| First Author | Rich BE | Year | 1997 |
| Journal | Immunology | Volume | 92 |
| Issue | 3 | Pages | 374-80 |
| PubMed ID | 9486111 | Mgi Jnum | J:43971 |
| Mgi Id | MGI:1099222 | Doi | 10.1046/j.1365-2567.1997.00353.x |
| Citation | Rich BE (1997) Autocrine expression of interleukin-7 rescues lymphoid expansion in interleukin-7-deficient mice. Immunology 92(3):374-80 |
| abstractText | The murine interleukin-7 (IL-7) gene was disrupted to examine the role of IL-7 in the lymphoid system. Expansion of lymphoid cells is sharply curtailed in IL-7-deficient mice. This is evident in a dramatic reduction but not elimination of lymphoid cells in the thymus, bone marrow and spleen. The few thymocytes present express CD4 and/or CD8 markers associated with T-cell maturation. Similarly, a limited number of B cells detected in the bone marrow rearrange and express immunoglobulin genes. Small but distinct populations of B and T cells are found in the spleens of IL-7-deficient mice. Thus the signal transmitted by IL-7 plays a central role in the expansion of lymphocytes while it is not absolutely required for their maturation. A transgene that directs expression of IL-7 to lymphoid cells was found to restore the numbers of thymocytes, bone marrow B-cell progenitors and splenic lymphocytes of IL-7-deficient mice to approximately normal levels. This genetic complementation confirms that the lymphoid defect is specifically due to the absence of IL-7 and demonstrates that the expansion of lymphoid cells in an organism is regulated by their exposure to IL-7. |
