA)
*The Max McGee Diabetes Research Center is affiliated with the Medical College of Wisconsin and Children’s Wisconsin.
If you would like more information or you would like to have your child join this study, Early Markers of Disease and Response to Therapy (DREAMT), please contact a study coordinator at (414) 955-4903.
*Individuals aged 6 – 55 years old that were diagnosed in the past 7 months may be eligible to join.
If your child is in this study, they will come to the Children’s Wisconsin research clinic in Milwaukee for 7 study visits over 2 years. Your child will complete a mixed meal tolerance test (MMTT) during the study visits. MMTTs involve not eating or drinking anything overnight, then drinking a nutritional drink, with blood samples drawn from an IV (a thin, flexible plastic tube in a vein in the arm) over 2 hours. The IV will be removed when the MMTT is done. Participation will also involve answering questions about your child’s typical diet, and collection of stool samples. At the second visit, your child will be given a probiotic or a placebo, which they will take by mouth 1 time a day for 6 months. You will speak to a member of the study team about the study and be asked to sign a consent form before your child begins the study. Your child will be compensated for their time. Each visit will take about 2.5 – 3 hours to complete. We will also work to coordinate some of your child’s clinic visits to occur during these study visits to reduce the number of trips and time spent at Children’s Wisconsin.If you would like more information or you would like to have your child join this study, Reducing Innate Inflammation in New Onset T1D with Lactobacillus Plantarum, please contact a study coordinator at (414) 955-4903.
*Individuals aged 3 – 45 years old that were diagnosed in the past 3 months may be eligible to join.
CD4+CD25+CD127hi cell frequency predicts disease progression in type 1 diabetes. Narsale A, Lam B, Moya R, Lu T, Mandelli A, Gotuzzo I, Pessina B, Giamporcaro G, Geoffrey R, Buchanan K, Harris M, Bergot AS, Thomas R, Hessner MJ, Battaglia M, Serti E, Davies JD.JCI Insight. 2021 Jan 25;6(2):e136114. doi: 10.1172/jci.insight.136114.PMID: 33301420
Lactobacillus plantarum 299v probiotic supplementation in men with stable coronary artery disease suppresses systemic inflammation.Hofeld BC, Puppala VK, Tyagi S, Ahn KW, Anger A, Jia S, Salzman NH, Hessner MJ, Widlansky ME. Sci Rep. 2021 Feb 17;11(1):3972. doi: 10.1038/s41598-021-83252-7.PMID: 33597583
Allred MG, Chimenti MS, Ciecko AE, Chen YG, Lieberman SM. Characterization of Type I Interferon-Associated Chemokines and Cytokines in Lacrimal Glands of Nonobese Diabetic Mice. Int J Mol Sci. 2021 Apr 5;22(7). doi: 10.3390/ijms22073767. PubMed PMID: 33916486; PubMed Central PMCID: PMC8038628.
Khatun A, Kasmani MY, Zander R, Schauder DM, Snook JP, Shen J, Wu X, Burns R, Chen YG, Lin CW, Williams MA, Cui W. Single-cell lineage mapping of a diverse virus-specific naive CD4 T cell repertoire. J Exp Med. 2021 Mar 1;218(3). doi: 10.1084/jem.20200650. PubMed PMID: 33201171; PubMed Central PMCID: PMC7676493.
Lipid mediators and biomarkers associated with type 1 diabetes development.Nelson AJ, Stephenson DJ, Bone RN, Cardona CL, Park MA, Tusing YG, Lei X, Kokotos G, Graves CL, Mathews CE, Kramer J, Hessner MJ, Chalfant CE, Ramanadham S. JCI Insight. 2020 Aug 20;5(16):e138034. doi: 10.1172/jci.insight.138034.PMID: 32814707
Broadening Our Understanding Type 1 Diabetes Heterogeneity by Exploring Effects of Race/Ethnicity on Disease Trajectory.Hessner MJ, Cabrera SM.J Clin Endocrinol Metab. 2020 Dec 1;105(12):e4961-3. doi: 10.1210/clinem/dgaa375. PMID: 32542394 No abstract available.
