Immune Function and the Progression to T1D

University of Florida

Status: Enrolling

Conditions: Type 1 Diabetes

Treatments: Other: blood draw

Study type: Observational

Funder types: Other; NIH

Identifiers

NCT05899439

P01AI042288 (U.S. NIH Grant/Contract)

PRO00043521 (Other Identifier)

IRB201400709

Details and patient eligibility

About

To elucidate the mechanisms by which type 1 diabetes-associated genes; IFIH1, TYK2, IKZF4, as well as total genetic risk, impart functional immunoregulatory abnormalities that result in expansion of self-reactive adaptive immune cells, defective regulatory/effector mechanisms in T cells, inflammatory antigen presenting cells, and abnormal immune function in T cells and B cells.

Full description

Newly proposed studies will identify the inflammatory cues that draw immune cells into islets for disease initiation (Project 1); probe the motility of immune cells through inflamed vasculature to the target organ and antigen priming sites within secondary lymphatics (Project 2); and characterize the T1D-associated adaptive immune signatures in blood and immune tissues (Project 3).

The overall hypothesis of the renewed P01 states: 1) the impact of T1D-risk variants will vary by tissue, cell subset, and activation state, and 2) risk variants, cellular stress, and defects in immunologic pathways are key to engender the autoimmune destruction of pancreatic B-cells that results in T1D.

Enrollment: 2,800 estimated patients

Sex: All

Ages: Under 100 years old

Volunteers: Accepts Healthy Volunteers

Inclusion and exclusion criteria

Inclusion Criteria: able to have blood drawn -

Exclusion Criteria: none

Trial design

2,800 participants in 2 patient groups

Subjects with diabetes age 0 to 100 years

Description:

People who have not been diagnosed with type 1 diabetes

Treatment:

Other: blood draw

Subjects with type 1 diabetes age 0 to 100 years

Description:

People who have been diagnosed with type 1 diabetes

Treatment:

Other: blood draw