|
 |
|||||||||||||||||||
|
|||||||||||||||||||
|
|||||||||||||||||||
 |
 |
|
|
Relevant Models of Protection from, and Induction of, Type 1 Diabetes
a Department of Pathology and Microbiology, University of Nebraska Medical Center, Nebraska Medical Center, Omaha, Nebraska, USA b Department of Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, Nebraska, USA
Key Words: enterovirus • coxsackievirus • non-obese diabetic mice • NOD mice • type 1 diabetes • T1D •  • cells • IL-4
Address for correspondence: Steven Tracy, Department of Pathology and Microbiology, University of Nebraska Medical Center, 986495 Nebraska Medical Center, Omaha NE 68198. Voice: +402-559-7747; fax:+ 402-559-4077. stracy{at}unmc.edu
Human enteroviruses (HEVs) like the group B coxsackieviruses (CVBs) are prime candidates for infectious, environmental causes of human type 1 diabetes (T1D). Non-obese diabetic (NOD) female mice are well protected from T1D onset if inoculated with CVB when young. Older, prediabetic NOD mice can rapidly develop T1D following inoculation with CVB, mimicking clinical reports of disease-associated T1D onset. The ability to induce rapid T1D in NOD mice is linked to the rate of replication of the CVB strain in
cell cultures and pancreatic tissue, indicating that any CVB strain is potentially diabetogenic under the correct conditions. Rapid T1D onset is preceded by CVB replication in islet cells including cells. Although CVB strains do not productively infect healthy islets of young mice, CVBs can replicate in healthy islets in the presence of murine IL-4. These models expand much of what is known or suspected regarding the etiologic role of HEVs in human T1D.
This article has been cited by other articles:
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
 |