Debreceni IL, Chimenti MS, Serreze DV, Geurts AM, Chen YG, Lieberman SM. Toll-Like Receptor 7 Is Required for Lacrimal Gland Autoimmunity and Type 1 Diabetes Development in Male Nonobese Diabetic Mice. Int J Mol Sci. 2020 Dec 13;21(24). doi: 10.3390/ijms21249478. PubMed PMID: 33322152; PubMed Central PMCID: PMC7764018.
Lee H, Lee YS, Harenda Q, Pietrzak S, Oktay HZ, Schreiber S, Liao Y, Sonthalia S, Ciecko AE, Chen YG, Keles S, Sridharan R, Engin F. Beta Cell Dedifferentiation Induced by IRE1α Deletion Prevents Type 1 Diabetes. Cell Metab. 2020 Apr 7;31(4):822-836.e5. doi: 10.1016/j.cmet.2020.03.002. Epub 2020 Mar 26. PubMed PMID: 32220307; PubMed Central PMCID: PMC7346095.
Beta Cell Dedifferentiation Induced by IRE1α Deletion Prevents Type 1 Diabetes.Lee H, Lee YS, Harenda Q, Pietrzak S, Oktay HZ, Schreiber S, Liao Y, Sonthalia S, Ciecko AE, Chen YG, Keles S, Sridharan R, Engin F. Cell Metab. 2020 Apr 7;31(4):822-836.e5. doi: 10.1016/j.cmet.2020.03.002. Epub 2020 Mar 26. PMID: 32220307
CD226 Deletion Reduces Type 1 Diabetes in the NOD Mouse by Impairing Thymocyte Development and Peripheral T Cell Activation.Shapiro MR, Yeh WI, Longfield JR, Gallagher J, Infante CM, Wellford S, Posgai AL, Atkinson MA, Campbell-Thompson M, Lieberman SM, Serreze DV, Geurts AM, Chen YG, Brusko TM. Front Immunol. 2020 Sep 4;11:2180. doi: 10.3389/fimmu.2020.02180. eCollection 2020. PMID: 33013915
The CD137 Ligand Is Important for Type 1 Diabetes Development but Dispensable for the Homeostasis of Disease-Suppressive CD137+ FOXP3+ Regulatory CD4 T Cells.Foda BM, Ciecko AE, Serreze DV, Ridgway WM, Geurts AM, Chen YG. J Immunol. 2020 Jun 1;204(11):2887-2899. doi: 10.4049/jimmunol.1900485. Epub 2020 Apr 15.PMID: 32295876
Chen YG, Ciecko AE, Khaja S, Grzybowski M, Geurts AM, Lieberman SM. UBASH3A deficiency accelerates type 1 diabetes development and enhances salivary gland inflammation in NOD mice. Sci Rep. 2020 Jul 21;10(1):12019. doi: 10.1038/s41598-020-68956-6. PubMed PMID: 32694640; PubMed Central PMCID: PMC7374577.
Introducing the Endotype Concept to Address the Challenge of Disease Heterogeneity in Type 1 Diabetes.Battaglia M, Ahmed S, Anderson MS, Atkinson MA, Becker D, Bingley PJ, Bosi E, Brusko TM, DiMeglio LA, Evans-Molina C, Gitelman SE, Greenbaum CJ, Gottlieb PA, Herold KC, Hessner MJ, Knip M, Jacobsen L, Krischer JP, Long SA, Lundgren M, McKinney EF, Morgan NG, Oram RA, Pastinen T, Peters MC, Petrelli A, Qian X, Redondo MJ, Roep BO, Schatz D, Skibinski D, Peakman M. Diabetes Care. 2020 Jan;43(1):5-12. doi: 10.2337/dc19-0880. Epub 2019 Nov 21. PMID: 31753960
Cystic Fibrosis Plasma Blunts the Immune Response to Bacterial Infection.Zhang X, Pan A, Jia S, Ideozu JE, Woods K, Murkowski K, Hessner MJ, Simpson PM, Levy H. Am J Respir Cell Mol Biol. 2019 Sep;61(3):301-311. doi: 10.1165/rcmb.2018-0114OC. PMID: 30848661
Identification of molecular signatures of cystic fibrosis disease status with plasma-based functional genomics.Levy H, Jia S, Pan A, Zhang X, Kaldunski M, Nugent ML, Reske M, Feliciano RA, Quintero D, Renda MM, Woods KJ, Murkowski K, Johnson K, Verbsky J, Dasu T, Ideozu JE, McColley S, Quasney MW, Dahmer MK, Avner E, Farrell PM, Cannon CL, Jacob H, Simpson PM, Hessner MJ. Physiol Genomics. 2019 Jan 1;51(1):27-41. doi: 10.1152/physiolgenomics.00109.2018. Epub 2018 Dec 12. PMID: 30540547
