Abstract
T cell receptors for antigen (TCR) V-genes are under a very restrictive evolutionary pressure in order to maintain their biological activities of interacting with MHC class I or II molecules and processed peptides at the protein level. This is in contrast to immunoglobulin V-genes which can mutate more freely. As we have discussed before, 17 or less nucleotide differences between any two mouse light chain V-genes can be due to somatic mutations induced by antigens, allelic variations, and the combination of these two mechanisms. Thus, a cut-off of 17 nucleotide differences has been used to estimate the numbers of the other human and mouse immunoglobulin chain V-genes. Except for mouse heavy chains where experimental study is not yet available, our estimated numbers are in good agreement with experimental findings. For TCR V-genes, however, this cut-off value should be modified as illustrated in the present analysis. Our estimation of the number of human TCR chain V-genes is also in good agreement with the recent experimental study of sequencing 685 kb of that gene locus. Estimations for the numbers of human mouse a and chain V-genes will wait for future experimental verification.