The forthcoming transition in the focus of stem cell research from basic science in the development of therapies raises important questions of justice. This transition is marked by increasing interest in establishing banks of stem cell lines, both to facilitate research and in anticipation of the eventual use of stem cell-derived transplants to treat such diseases as amyotrophic lateral sclerosis, Parkinson's, and diabetes. (1) The creation of stem cell banks raises questions about who stands to benefit from these banks and their research and therapeutic applications. First, there is a question about who, financially, will have access to stem cell-based therapies. (2) Also, given that some nations have legislated against allowing the use of embryonic stem cells, there may be a question of who legally will have access to therapies derived from banked stem cell lines, particularly those of embryonic derivation.
A final issue, and the one we will discuss in this paper, is who biologically will have access to cell-based therapies. As we will show, the biological properties of stem cells themselves may make them less accessible to some potential recipients than to others, a situation we term the problem of biological access. Unless the problem of biological access is carefully addressed, an American stem cell bank may end up benefiting primarily white Americans, to the relative exclusion of the rest of the population. We must therefore ask which of all possible ways to structure an American stem cell bank is the most just.
Rejection and the Theoretical Solution of Autologous Grafts
The future promise of cell engineering is the ability to control cells and their functions. In the interim, however, it seems likely that cell-based treatment for disease and injury will be orchestrated through the transplantation of stem cells or their products. As with more conventional types of transplants, immune rejection is a major potential problem. Immune rejection is the principal reason that a given stem cell-based therapy for a specific disorder might be biologically less available to one patient than to another.
Immune rejection is mediated by our genetic makeup, specifically the set of genes which code for a type of protein called human leukocyte antigens (HLA). These HLA proteins are on the surface of virtually all cells in the body, including stem cells, and they play an important role in immune recognition and rejection. We have two copies of each of these genes, one inherited from each parent. There are multiple genes that code for HLA and we have two copies of each, one on each member of a chromosome pair. Some of the most important genes for the purposes of HLA-mediated immune recognition and response are HLA-A, HLA-B, and HLA-DR.
These genes are highly polymorphic, meaning they occur in variant forms, each of which is known as an allele. When an individual has two different alleles (one inherited from each parent), she is heterozygous for that allele. When, by chance, both parents pass on the same allele for a particular gene, their child is homozygous for that allele, meaning she has two identical copies of the allele.
Different methods exist for characterizing the alleles (either through serologic or DNA methods), and the alleles are usually given numeric codes, like 0101. To find someone's HLA type is to determine which alleles she has at specific locations on the chromosome. Three locations--A, B, and DR--and thus three sets of alleles, are particularly important to HLA-mediated immune functioning. A match entails the donor and the recipient having the same HLA-A, HLA-B, and HLA-DR alleles. (3)
An individual's HLA type is linked to her ancestry; however, even within a family there is variability in HLA expression. Identical twins have identical HLA because they have received the same genetic contribution from their parents. Siblings have a roughly one in four chance of sharing an HLA type. …