Interleukin-27 Is Essential for Type 1 Diabetes Development and Sjögren Syndrome-like Inflammation.Ciecko AE, Foda B, Barr JY, Ramanathan S, Atkinson MA, Serreze DV, Geurts AM, Lieberman SM, Chen YG. Cell Rep. 2019 Dec 3;29(10):3073-3086.e5. doi: 10.1016/j.celrep.2019.11.010. PMID: 31801074
Soluble CD137 Ameliorates Acute Type 1 Diabetes by Inducing T Cell Anergy.Itoh A, Ortiz L, Kachapati K, Wu Y, Adams D, Bednar K, Mukherjee S, Chougnet C, Mittler RS, Chen YG, Dolan L, Ridgway WM. Front Immunol. 2019 Nov 7;10:2566. doi: 10.3389/fimmu.2019.02566. eCollection 2019. PMID: 31787971
CD11c+ Cells Are Gatekeepers for Lymphocyte Trafficking to Infiltrated Islets During Type 1 Diabetes.Sandor AM, Lindsay RS, Dyjack N, Whitesell JC, Rios C, Bradley BJ, Haskins K, Serreze DV, Geurts AM, Chen YG, Seibold MA, Jacobelli J, Friedman RS. Front Immunol. 2019 Jan 31;10:99. doi: 10.3389/fimmu.2019.00099. eCollection 2019. PMID: 30766536
Gioia L, Holt M, Costanzo A, Sharma S, Abe B, Kain L, Nakayama M, Wan X, Su A, Mathews C, Chen YG, Unanue E, Teyton L. Position β57 of I-Ag7 controls early anti-insulin responses in NOD mice, linking an MHC susceptibility allele to type 1 diabetes onset. Sci Immunol. 2019 Aug 30;4(38). doi: 10.1126/sciimmunol.aaw6329. PubMed PMID: 31471352; PubMed Central PMCID: PMC6816460.
Forsberg MH, Foda B, Serreze DV, Chen YG. Combined congenic mapping and nuclease-based gene targeting for studying allele-specific effects of Tnfrsf9 within the Idd9.3 autoimmune diabetes locus. Sci Rep. 2019 Mar 13;9(1):4316. doi: 10.1038/s41598-019-40898-8. PubMed PMID: 30867509; PubMed Central PMCID: PMC6416332.
Henschel AM, Cabrera SM, Kaldunski ML, Jia S, Geoffrey R, Roethle MF, Lam V, Chen YG, Wang X, Salzman NH, Hessner MJ. Modulation of the diet and gastrointestinal microbiota normalizes systemic inflammation and β-cell chemokine expression associated with autoimmune diabetes susceptibility. PLoS One. 2018 Jan 2;13(1):e0190351. doi: 10.1371/journal.pone.0190351. eCollection 2018.PMID: 29293587
A Serum-Induced Transcriptome and Serum Cytokine Signature Obtained at Diagnosis Correlates with the Development of Early Pancreatic Ductal Adenocarcinoma Metastasis.Tsai S, McOlash L, Jia S, Zhang J, Simpson P, Kaldunski ML, Aldakkak M, Grewal J, Palen K, Dwinell MB, Johnson BD, Mackinnon A, Hessner MJ, Gershan JA. Cancer Epidemiol Biomarkers Prev. 2019 Apr;28(4):680-689. doi: 10.1158/1055-9965.EPI-18-0813. Epub 2018 Dec 7. PMID: 30530849
The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and Recommendations for the Future.Chen YG, Mathews CE, Driver JP. Front Endocrinol (Lausanne). 2018 Feb 23;9:51. doi: 10.3389/fendo.2018.00051. eCollection 2018. PMID: 29527189
Innate immune activity as a predictor of persistent insulin secretion and association with responsiveness to CTLA4-Ig treatment in recent-onset type 1 diabetes.Cabrera SM, Engle S, Kaldunski M, Jia S, Geoffrey R, Simpson P, Szabo A, Speake C, Greenbaum CJ; Type 1 Diabetes TrialNet CTLA4-Ig (Abatacept) Study Group, Chen YG, Hessner MJ. Diabetologia. 2018 Nov;61(11):2356-2370. doi: 10.1007/s00125-018-4708-x. Epub 2018 Aug 30. PMID: 30167736
