| Abstract: |
After puberty, the thymus undergoes a dramatic loss in volume, in weight and in the number of thymocytes, a phenomenon termed age-associated thymic involution. Recently, it was reported that age-associated thymic involution did not occur in mice expressing a rearranged transgenic (Tg) TCRαβ receptor. This finding implied that an age-associated defect in TCR rearrangement was the major, if not the only, cause for thymic involution. Here, we examined thymic involution in three other widely used MHC class I- restricted TCRαβ Tg mouse strains and compared it with that in non-Tg mice. In all three TCRαβ Tg strains, as in control mice, thymocyte numbers were reduced by ~90% between 2 and 24 mo of age. The presence or absence of the selecting MHC molecules did not alter this age-associated cell loss. Our results indicate that the expression of a rearranged TCR alone cannot, by itself, prevent thymic involution. Consequently, other presently unknown factors must also contribute to this phenomenon. |
| Keywords: |
controlled study; nonhuman; animal cell; mouse; animals; mice; gene expression; mice, inbred c57bl; mice, transgenic; t lymphocyte receptor; gene rearrangement; thymus; thymus gland; transgene; immunophenotyping; cell count; aging; t-lymphocyte subsets; major histocompatibility complex; organ size; involution; thymocyte; transgenes; lymphocyte count; receptors, antigen, t-cell, alpha-beta; organ weight; major histocompatibility complex restriction; major histocompatibility antigen; cell loss; male; female; priority journal; article; gene rearrangement, alpha-chain t-cell antigen receptor; gene rearrangement, beta-chain t-cell antigen receptor
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