Chester Alper, MD
| Department | Hematology/Oncology |
 |
| Hospital Title | Senior Investigator, CBR Institute | |
| Academic Title | Professor of Pediatrics | |
| Phone | 617-278-3333 | |
| Fax | 617-278-3493 | |
| Chester Alper | ||
| Location |
CBR Institute for Biomedical Research 800 Huntington Avenue Boston MA 02115 |
Research Overview
The Alper lab studies the genetics of immune function in humans, particularly within the genes of the major histocompatibility complex (MHC) of chromosome 6. Many human diseases of unknown origin, but mostly involving immune reactions against the patients' own tissues, show associations with the MHC.
Specifically, Alper and colleagues investigate the relationship between genetic differences in the human MHC with differences in the immune function of a variety of "white blood cells," or leukocytes. Gene products of the human MHC are also sometimes called human leukocyte antigens (HLA), and are major proteins expressed on and within leukocytes. Many of these proteins are used by the body to differentiate "self" from foreign cells, and HLA proteins play a critical role in organ and tissue recognition and rejection after transplantation as well as in detecting foreign pathogens.
Hundreds of genes are located within the human MHC. As would be expected for a region that contains proteins that help define "self," this region is among the most diverse of the human genome. Although the lab has studied the MHC genetics of a number of immune functions and diseases, they are currently focused on six specific areas. These are complement, the cellular immune response to hepatitis B vaccine, immunoglobulin deficiency (particularly IgA deficiency), natural killer cell repertoire and function, dendritic cell structure and function, and the genetic mechanisms of autoimmunity. The Alper lab often studies the blood of donors bearing conserved extended MHC haplotypes to explore control by these genes.
About Chester Alper
Chester Alper received an MD from Harvard Medical School. He completed an internship and residency at Boston City Hospital.
Key Publications
- Husain Z, Holodick N, Day C, Szymanski I, Alper CA. 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; 26:113-25.
- Alper CA, Larsen CE, Dubey DP, Awdeh ZL, Fici DA, Yunis EJ. The haplotype structure of the human major histocompatibility complex. Hum Immunol. 2006; 67:73-84.
- Alper CA, Xu J, Cosmopoulos K, Dolinski B, Stein R, Uko G, Larsen CE, Dubey DP, Densen P, Truedsson L, Sturfelt G, Sjoholm AG. Immunoglobulin deficiencies and susceptibility to infection among homozygotes and heterozygotes for C2 deficiencyL. Journal of Clinical Immunology 2003; 23: 297-305.