Jiang F, Zhou JY, Wu J, Tian F, Zhu XX, Zhu CL, Yang BL, Chen YG. Yangyin Runchang Decoction Improves Intestinal Motility in Mice with Atropine/Diphenoxylate-Induced Slow-Transit Constipation. Evid Based Complement Alternat Med. 2017;2017:4249016. doi: 10.1155/2017/4249016. Epub 2017 Dec 18. PMID: 29403536
Ideozu JE, Zhang X, Pan A, Ashrafi Z, Woods KJ, Hessner MJ, Simpson P, Levy H. Increased Expression of Plasma-Induced ABCC1 mRNA in Cystic Fibrosis. Int J Mol Sci. 2017 Aug 11;18(8). pii: E1752. doi: 10.3390/ijms18081752. PMID: 28800122
Palatnik A, Ye S, Kendziorski C, Iden M, Zigman JS, Hessner, Identification of a serum-induced transcriptional signature associated with metastatic cervical cancer . Rader JS. PLoS One. 2017 Aug 30;12(8):e0181242. doi: 10.1371/journal.pone.0181242. eCollection 2017. PMID: 28854209
Fawley J, Koehler S, Cabrera S, Lam V, Fredrich K, Hessner M, Salzman N, Gourlay D. Intestinal alkaline phosphatase deficiency leads to dysbiosis and bacterial translocation in the newborn intestine. J Surg Res. 2017 Oct;218:35-42. doi: 10.1016/j.jss.2017.03.049. Epub 2017 Apr 13. PMID: 28985873
Lin B, Ciecko AE, MacKinney E, Serreze DV, Chen YG. Congenic mapping identifies a novel Idd9 subregion regulating type 1 diabetes in NOD mice. Immunogenetics. 2017 Mar;69(3):193-198. Epub 2016 Oct 28. PMID: 27796442
Driver JP, Racine JJ, Ye C, Lamont DJ, Newby BN, Leeth CM, Chapman HD, Brusko TM, Chen YG, Mathews CE, Serreze DV. Interferon-γ Limits Diabetogenic CD8+ T-Cell Effector Responses in Type 1 Diabetes. Diabetes. 2017 Mar;66(3):710-721. Epub 2016 Dec 5. PMID: 27920091
Forsberg MH, Ciecko AE, Bednar KJ, Itoh A, Kachapati K, Ridgway WM, Chen YG. CD137 Plays Both Pathogenic and Protective Roles in Type 1 Diabetes Development in NOD Mice. J Immunol. 2017 Mar 31. pii: 1601851. [Epub ahead of print]. PMID:28363905
Regnell SE, Hessner MJ, Jia S, Åkesson L, Stenlund H, Moritz T, La Torre D, Lernmark Å. Longitudinal analysis of hepatic transcriptome and serum metabolome demonstrates altered lipid metabolism following the onset of hyperglycemia in spontaneously diabetic biobreeding rats. PLoS One. 2017 Feb 3;12(2):e0171372. PMID: 28192442
Gao S, Wolanyk N, Chen Y, Jia S, Hessner MJ, Wang X. Investigation of coordination and order in transcription regulation of innate and adaptive immunity genes in type 1 diabetes. BMC Med Genomics. 2017 Jan 31;10(1):7. PMID: 28143555
Haribhai D, Luo X, Chen J, Jia S, Shi L, Schroeder JA, Weiler H, Aster RH, Hessner MJ, Hu J, Williams CB, Shi Q. TGF-β1 along with other platelet contents augments Treg cells to suppress anti-FVIII immune responses in hemophilia A mice. Blood Adv. 2016 Dec 13;1(2):139-151. PMID: 28164173
Cepero-Donates Y, Lacraz G, Ghobadi F, Rakotoarivelo V, Orkhis S, Mayhue M, Chen YG, Rola-Pleszczynski M, Menendez A, Ilangumaran S, Ramanathan S. Interleukin-15-mediated inflammation promotes non-alcoholic fatty liver disease. Cytokine 2016 Jun;82:102-11 PMID: 26868085
Cepero-Donates Y, Rakotoarivelo V, Mayhue M, Ma A, Chen YG, Ramanathan S. Homeostasis of IL-15 dependent lymphocyte subsets in the liver. Cytokine 2016 Jun;82:95-101 PMID: 26778709
Tsao CC, Tsao PN, Chen YG, Chuang YH. Repeated Activation of Lung Invariant NKT Cells Results in Chronic Obstructive Pulmonary Disease-Like Symptoms. PLoS One 2016;11(1):e0147710 PMID: 26811900
