The Journal of Immunology, Vol 159, Issue 6 2712-2719, Copyright © 1997 by American Association of Immunologists

ARTICLES

Primary B cell development is impaired in mice with defects of the pituitary/thyroid axis

E Montecino-Rodriguez, RG Clark, L Powell-Braxton and K Dorshkind
Department of Pathology and Laboratory Medicine and The Jonsson Comprehensive Cancer Center, School of Medicine, University of California, Los Angeles 90095, USA.

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.

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