Suppression of streptococcal cell wall–induced arthritis by human chorionic gonadotropin

Song, Xiaoyu; Zeng, Li; Jin, Wenwen; Pilo, Carey M.; Frank, Mark; Wahl, Sharon M.

doi:10.1002/1529-0131(200009)43:9<2064::aid-anr18>3.0.co;2-z

Cited by 28 publications

(18 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…TGF-β1 has been shown to be therapeutic in several different animal models when expressed systemically from muscle tissue [26,27]. This suggests that elevated serum levels of TGF-β1 can reduce general inflammation as well as inhibit IL-1β and tumor necrosis factor alpha production, resulting in a systemic therapeutic effect.…”

Section: Discussionmentioning

confidence: 99%

Adverse effects of adenovirus-mediated gene transfer of human transforming growth factor beta 1 into rabbit knees

et al. 2003

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Adverse effects of adenovirus-mediated gene transfer of human transforming growth factor beta 1 into rabbit knees

et al. 2003

View full text Add to dashboard Cite

“…This suggests that hCG may also exert its protective effect on Tg26 mice by suppressing TNF-␣-induced activation pathways. Similarly, the suppression of streptococcus cell wall-induced arthritis by hCG may be mediated through the reduction of TNF-␣ levels (33). Evidence that hCG actually can suppress TNF-␣-induced pathways, particularly NF-B and AP-1, was recently provided by Manna and colleagues (22).…”

Section: Tnf-␣ Levels In Sera Of Anti-tnf-␣-and Hcg-treated Micementioning

confidence: 99%

Elevated Levels of Tumor Necrosis Factor Alpha (TNF-α) in Human Immunodeficiency Virus Type 1-Transgenic Mice: Prevention of Death by Antibody to TNF-α

Devadas

Notkins

2002

J Virol

View full text Add to dashboard Cite

Homozygous human immunodeficiency virus type 1 (HIV-1)-transgenic mice (Tg26) appear normal at birth but die within 3 to 4 weeks. The skin of these animals shows diffuse scaling and high-level expression of both HIV-1 mRNA and gp120. Previous experiments showed that treatment with human chorionic gonadatropin (hCG) prevented death and the expression of HIV-1 mRNA and gp120. The present experiments were initiated to study the role of tumor necrosis factor alpha (TNF-␣) in HIV-1-induced pathology. Examination of the sera of Tg26 mice revealed a 50-fold increase in TNF-␣ levels compared to those in nontransgenic mice. Treatment with antibody to TNF-␣ prevented death, resulted in near normal growth, and produced a marked decrease in skin lesions and a profound reduction in the expression of HIV-1 mRNA and gp120. Both TNF-␣ antibody and hCG reduced TNF-␣ levels in sera by approximately 75%. We conclude that TNF-␣ contributes in a major way to HIV-1-induced pathology in transgenic mice and that both hCG and antibody to TNF-␣ prevent the development of pathology by suppressing the level of TNF-␣.

show abstract

“…We used the HPA-1(24-45) peptide and also a shorter peptide with an extended N-terminal sequence (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39) in both the Leu33 (HPA-1a) and Pro33 (HPA-1b) forms in T cell proliferation assays to detect responding T cells from women who had been alloimmunized by pregnancy. Most samples were taken from patients during pregnancy or postpartum.…”

Section: Introductionmentioning

confidence: 99%

Reactivity of T cells from women with antibodies to the human platelet antigen (HPA)-1a to peptides encompassing the HPA-1 polymorphism

Jackson

Soothill

et al. 2005

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SummaryThe human platelet antigen-1a (HPA-1a) is the most common alloantigenic target in fetal and neonatal alloimmune thrombocytopenia (NAIT). Treatment currently depends on the outcome in previous pregnancies. HPA-1 specific T cell responses were determined in 14 HPA-1a alloimmunized women during or after pregnancies affected by NAIT. Peripheral blood mononuclear cells were incubated with peptides encompassing the Leu33Pro polymorphism (residues 20-39 and 24-45 in both Leu33 (HPA-1a) and Pro33 (HPA1b) forms) or control recall antigens in the presence of autologous sera and T cell proliferation was measured by 3 H-thymidine incorporation. Control antenatal and postpartum sera suppressed T cell proliferation and use of such sera was avoided. Most patients (86%) responded to the HPA-1a peptides with 64% also having weaker T cell proliferation to the HPA-1b peptides; 14% had no activity towards any peptide despite responding to control antigens. Administration of IVIG during pregnancy appeared to reduce T cell reactivity to HPA-1 peptides. Postnatal anti-HPA-1a T cell responses from women who had a severe history of NAIT (an intracranial haemorrhage in a previous fetus) were greater than those from women with a mild history. This assay may have the potential to predict disease severity if performed prior to or early in pregnancy.

show abstract

Suppression of streptococcal cell wall–induced arthritis by human chorionic gonadotropin

Abstract: These findings indicate that HCG exerts a protective effect in this experimental arthritis model, through modulation of inflammatory mediators.

Cited by 28 publications

References 45 publications

Adverse effects of adenovirus-mediated gene transfer of human transforming growth factor beta 1 into rabbit knees

Adverse effects of adenovirus-mediated gene transfer of human transforming growth factor beta 1 into rabbit knees

Elevated Levels of Tumor Necrosis Factor Alpha (TNF-α) in Human Immunodeficiency Virus Type 1-Transgenic Mice: Prevention of Death by Antibody to TNF-α

Reactivity of T cells from women with antibodies to the human platelet antigen (HPA)-1a to peptides encompassing the HPA-1 polymorphism

Contact Info

Product

Resources

About