Olsen JA, Kenna LA, Spelios MG, Hessner MJ, Akirav EM. Circulating Differentially Methylated Amylin DNA as a Biomarker of β-Cell Loss in Type 1 Diabetes. PLoS One 2016;11(4):e0152662 PMID: 27111653
Stelloh C, Reimer MH, Pulakanti K, Blinka S, Peterson J, Pinello L, Jia S, Roumiantsev S, Hessner MJ, Milanovich S, Yuan GC, Rao S. The cohesin-associated protein Wapal is required for proper Polycomb-mediated gene silencing. Epigenetics Chromatin 2016;9:14 PMID: 27087855
Haribhai D, Ziegelbauer J, Jia S, Upchurch K, Yan K, Schmitt EG, Salzman NH, Simpson P, Hessner MJ, Chatila TA, Williams CB. Alternatively Activated Macrophages Boost Induced Regulatory T and Th17 Cell Responses during Immunotherapy for Colitis. J Immunol 2016 Apr 15;196(8):3305-17 PMID: 26927797
Cabrera SM, Wang X, Chen YG, Jia S, Kaldunski ML, Greenbaum CJ. Interleukin-1 antagonism moderates the inflammatory state associated with Type 1 diabetes during clinical trials conducted at disease onset. Type 1 Diabetes TrialNet Canakinumab Study Group, Mandrup-Poulsen T, AIDA Study Group, Hessner MJ) Eur J Immunol 2016 Apr;46(4):1030-46 PMID: 26692253
Gurram B, Salzman NH, Kaldunski ML, Jia S, Li BU, Stephens M, Sood MR, Hessner MJ. Plasma-induced signatures reveal an extracellular milieu possessing an immunoregulatory bias in treatment-naive paediatric inflammatory bowel disease. Clin Exp Immunol 2016 Apr;184(1):36-49 PMID: 26660358Cabrera SM, Chen YG, Hagopian WA, Hessner MJ. Blood-based signatures in type 1 diabetes. Diabetologia 2016 Mar;59(3):414-25 PMID: 26699650
Fisher MM, Cabrera SM, Imel EA. Successful treatment of neonatal severe hyperparathyroidism with cinacalcet in two patients. Endocrinol Diabetes Metab Case Rep. 2015;2015:150040. doi: 10.1530/EDM-15-0040. Epub 2015 Jun 18. PMID: 26161261
Liang HP, Kerschen EJ, Hernandez I, Basu S, Zogg M, Botros F, Jia S, Hessner MJ, Griffin JH, Ruf W, Weiler H. EPCR-dependent PAR2 activation by the blood coagulation initiation complex regulates LPS-triggered interferon responses in mice. Blood. 2015 Apr 30;125(18):2845-54. doi: 10.1182/blood-2014-11-610717. Epub 2015 Mar 2. PMID: 25733582
Gehrand AL, Kaldunski ML, Bruder ED, Jia S, Hessner MJ, Raff H. Intermittent neonatal hypoxia elicits the upregulation of inflammatory-related genes in adult male rats through long-lasting programming effects. Physiol Rep 2015 Dec;3(12): PMID: 26660555
Presa M, Chen YG, Grier AE, Leiter EH, Brehm MA, Greiner DL, Shultz LD, Serreze DV. The Presence and Preferential Activation of Regulatory T Cells Diminish Adoptive Transfer of Autoimmune Diabetes by Polyclonal Nonobese Diabetic (NOD) T Cell Effectors into NSG versus NOD-scid Mice. J Immunol 2015 Oct 1;195(7):3011-9 PMID: 26283479
Fisher MM, Cabrera SM, Imel EA. Successful treatment of neonatal severe hyperparathyroidism with cinacalcet in two patients. Endocrinol Diabetes Metab Case Rep 2015;2015:150040 PMID: 26161261
Liang HP, Kerschen EJ, Basu S, Hernandez I, Zogg M, Jia S, Hessner MJ, Toso R, Rezaie AR, Fernández JA, Camire RM, Ruf W, Griffin JH, Weiler H. Coagulation factor V mediates inhibition of tissue factor signaling by activated protein C in mice. Blood. 2015 Sep 4. pii: blood-2015-05-644401. PMID: 26341257
Cabrera SM, Henschel AM, Hessner MJ. Innate inflammation in type 1 diabetes. Transl Res. 2015 Apr 29. pii: S1931-5244(15)00137-1. PMID: 2598092. Review.
