Suppression of Immunoglobulin Secretion by Soluble Annexin II

Aarli, Å.; Matre, R.

doi:10.1046/j.1365-3083.1998.00436.x

Cited by 9 publications

(8 citation statements)

References 35 publications

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“…In view of previous reports (8–11) our negative results using similar assays were unexpected, but the most likely explanation is that the active form of AXII remained intracellular, and therefore did not have any direct effect on other cells. We did not detect AXII on the cell surface.…”

Section: Discussionsupporting

confidence: 51%

No immunosuppressive effect of transfected annexin II

Hansen

2002

APMIS

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Annexin II (AXII) was reported to suppress lymphoproliferation and immunoglobulin production. To investigate this further, the AXII-negative human B-lymphoma cell line Raji was transfected with AXII followed by transfection with p11. Stable transfectants were generated. In vitro immunological effects of Raji, Raji-AXII and Raji-AXII-p11 were compared by using irradiated cells as stimulators for PBM in mixed lymphocyte reactions or by adding the supernatants to lymphoproliferation or ELISPOT cultures. None of the assays provided evidence of significant immunosuppression by AXII. Thus, expression of AXII or AXII plus p11 does not by itself give a cell immunosuppressive ability.

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Section: Discussionsupporting

confidence: 51%

No immunosuppressive effect of transfected annexin II

Hansen

2002

APMIS

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“…CalM can also regulate ER transcriptional activity by its direct association with ER and interact with myosin light chain kinase to control uterine muscle contraction (23)(24)(25)(26). CalP, a member of the annexin family, plays a role in immunomodulation (27). Sik-SP is conserved with a gene family nop5/sik1 that encodes components of small nucleolar ribonucleoprotein complexes.…”

mentioning

confidence: 99%

Estrogen Targets Genes Involved in Protein Processing, Calcium Homeostasis, and Wnt Signaling in the Mouse Uterus Independent of Estrogen Receptor-α and -β

Das¹,

Tan²,

Raja³

et al. 2000

Journal of Biological Chemistry

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Estrogen actions in target organs are normally mediated via activation of nuclear estrogen receptors (ERs). By using mRNA differential display technique, we show, herein, that estradiol-17␤ (E 2 ) and its catechol metabolite 4-hydroxy-E 2 (4OHE 2 ) can modulate uterine gene expression in ER␣(؊/؊) mice. Whereas administration of E 2 or 4OHE 2 rapidly up-regulated (4 -8-fold) the expression of immunoglobulin heavy chain binding protein (Bip), calpactin I (CalP), calmodulin (CalM), and Sik similar protein (Sik-SP) genes in ovariectomized wildtype or ER␣(؊/؊) mice, the expression of secreted frizzled related protein-2 (SFRP-2) gene was down-regulated (4-fold). Bip, CalP, and CalM are calcium-binding proteins and implicated in calcium homeostasis, whereas SFRP-2 is a negative regulator of Wnt signaling. Bip and Sik-SP also possess chaperone-like functions. Administration of ICI-182,780 or cycloheximide failed to influence these estrogenic responses, demonstrating that these effects occur independent of ER␣, ER␤, or protein synthesis. In situ hybridization showed differential cell-specific expression of these genes in wild-type and ER␣(؊/؊) uteri. Although progesterone can antagonize or synergize estrogen actions, it had minimal effects on these estrogenic responses. Collectively, the results demonstrate that estrogens have a unique ability to influence specific genes in the uterus not involving classical nuclear ERs.Estrogens regulate diverse physiological responses including normal functioning of the reproductive and cardiovascular systems and bone metabolism (1-3). The uterus is a primary target for various estrogenic responses during the cycle and pregnancy. In the mouse, estrogen induces uterine epithelial cell proliferation, and together with progesterone (P 4 ) 1 it directs stromal cell proliferation and epithelial cell differentiation. These coordinated estrogen and P 4 interactions prepare the uterus to the receptive state for implantation (reviewed in Ref. 4). The mechanism by which estrogen renders the P 4 -primed uterus receptive for implantation is not clearly understood.Estrogen actions are primarily executed by its binding to nuclear estrogen receptors, ER␣ and/or ER␤, which are ligandinducible transcription factors (5, 6). They modulate transcription of genes by virtue of their binding as hormone receptor complexes to specific DNA sequences (hormone response elements) in target promoters (5, 6). Despite the classical estrogenic actions, there is increasing evidence that gene transactivation or modulation of cell functions by estrogens is also mediated independent of nuclear ERs (7-10). In many cells, a myriad of estrogenic effects occurs rapidly within seconds or minutes. These responses do not require RNA or protein synthesis and are considered to be mediated by estrogen binding to the plasma membrane (10 -12). For example, increases in intracellular cAMP, calcium influx, inositol triphosphate, and release of prolactin are all attributed to membrane-mediated estrogen actions (10 -12). Although the pre...

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“…Annexin II is secreted by the placenta and might inhibit lymphoproliferation and secretion of maternal immunoglobulins (Fig. 6), (Aarli and Matre, 1998).…”

Section: Means Of Tolerancementioning

confidence: 99%

Pregnancy and the immune system: between tolerance and rejection

Thellin

Heinen

2003

Toxicology

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Interactions between the conceptus and the mother are bi-directional: the feto-placental tissues need nutrition and a suitable environment in homeostatic condition whereas the mother influenced by the placental factors adapts her metabolism and immune system. Many different mechanisms acting locally or at distance ensure tolerance of the semiallogeneic graft by the maternal natural and adaptive immune defences. In front of this tolerance, mechanisms exist ensuring rejection of the conceptus by the mother (spontaneous abortion) through rupture of one or more tolerance mechanisms, notably in stress situations endangering the mother. Thus outcome of a pregnancy is dependent on efficiently working tolerance mechanisms, and rupture of such mechanisms can lead to rejection. The balance of influence leading either to tolerance or rejection is under control of internal (maternal and fetal) and external (environmental) factors. Rejection, if triggered, mainly occurs through immune-induced inflammation, tissue degradation and coagulation. #

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Suppression of Immunoglobulin Secretion by Soluble Annexin II

Cited by 9 publications

References 35 publications

No immunosuppressive effect of transfected annexin II

No immunosuppressive effect of transfected annexin II

Estrogen Targets Genes Involved in Protein Processing, Calcium Homeostasis, and Wnt Signaling in the Mouse Uterus Independent of Estrogen Receptor-α and -β

Pregnancy and the immune system: between tolerance and rejection

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