Estradiol prevents and testosterone promotes Fas-dependent apoptosis in CD4+                 Th2 cells by altering Bcl 2 expression

Huber, Sally A.; Kupperman, J.; Newell, M. K.

doi:10.1177/096120339900800511

Cited by 81 publications

(54 citation statements)

References 19 publications

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“…Such effects may be mediated through any of several mechanisms described in other rodents. In mice, castration increases thymus size and proliferation of T lymphocytes (10,36), and testosterone reverses these effects (11,36) through a direct action on membrane-bound androgen receptors (2,25). Testosterone induces apoptosis in CD4ϩ and CD4ϩCD8ϩ lymphocytes, in part by increasing production of the proinflammatory cytokine TNF-␣ (23).…”

Section: Discussionmentioning

confidence: 99%

Gonadal hormone-dependent and -independent regulation of immune function by photoperiod in Siberian hamsters

Prendergast¹,

Baillie²,

Dhabhar³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Siberian hamsters (Phodopus sungorus) exhibit changes in reproductive and immune function in response to seasonal variations in day length. Exposure to short days induces gonadal regression and inhibits testosterone secretion. In parallel, short days enhance immune function: increasing leukocyte numbers and attenuating cytokine and behavioral responses to infection. We examined whether photoperiodic changes in leukocyte phenotypes and sickness behaviors are dependent on concurrent photoperiodic changes in gonadal function. Male hamsters were gonadectomized or sham-gonadectomized and either exposed to short days (9 h light/day; SD) or kept in their natal long-day (15 h light/day; LD) photoperiod for 10 -13 wk. Blood samples were obtained for leukocyte enumeration, and hamsters were challenged with bacterial LPS, which induced behavioral (anorexia, reductions in nest building) and somatic (weight loss) sickness responses. Among gonad-intact hamsters, exposure to SD increased total and CD62Lϩ lymphocytes and CD3ϩ T lymphocytes in blood and significantly attenuated LPSinduced sickness responses. Independent of photoperiod, castration alone increased total and CD62Lϩ lymphocyte and CD3ϩ T lymphocyte numbers and attenuated somatic and anorexic sickness responses. Among castrated hamsters, SD exposure increased lymphocyte numbers and suppressed sickness behaviors. In castrated hamsters, the magnitude of most immunological effects of SD were diminished relative to those evident in gonad-intact hamsters. The SD phenotype in several measures of immunity can be instated via elimination of gonadal hormones alone; however, photoperiodic effects on immune function persist even in castrated hamsters. Thus, photoperiod affects the immune system and neural-immune interactions underlying sickness behaviors via gonadal hormone-dependent and -independent mechanisms. seasonality; sickness behaviors; infection; neural-immune interactions SEASONAL CHANGES IN PHYSIOLOGY and behavior are legion, most notably in reproductive function (8). Many mammals have evolved mechanisms that permit cessation of reproduction during intervals of the year when environmental conditions of food availability and ambient temperature are unfavorable for successful weaning of offspring (44,47). In nonequatorial regions, changes in day length (photoperiod) predict these environmental constraints (46) and function as proximate cues for triggering anticipatory changes in reproductive physiology and behavior. In long-day breeders, decreasing photoperiods of late-summer trigger gonadal atrophy, withdrawal of gonadal hormone secretion, and cessation of sex behaviors (8). The full complement of changes in the reproductive system can be elicited in the laboratory by exposing reproductively photoperiodic animals to winter-like day lengths (Ͻ12 h of light/day) (22).Seasonal changes in immune function also occur in wild and laboratory animals (34), and a growing body of research indicates photoperiod likewise drives these cycles. Among long-day breeding rodents, many a...

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Section: Discussionmentioning

confidence: 99%

Gonadal hormone-dependent and -independent regulation of immune function by photoperiod in Siberian hamsters

Prendergast¹,

Baillie²,

Dhabhar³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…[36][37][38] Consistent with the decrease of TNF-␣ and IFN-␥ production in cardiac allografts, local overexpression of Bcl-2 resulted in the reduced expression of ICAM-1 and VCAM-1. In addition, Huber et al 39 recently reported that increased Bcl-2 expression on T H 2 cells led to the selective survival of T H 2 cells in the mouse viral myocarditis model. In contrast, we show that the local overexpression of Bcl-2 in cardiac allografts has a significant influence on T H 1-type immune responses but not on T H 2-type immune responses.…”

Section: Org Frommentioning

confidence: 99%

Cardiomyocyte-specific Bcl-2 overexpression attenuates ischemia-reperfusion injury, immune response during acute rejection, and graft coronary artery disease

Tanaka

Nakae

Terry

et al. 2004

Blood

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After cardiac transplantation, graft damage occurs secondary to ischemia-reperfusion injury and acute rejection. This damage ultimately leads to the development of graft coronary artery disease (GCAD), which limits long-term graft survival. Apoptosis is directly involved in graft injury, contributing to the development of GCAD. To assess the role of the antiapoptotic factor Bcl-2 in the process of GCAD, we transplanted hearts from FVB transgenic mice overexpressing human Bcl-2 under the control of ␣-myosin heavy chain promoter into allogenic C57BL/6 mice. Bcl-2 overexpression led to reduced cytochrome c-mediated caspase-9-dependent cardiomyocyte apoptosis and local inflammation (neutrophil infiltration and proinflammatory cytokine production) in cardiac allografts during ischemia-reperfusion injury and also led to reduced immune responses (inflammatory cell infiltration, production of T H 1 cytokines and chemokines, and expression of adhesion molecules) during acute and chronic rejection without affecting host CD4 ؉ and CD8 ؉ cell responses in the spleen. Thus, local Bcl-2 expression directly contributes to the modulation of local immune responses in allograft rejection, resulting in attenuated GCAD. In conclusion, our findings suggest that the modulation of Bcl-2 expression by pharmacologic up-regulation or gene transfer may be of clinical benefit in the short-and long-term function of cardiac allografts.

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“…Figure 5 shows the percentages of cells -10 -8 M) of 17β-estradiol might slightly increase the cells not stimulated by mitogen in the late phase of apoptosis. Some previous reports 33,34) said that the low-level 17β-estradiol suppressed lymphocyte apoptosis. It might be suggested that 17β-estradiol prevents the change of membrane conformation between the late apoptotic phase and the final debris phase.…”

Section: Resultsmentioning

confidence: 93%

Apoptosis Induction of Mouse Splenic Cells by Exposure to High-Level 17.BETA.-Estradiol and Endocrine Disrupting Chemicals

Sakazaki

Ueno

Nakamuro

2004

JOURNAL OF HEALTH SCIENCE

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Estradiol prevents and testosterone promotes Fas-dependent apoptosis in CD4+ Th2 cells by altering Bcl 2 expression

Cited by 81 publications

References 19 publications

Gonadal hormone-dependent and -independent regulation of immune function by photoperiod in Siberian hamsters

Gonadal hormone-dependent and -independent regulation of immune function by photoperiod in Siberian hamsters

Cardiomyocyte-specific Bcl-2 overexpression attenuates ischemia-reperfusion injury, immune response during acute rejection, and graft coronary artery disease

Apoptosis Induction of Mouse Splenic Cells by Exposure to High-Level 17.BETA.-Estradiol and Endocrine Disrupting Chemicals

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