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JCI table of contents, January 15 2003

ritical role in lactation, prolactin is thought to affect cells of the immune system and augment autoimmunity. Both B and T cells express prolactin receptors, and the hormone has been shown to influence T cell development and proliferation. Focusing on the effects of prolactin on B cells, Betty Diamond and colleagues found (see pages 275-283) that a two-fold increase in prolactin can break tolerance to certain self-antigens and induce lupus-like disease in a transgenic mouse model. Increased prolactin levels affected B cell development and maturation, and promoted the survival of high-affinity autoreactive B cells that would normally undergo deletion. While these alterations were consistently observed in one genetic background, they were not seen in a second mouse strain, suggesting that susceptibility to hormone-mediated autoantibody development is genetically determined.

CONTACT:
Betty Diamond
Albert Einstein College of Medicine
Department of Microbiology & Immunology and Dept. of Medicine
1300 Morris Park Avenue
Room 405, Forchheimer Building
Bronx, NY 10461
USA
Phone 1: 718/430-4081
Phone 2: 718/430-2811 ext. 4081
Fax 1: 718-430-8711
E-mail: diamond@aecom.yu.edu

View the PDF of this article at: https://www.the-jci.org/press/16530.pdf

Direct Injection of Genetically Engineered Fibroblasts Corrects Epidermolysis Bullosa Skin

Dystrophic epidermolysis bullosa refers to a family of severe skin disorders caused by mutations in the type VII collagen gene (COL7A1). Patients lack anchoring fibrils that ensure adhesion of the epidermis to the dermis and develop subepidermal blisters in response to minor mechanical stress. The current lack of treatment is an impetus to develop gene therapy strategies that will restore anchoring fibrils.
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Contact: Brooke Grindlinger, PhD
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
16-Jan-2003


Page: 1 2 3 4 5 6 7

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