Response to Comment on: Meagher et al. Neutralization of Interleukin-16 Protects Nonobese Diabetic Mice From Autoimmune Type 1 Diabetes by a CCL4-Dependent Mechanism. Diabetes 2010;59:2862–2871
- Craig Meagher1,
- William Cruikshank2 and
- Terry L. Delovitch1
- From the 1Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada; and
- 2The Pulmonary Center, Boston University, Boston, Massachusetts
- Corresponding author: Terry L. Delovitch, del{at}robarts.ca.
We thank Vendrame and Dotta (1) for their interesting perspective regarding our recently published study investigating the role of interleukin-16 (IL-16) in the development of insulitis and type 1 diabetes in female NOD mice (2). On the basis of previous studies correlating suboptimal activation of caspase-3 with the development of autoimmunity in the clinical setting (3,4), they propose a similar condition might exist in NOD mice, resulting …
In this Issue
February 2011, 60(2)
Response to Comment on: Meagher et al. Neutralization of Interleukin-16 Protects Nonobese Diabetic Mice From Autoimmune Type 1 Diabetes by a CCL4-Dependent Mechanism. Diabetes 2010;59:2862–2871
