The primary interest of this laboratory is the control by genes of the human major histocompatibility complex (MHC) of immune function. Current projects deal with MHC gene influence on NK cell receptor repertoire, T cell antigen receptor repertoire and the human immune response, on immunoglobulin deficiencies, on autoimmune diseases, and on dendritic cell surface molecules and function. We are examining genetic determination of the human immune response and nonresponse to the hepatitis B vaccine and tetanus toxoid peptides using these as models. Because it is central in MHC-influenced autoimmune diseases such as juvenile onset diabetes, multiple sclerosis, and gluten-sensitive enteropathy, we are particularly interested in unravelling the mechanisms involved in incomplete penetrance of MHC susceptibility genes. We have developed ways to analyze modes of inheritance of incompletely penetrant MHC traits and of localizing and ultimately identifying specific susceptibility genes. We are currently using these methods to explore MHC-determined functions and defects in humans.
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Papers & Publications:
1. Alper CA, CE Larsen, DP Dubey, ZL Awdeh, DA Fici, EJ Yunis. The haplotype structure of the human major histocompatibility complex. Hum Immunol. 2006; 67: 73-84.
2. Husain Z, N Holodick, C Day, I Szymanski, CA Alper. Increased apoptosis of CD20+ IgA+ B cells is the basis for IgA deficiency: the molecular mechanism for correction in vitro by IL-10 and CD40L. J Clin Immunol. 2006; 26: 113-125.
3. Alper CA, Z Husain, CE Larsen, DP Dubey, R Stein, C Day, A Baker, H Beyan, M Hawa, TO Ola, RD Leslie. Incomplete penetrance of susceptibility genes for MHC-determined immunoglobulin deficiencies in monozygotic twins discordant for type 1 diabetes. J Autoimmun. 2006; 27: 89-95.
4. Bilbao JR, B Calvo, AM Aransay, A Martin-Pagola, G Pérez de Nanclares, TA Aly, I Rica, JC Vitoria, S Gaztambide, J Noble, PR Fain, ZL Awdeh, CA Alper, L Castaño. Conserved extended haplotypes discriminate HLA-DR3-homozygous Basque patients with type 1 diabetes mellitus and celiac disease. Genes Immun. 2006; 7: 550-554.
5. Awdeh ZL, EJ Yunis, MJ Audeh, D Fici, A Pugliese, CE Larsen, CA Alper. A genetic explanation for the rising incidence of type 1 diabetes, a polygenic disease. J Autoimmun. 2006; 27: 174-181. |
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