Dr. Robert
P.
Kimberly
Department of Medicine
Division of Clinical Immunology and Rheumatology
THT 429, 1900 University Blvd.
Birmingham, AL 35294
Phone: 205-934-5306
Fax: 205-934-1564
E-mail: rpk@uab.edu
Number of Human Subjects projects reported: 1
| UAB-04-X040607001 | "Program in the Functional Genomics of Autoimmunity and Immunobiology" |
"Program in the Functional Genomics of Autoimmunity and Immunobiology"
Principal Investigator: Dr. Robert P. Kimberly, University of Alabama at Birmingham
Project started in: 2004
This project ended in fiscal year 2005.
Funding for Human Subjects Research:
This project does not involve the use of multiple protocols/subprojects.
Institutional Review Board (IRB) Review:
Type of Review:
Expedited
Approving Institution: University of Alabama at Birmingham
Most recent approval: 07/20/05
IRB approval number: X040607001
Number of human subjects who participated in this project/protocol/subproject in the last reporting period: 1507
Reporting period for number of human subjects:
Fiscal Year 2005
Type(s) of Human Subjects Involvement:
Polymeric immunoglobulin receptor (pIgR) is a transmembrane glycoprotein on the basolateral surface of secretory epithelial cells. It mediates the transport of dimeric IgA and polymeric IgM across mucosal epithelia. Regulation of IgA transport through pIgR may play an important role in the levels of IgA and its relation to pathogenesis. pIgR is located on human chromosome 1q32, a region of genetic linkage for systemic lupus erythematosis (SLE), and is a strong candidate gene for SLE susceptibility. We used direct sequencing techniques to identify single nucleotide polymorphisms (SNPs) in the pIgR gene in Caucasian and African American controls and SLE patients and to test for association with SLE phenotype. The study cohort comprises of 50 controls and 50 SLE patients from the African American and Caucasian ethnic groups. Four significant SNPs in the pIgR gene were identified by DNA direct sequencing in 191 ethnically diverse donors. Some of SNP alleles were enriched in SLE patient groups, indicating these SNPs may play important roles in autoimmune and other inflammatory diseases.