Profile Frank Conrad

Diabetes is the fifth deadliest disease in the US (American Diabetes Association), with autoimmune Type 1 Diabetes (T1D) accounting for more cases than all other chronic illnesses of childhood combined. T1D is known to result from the infiltration of the Islets of Langerhans with immune cells (including lymphocytes) that destroy insulin producing beta-cells of the pancreas. Ultimately, this reduces insulin production, limiting the body’s ability to convert sugars into energy. Depletion of beta-cells in T1D is widely thought to involve CD4+ and CD8+ T-cells as effectors. However the mechanisms that contribute to the activation of insulin specific T-cells remain unclear.

Compelling evidence indicates that B cells are required for development of T1D in the NOD mouse model. Offending cells must be of appropriate specificity (i.e. anti-insulin), but needn’t produce antibody. B cells may play a similar role in T1D in humans, as studies of pre-diabetic patients have found that anti-Islet and anti-insulin antibodies are predictive of disease onset but do not directly contribute to pancreatic damage. Thus an understanding of how and why B cells contribute to T1D may reveal new targets for therapeutic intervention.