Mucosal Innate Immune Factors in Secretions from High-Risk Individuals Immunized with a Bivalent gp120 Vaccine

2007 ◽  
Vol 23 (5) ◽  
pp. 748-754 ◽  
Author(s):  
James E. Cummins Jr. ◽  
Maxine Denniston ◽  
Kenneth H. Mayer ◽  
Robert Pickard ◽  
Richard M. Novak ◽  
...  
Therapy ◽  
2021 ◽  
Vol 4_2021 ◽  
pp. 41-47
Author(s):  
Vinnitskaya A.B. Vinnitskaya ◽  
Svitich O.A. Svitich ◽  
Golenkov A.K. Golenkov ◽  
Klinushkina E.F. Klinushkina ◽  
Zaitseva T.A. Zaitseva ◽  
...  

2011 ◽  
Vol 7 (3) ◽  
pp. e1001309 ◽  
Author(s):  
Ricardo S. Ramiro ◽  
João Alpedrinha ◽  
Lucy Carter ◽  
Andy Gardner ◽  
Sarah E. Reece

2020 ◽  
pp. 175342592095520
Author(s):  
YunQiang Zhang ◽  
YunLu Zhang ◽  
ZiKui Liu

Modern scientific research has shown that Acanthopanax senticosus (AS) can regulate the innate immunity of healthy animals, thus affecting the health of animals. However, there are few systematic reports on the changes of innate immune indices of healthy animals after consuming AS. The purpose of this project was to study the effect on healthy mice’s innate immunity and changes of related immune factors induced by feeding AS root powder supplementation. The results showed that the killing rate of natural cells increased in a dose-dependent manner in a certain time period. Compared to the control group, the treatment groups (T1, T2 and T3) improved significantly in the innate immune index (lysozyme, β-defensin-2 and duodenal secretory IgA (SIgA) to varying degrees) and induced corresponding changes of immune factors at certain time periods. The correlation between SIgA and IFN-γ in mouse serum was enhanced, and the higher the concentration of AS in the diet, the stronger the correlation was. However, there was no significant difference in growth performance among groups. It is proved that AS supplementation can enhance innate immunity and change several relevant immune factors and cells of healthy mice without affecting growth performance.


2020 ◽  
Vol 11 ◽  
Author(s):  
Nátalli Zanete Pereira ◽  
Anna Cláudia Calvielli Castelo Branco ◽  
Kelly Cristina Gomes Manfrere ◽  
Josenilson Feitosa de Lima ◽  
Fabio Seiti Yamada Yoshikawa ◽  
...  

2014 ◽  
Vol 20 (11) ◽  
pp. 1942-1949 ◽  
Author(s):  
Jonathan Landy ◽  
Hafid O. Al-Hassi ◽  
Emma Ronde ◽  
Nick R. English ◽  
Elizabeth R. Mann ◽  
...  
Keyword(s):  

2019 ◽  
Vol 5_2019 ◽  
pp. 125-132
Author(s):  
Dobrokhotova Yu.E. Dobrokhotova ◽  
Gankovskaya L.V. Gankovskaya ◽  
Borovkova E.I. Borovkova ◽  
Zaidieva Z.S. Zaidieva Z ◽  
Skalnaya V.S. Skalnaya ◽  
...  

mBio ◽  
2015 ◽  
Vol 6 (6) ◽  
Author(s):  
Shiyuan Hong ◽  
Shouqiang Cheng ◽  
Andre Iovane ◽  
Laimonis A. Laimins

ABSTRACTThe life cycle of high-risk human papillomaviruses (HPVs) is dependent upon epithelial differentiation. Following infection of basal cells, HPV genomes are stably maintained at low copy numbers, and productive replication or amplification is restricted to highly differentiated suprabasal cells. In high-risk HPV infections, the ATM pathway is constitutively activated in the absence of external DNA-damaging agents and is required for productive viral replication. The ataxia telangiectasia (ATM) pathway repairs double-strand breaks in DNA, while the ataxia telangiectasia and Rad3-related (ATR) pathway targets single-strand breaks. Our studies show that the ATR pathway, like the ATM pathway, is activated in HPV-positive cells and that inhibitors of ATR or CHK1 phosphorylation block both amplification and late viral gene expression in differentiated cells while moderately reducing stable copy numbers in undifferentiated cells. TopBP1 is a critical upstream activator of the ATR pathway and is expressed at elevated levels in HPV-positive cells. This increased expression of TopBP1 is necessary for ATR/CHK1 activation in HPV-positive cells, and knockdown blocks amplification. Furthermore, TopBP1 activation is shown to be regulated at the level of transcription initiation by the innate immune regulator STAT-5, which is activated by HPV proteins. STAT-5 has also been shown to be a regulator of the ATM response, demonstrating that these two pathways are coordinately regulated in HPV-positive cells. These findings identify a novel link between the innate immune response and activation of the ATR DNA damage response in regulating the life cycle of high-risk HPVs.IMPORTANCEHigh-risk human papillomaviruses (HPVs) are the causative agents of cervical and other anogenital cancers, as well as many oral cancers. HPVs infect epithelial cells and restrict productive viral replication or amplification and virion production to differentiated cells. Our studies demonstrate that HPVs activate the ATR single-strand DNA repair pathway and this activation is necessary for HPV genome amplification. The innate immune regulator STAT-5 is shown to regulate transcription of the ATR binding factor TopBP1, and this is critical for the induction of the ATR pathway. Our study identifies important links between innate immune signaling, the ATR DNA damage pathway, and productive HPV replication that may lead to the characterization of new targets for the development of therapeutics to treat HPV-induced infections.


2019 ◽  
Vol 16 (3) ◽  
pp. 545-553
Author(s):  
Sawsan Hassan Mahassni

Saudi Arabia has one of the highest adult overweight and obesity rates, especially in females, leading to increased mortality, morbidity, infections, and risk for many diseases. This study determined the counts and percents of lymphocyte subtypes (CD3, CD4, CD8, and CD16 +CD56 cells) and serum IgG, IgA, and IgM concentrations in blood samples collected from sixty-four Saudi female university employees with an age range of 24-52 years. There is only one other study on the counts/numbers of lymphocyte subtypes in overweight and obese Saudi females. Anthropometric measurements were used to categorize the subjects into groups according to the body mass index (BMI), waist-to-hip ratio (WHR), and waist circumference (WC). Results were all compared to the controls. Antibody concentrations were not significantly different. The CD3and CD4 counts were significantly higher for the obese BMI group and the overweight and obese BMI, respectively. The high-risk WHR group had a significantly lower CD 3% and a significantly higher CD16 + CD56 count. The high-risk WC group had significantly higher CD3 and CD4 counts and a significantly lower CD16 + CD56%. Thus, obesity leads to changes in the cellular adaptive and innate immune systems, while not affecting the humoral adaptive immune system.


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