This study demonstrates that IL-7 is a nonredundant cytokine essential for the development of T and B cells. Researchers inactivated the IL-7 gene in mice using gene-targeting techniques and observed severe lymphopenia in peripheral blood and lymphoid organs. Bone marrow B lymphopoiesis was blocked at the transition from pro-B to pre-B cells, while thymic cellularity was reduced 20-fold but retained normal CD4 and CD8 distribution. Splenic T cellularity was reduced 10-fold, and splenic B cells showed an abnormal population of immature B cells. Despite these defects, remaining lymphocytes showed normal responsiveness to mitogenic stimuli. These findings indicate that IL-7 is critical for proper T and B cell development. The IL-7-deficient mice are the first example of a single cytokine-deficient mouse with severe lymphoid abnormalities. The study also highlights the importance of IL-7 in lymphoid development, as it is not redundant and is essential for normal lymphocyte development. The results suggest that IL-7 is a unique and nonredundant cytokine, with no other cytokine being as essential for lymphoid development as IL-7. The study also shows that the absence of IL-7 leads to a stable phenotype of severe peripheral blood lymphopenia, which can be traced back to abnormal B lymphopoiesis in the bone marrow. The data indicate that the transition between pro-B and pre-B cells is blocked, and that the differentiation of B cells to pre-B cells is absolutely dependent on IL-7. The study also shows that the remaining splenic T cell populations show normal staining patterns of CD4, CD8, and CD3. The results suggest that IL-7 is essential for the development and expansion of lymphocytes, and that its absence leads to severe lymphopenia. The study also shows that the phenotype of IL-7-deficient mice is similar to that of IL-2Rγ-deficient mice, even though this receptor subunit is shared by at least four other cytokines. The study concludes that IL-7 is a unique and nonredundant cytokine essential for normal lymphocyte development.This study demonstrates that IL-7 is a nonredundant cytokine essential for the development of T and B cells. Researchers inactivated the IL-7 gene in mice using gene-targeting techniques and observed severe lymphopenia in peripheral blood and lymphoid organs. Bone marrow B lymphopoiesis was blocked at the transition from pro-B to pre-B cells, while thymic cellularity was reduced 20-fold but retained normal CD4 and CD8 distribution. Splenic T cellularity was reduced 10-fold, and splenic B cells showed an abnormal population of immature B cells. Despite these defects, remaining lymphocytes showed normal responsiveness to mitogenic stimuli. These findings indicate that IL-7 is critical for proper T and B cell development. The IL-7-deficient mice are the first example of a single cytokine-deficient mouse with severe lymphoid abnormalities. The study also highlights the importance of IL-7 in lymphoid development, as it is not redundant and is essential for normal lymphocyte development. The results suggest that IL-7 is a unique and nonredundant cytokine, with no other cytokine being as essential for lymphoid development as IL-7. The study also shows that the absence of IL-7 leads to a stable phenotype of severe peripheral blood lymphopenia, which can be traced back to abnormal B lymphopoiesis in the bone marrow. The data indicate that the transition between pro-B and pre-B cells is blocked, and that the differentiation of B cells to pre-B cells is absolutely dependent on IL-7. The study also shows that the remaining splenic T cell populations show normal staining patterns of CD4, CD8, and CD3. The results suggest that IL-7 is essential for the development and expansion of lymphocytes, and that its absence leads to severe lymphopenia. The study also shows that the phenotype of IL-7-deficient mice is similar to that of IL-2Rγ-deficient mice, even though this receptor subunit is shared by at least four other cytokines. The study concludes that IL-7 is a unique and nonredundant cytokine essential for normal lymphocyte development.