Roles of Prolactin and Gonadotropin-Releasing Hormone in Rheumatic Diseases

Walker, Sara E.; Jacobson, Jill D.

doi:10.1016/s0889-857x(05)70166-6

Cited by 82 publications

(52 citation statements)

References 87 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…On the other hand, they also demonstrated sexually dimorphic actions (disease severity was higher in females) of GnRH agonists even in gonadectomised mice. Based on their data, it was hypothesised that differences in responsiveness to GnRH might be due to gender differences in expression of GnRH-R or due to gender differences in expression of G proteins (Jacobson et al 1999a, Jacobson 2000, Walker & Jacobson 2000. These explanations might partially explain gender differences in immune function.…”

Section: Impact Of Gnrh On Autoimmunity and Gender-specific Immune Rementioning

confidence: 99%

The hypothalamic-pituitary-gonadal axis: immune function and autoimmunity

Tanrıverdi¹,

Silveira²,

MacColl³

et al. 2003

Journal of Endocrinology

274

187

View full text Add to dashboard Cite

show abstract

Section: Impact Of Gnrh On Autoimmunity and Gender-specific Immune Rementioning

confidence: 99%

The hypothalamic-pituitary-gonadal axis: immune function and autoimmunity

Tanrıverdi¹,

Silveira²,

MacColl³

et al. 2003

Journal of Endocrinology

274

187

View full text Add to dashboard Cite

show abstract

“…Prolactin is a polypeptide pituitary sex hormone with relative concentration differences between sexes (69,70) and a broad array of immunoregulatory proper- ties (7,8). Estradiol stimulates prolactin secretion, and prolactin suppresses gonadal steroid synthesis (69,70).…”

Section: Serum Prolactinmentioning

confidence: 99%

“…As recently reviewed (4), biologic differences between the sexes occur at genetic (X and Y chromosome-mediated), endocrinologic, metabolic, and environmental levels. However, the report in 1944 (5) of SLE flares corresponding to menstrual cyclicity focused an era of investigations on the potential contributions of estrogens, androgens, and prolactin to the development of SLE (6)(7)(8). Substantial evidence of immunoregulatory actions of 17␤-estradiol (estradiol), testosterone, progesterone, dehydroepiandrosterone/dehydroepiandrosterone sulfate (DHEA/DHEAS), and prolactin supports the concept that sex hormones modulate the incidence and severity of disease in patients with SLE (3,9).…”

Section: Introductionmentioning

confidence: 99%

Sex hormones and systemic lupus erythematosus: Review and meta‐analysis

McMurray¹,

May²

2003

Arthritis & Rheumatism

149

120

View full text Add to dashboard Cite

“…Because sex hormone manipulation can alter the severity of murine lupus (reviewed in Refs. [5][6][7], it has been thought that hormones may act as modulators of disease expression in systemic lupus erythematosus (SLE) 3 (8). Studies in murine lupus, particularly the New Zealand Black/White (NZB/W) model, have supported this hypothesis.…”

mentioning

confidence: 99%

Increased Severity of Murine Lupus in Female Mice Is Due to Enhanced Expansion of Pathogenic T Cells

Lang

Nguyen

Papadimitriou

et al. 2003

The Journal of Immunology

View full text Add to dashboard Cite

A strong female predominance is a well-recognized feature of human lupus. The mechanism by which sex influences disease expression and severity is not fully understood. To address this question, we used the parent-into-F1 (p→F1) model of chronic graft-vs-host disease (cGVHD) in which lupus-like humoral autoimmunity and renal disease are induced in normal F1 mice. An advantage of this model is that the pathogenic T cells driving disease (donor strain) can be studied separately from nonspecifically activated T cells (host strain). We observed that lupus-like disease using female donor and host mice (f→F cGVHD) is characterized by more severe long-term disease (glomerulonephritis) than with male donor and host (m→M cGVHD). Interestingly, differences in disease parameters could be seen at 2 wk after parental cell transfer, as evidenced by a 2- to 3-fold greater engraftment of donor CD4+ T cells in f→F cGVHD mice, which persisted throughout disease course. Enhanced engraftment of donor CD4+ T cells in f→F cGVHD mice was not due to differences in splenic homing, alloreactive precursor frequency, initial proliferation rates, or apoptotic rates, but rather to sustained high proliferation rates during wk 2 of disease compared with m→M cGVHD mice. Crossover studies (m→F, f→M) demonstrated that enhanced donor CD4+ T cell proliferation and engraftment segregate with the sex of the host. These results demonstrate that the sex of the recipient can influence the expansion of pathogenic T cells, thus increasing long-term the burden of autoreactive T cells and resulting in greater disease severity.

show abstract

Roles of Prolactin and Gonadotropin-Releasing Hormone in Rheumatic Diseases

Cited by 82 publications

References 87 publications

The hypothalamic-pituitary-gonadal axis: immune function and autoimmunity

The hypothalamic-pituitary-gonadal axis: immune function and autoimmunity

Sex hormones and systemic lupus erythematosus: Review and meta‐analysis

Increased Severity of Murine Lupus in Female Mice Is Due to Enhanced Expansion of Pathogenic T Cells

Contact Info

Product

Resources

About