RESEARCH - The role of the sex hormones estrogen and prolactin on the regulation of autoreactive B cells

January 5, 2007

Sex and systemic lupus erythematosus: the role of the sex hormones estrogen

and prolactin on the regulation of autoreactive B cells.

Systemic lupus erythematosus and Sjogren syndrome

Current Opinion in Rheumatology. 18(5):456-461, September 2006.

Abstract:

Purpose of review: For many decades, it has been speculated that sex

hormones play a role in systemic lupus erythematosus. Recent data

accumulated during the past few years provide striking evidence that

hormonal modulation of B cells can have a profound impact on the survival,

maturation and repertoire selection of autoreactive B cells and begin to

explain the sex bias associated with the condition.

Recent findings: While there are still insufficient clinical data to define

a role for estrogen or prolactin in human systemic lupus erythematosus,

recent studies of anti-DNA antibody transgenic mice clearly demonstrate that

an elevation in either estrogen or prolactin breaks tolerance of high

affinity DNA-reactive B cells and induces a lupus phenotype. B cells with

the same antigenic specificities are rescued by either estrogen or

prolactin, but estrogen promotes the survival and activation of the T

independent marginal zone B cell subset, while prolactin promotes the

survival and activation of the T dependent follicular B cell subset.

Summary: Elevations in the levels of estrogen or prolactin can promote the

survival and activation of high affinity autoreactive B cells. These

hormones engage different B cell pathways to interfere with B cell

tolerance. The identification of systemic lupus erythematosus patients with

either an estrogen-responsive or prolactin-responsive disease will further

the development of therapeutics that can specifically modulate hormonal

responses.

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Not an MD

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