These lckpr-bcl-XL transgenic mice express a human B-cell leukemia/lymphoma 2 like, 1 (BCL2L1 or BCL-XL) cDNA sequence, under the control of a mouse lymphocyte protein tyrosine kinase proximal promoter (Lckpr). Mice that are heterozygous for this transgene are viable, fertile, and normal in size. Lckpr drives BCL-XL expression within all thymocyte subsets and protects thymocytes from a variety of apoptotic stimuli, including γ irradiation, glucocorticoids, and anti-CD3 treatment. This BCL-XL overexpression alters thymocyte maturation, resulting in an increase in CD3int/hi and a decrease in CD3lo thymocytes, along with an increase in intermediate CD4+8lo and CD4lo8+ thymocytes. They also exhibit an increase in single positive CD8 T cells in the spleen. Overexpression of BCL-XL causes down-regulation of B-cell leukemia/lymphoma 2 (BCL-2) and represses cell death observed in BCL-2 null mice, suggesting a redundant cell survival pathway. These mice may be used for studying development, maturation, and apoptosis of thymocytes.
