scholarly journals The relationship between the frequency of the common cold and the activities of natural killer cells

2000 ◽  
Vol 4 (4) ◽  
pp. 212-216 ◽  
Author(s):  
Ming Xu ◽  
Takashi Muto ◽  
Tosio Yabe ◽  
Fumiko Nagao ◽  
Yasushi Fukuwatart ◽  
...  
Keyword(s):  
Natural Killer Cells ◽  
Natural Killer ◽  
Common Cold ◽  
Killer Cells ◽  
The Common ◽  
The Relationship

scholarly journals NKG2D functions as an activating receptor on natural killer cells in the common marmoset (Callithrix jacchus)

2014 ◽  
Vol 26 (11) ◽  
pp. 597-606 ◽  
Author(s):  
Masamichi Watanabe ◽  
Yohei Kudo ◽  
Mitsuko Kawano ◽  
Masafumi Nakayama ◽  
Kyohei Nakamura ◽  
...  
Keyword(s):  
Natural Killer Cells ◽  
Natural Killer ◽  
Common Marmoset ◽  
Callithrix Jacchus ◽  
Killer Cells ◽  
The Common ◽  
Activating Receptor

scholarly journals Impact of Zygosity in Bimodal Phenotype Distributions

2016 ◽  
Author(s):  
Thomas Holst-Hansen ◽  
Elena Abad ◽  
Aura Muntasell ◽  
Miguel López-Botet ◽  
Mogens H. Jensen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Expression Profile ◽  
Positive Feedback ◽  
Expression Profiles ◽  
Receptor Protein ◽  
Killer Cells ◽  
Regulatory Circuit ◽  
The Relationship

AbstractAllele number, or zygosity, is a clear determinant of gene expression in diploid cells. But the relationship between the number of copies of a gene and its expression can be hard to anticipate, especially when the gene in question is embedded in a regulatory circuit that contains feedbacks. Here we study this question making use of the natural genetic variability of human populations, which allows us to compare the expression profiles of a receptor protein in natural killer cells between donors infected with human cytomegalovirus (HCMV) with one or two copies of the allele. Crucially, the distribution of gene expression in many of the donors is bimodal, indicative of the presence of a positive feedback somewhere in the regulatory environment of the gene. Three separate gene-circuit models differing in the location of the positive feedback with respect to the gene can all reproduce well the homozygous data. However, when the resulting fitted models are applied to the hemizygous donors, only one model (the one with the positive feedback located at the level of gene transcription) reproduces the experimentally observed gene-expression profile. In that way, our work shows that zygosity can help us relate structure and function of gene regulatory networks.Author SummaryNearly all mammalian cells, including human cells, have two copies of each chromosome, and thus possess two potentially different copies of each gene (which might be in some cases non-functional or even absent). Naïively one might expect that two identical copies of the gene would lead to the protein being expressed at twice the rate, but many factors can alter this simple calculation. One of these factors is the existence of feedback mechanisms affecting in one way or another the regulatory circuit in which our gene of interest is embedded. Here we study the relationship between the number of gene copies and the expression of a receptor protein that plays a crucial role in the recognition of pathogens by natural killer cells, which are important elements of the innate immune system. Experimental data of virus-infected donors reveals a bimodal expression profile of this receptor, typical of a positive feedback, and a clear difference between donors with one or two copies of the gene. Mathematical modeling allows us to find the likely location of the feedback loop within the gene’s regulatory circuit, by requiring the correct model to reproduce the expression profiles of both types of donors.

scholarly journals Effect of Apatinib on Serum CD4+CD25+ T cells, NK Cells, and T Cells Subgroup in Malignant Tumor

2019 ◽  
Vol 18 ◽  
pp. 153303381989366
Author(s):  
Hui-Qin Luo ◽  
Yi-Fu He ◽  
Wen-Ju Chen ◽  
Ying Yan ◽  
Shu-Sheng Wu ◽  
...  
Keyword(s):  
T Cells ◽  
Prognostic Factors ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Progression Free Survival ◽  
Control Group ◽  
Killer Cells ◽  
Free Survival ◽  
Median Progression Free Survival ◽  
The Relationship

Objective: The immune makers including CD4+CD25+ T cells, natural killer cells, and T cells subgroup were retrospectively analyzed to find the relationship between apatinib and the immune system in the patients treated with apatinib. Method: Forty-two patients with advanced malignant tumors orally took apatinib as treatment and 16 patients with the same situation did not take apatinib as a control group. These patients were all included in the study, and they orally received apatinib 500 mg daily as monotherapy or combination. The treatment was continued until disease progression or intolerable toxicity. CD4+CD25+ T cells, natural killer cells, and T cells subgroup were detected before and 1 month after therapy for all the patients. The relationship between the changing number of immune cells and progression-free survival was analyzed in this study. Result: For the apatinib group, the rate of CD4+CD25+ T cells significantly increased ( P = .048). The median progression-free survival was 3.25 months for the 42 patients. The median progression-free survival in the patients with the rate of CD4+CD25+ T cells increased and decreased was 5.8 months and 2.9 months, respectively ( P = .012). Multivariate analysis found the increased rate of CD4+CD25+ T cells was an independent prognostic factor for a longer progression-free survival. The rate of natural killer cells and T cells subgroup did not change much after apatinib therapy, and they were not independent prognostic factors for progression-free survival. Conclusion: The rate of CD4+CD25+ T cells is very important in patients with apatinib treatment. The changing number of CD4+CD25+ T cells may be a good indicator for apatinib prognosis. Natural killer cells and T cells subgroup did not change much after apatinib, and they were not independent prognostic factors for progression-free survival.

Heterozygosity for the common perforin mutation, p.A91V, impairs the cytotoxicity of primary natural killer cells from healthy individuals

2015 ◽  
Vol 93 (6) ◽  
pp. 575-580 ◽  
Author(s):  
Imran G House ◽  
Kevin Thia ◽  
Amelia J Brennan ◽  
Richard Tothill ◽  
Alexander Dobrovic ◽  
...  
Keyword(s):  
Natural Killer Cells ◽  
Natural Killer ◽  
Healthy Individuals ◽  
Killer Cells ◽  
The Common
Sign in / Sign up

Export Citation Format

Share Document