Qin W, Dion SL, Kutny PM, Zhang Y, Cheng A, Jillette NL, Malhotra A, Geurts AM, Chen YG, Wang H. Efficient CRISPR/Cas9-Mediated Genome Editing in Mice by Zygote Electroporation of Nuclease. Genetics. 2015 Mar 27. pii: genetics.115.176594. PMID: 25819794
Liang HP, Kerschen EJ, Hernandez I, Basu S, Zogg M, Botros F, Jia S, Hessner MJ, Griffin JH, Ruf W, Weiler H. EPCR-dependent PAR2 activation by the blood coagulation initiation complex regulates LPS-triggered interferon responses in mice. Blood. 2015 Apr 30;125(18):2845-54. PMID: 25733582. Epub 2015 Mar 2
Ehrhardt MJ, Karst J, Donohoue PA, Maheshwari M, McClain KL, Bingen K, Kelly ME. Recognition and treatment of concurrent active and neurodegenerative langerhans cell histiocytosis: a case report. J Pediatr Hematol Oncol. 2015 Jan;37(1):e37-40. PMID:24322503
Chen YG, Cabrera SM, Jia S, Kaldunski ML, Kramer J, Cheong S, Geoffrey R, Roethle MF, Woodliff JE, Greenbaum CJ, Wang X, Hessner MJ. Molecular signatures differentiate immune states in type 1 diabetic families. Diabetes. 2014 Nov;63(11):3960-73. doi: 10.2337/db14-0214. Epub 2014 Apr 23.
Tsaih SW, Holl K, Jia S, Kaldunski M, Tschannen M, He H, Andrae JW, Li SH, Stoddard A, Wiederhold A, Parrington J, Ruas da Silva M, Galione A, Meigs J; Meta-Analyses of Glucose and Insulin-Related Traits Consortium (MAGIC) Investigators, Hoffmann RG, Simpson P, Jacob H, Hessner M, Solberg Woods LC. Identification of a novel gene for diabetic traits in rats, mice, and humans. Genetics. 2014 Sep;198(1):17-29. doi: 10.1534/genetics.114.162982. PMID: 25236446
Chelvakumar G, Levin L, Polfuss M, Hovis S, Donohoue P, Kotowski A. Perception and documentation of weight management practices in pediatric primary care. WMJ. 2014 Aug; 113(4):149-53; quiz 154. PMID:25211802
Chen YG, Forsberg MH, Khaja S, Ciecko AE, Hessner MJ, Geurts AM. Gene targeting in NOD mouse embryos using zinc-finger nucleases. Diabetes. 2014 Jan. Epub 2013 Aug 23. PMID:23974926
Cort L, Habib M, Eberwine RA, Hessner MJ, Mordes JP, Blankenhorn EP. Diubiquitin (Ubd) is a susceptibility gene for virus-triggered autoimmune diabetes in rats. Genes Immun. 2014 Jan 23. [Epub ahead of print] PMID:24452267
Levy H, Reske M, Bersie R, Barbieri J, Jia S, Kaldunski M, Simpson P, Laxova A, Farrell PM, Hessner MJ. Host Microarray Molecular Signature and Serologic Evaluation of Stages of Pseudomonas aeruginosa Infection in Cystic Fibrosis. Ann Am Thorac Soc. 2014 Jan 11. [In Press] PMID:24437430