| First Author | Montecino-Rodriguez E | Year | 1997 |
| Journal | J Immunol | Volume | 159 |
| Issue | 6 | Pages | 2712-9 |
| PubMed ID | 9300691 | Mgi Jnum | J:110683 |
| Mgi Id | MGI:3640879 | Doi | 10.4049/jimmunol.159.6.2712 |
| Citation | Montecino-Rodriguez E, et al. (1997) Primary B cell development is impaired in mice with defects of the pituitary/thyroid axis. J Immunol 159(6):2712-9 |
| abstractText | There has been considerable speculation that hormones produced in the anterior pituitary gland act as positive regulators of primary B cell development in the bone marrow. In order to identify endocrine factors that have such a role, B cell differentiation was examined in a panel of mice with genetic mutations that result in compromised production of one or more anterior pituitary hormones. This analysis demonstrated that the frequency of B lineage cells is significantly reduced in the dwarf and hypothyroid strains of mice, which have defects in the pituitary/thyroid axis, and that the production of normal numbers of pre-B cells is particularly dependent upon thyroid hormones. B cell development was normal in Little and IGF-I knockout animals, which have defects in the production of growth hormone and/or insulin-like growth factor I. The dependence of B lymphopoiesis on thyroid hormones appeared to be specific for that lineage, as myelopoiesis and thymopoiesis were normal in dwarf and hypothyroid mice. In addition to describing a specific endocrine hormone involved in the regulation of B cell development, these data provide evidence that normal production of bone marrow B lineage cells is dependent on extramedullary signals. |
