log
     Login   |   Register   
img
 
 
Cell size dependent migration of T-cells latently infected with HIV
Kathrin Bohn-Wippert and Roy D. Dar
Editorial: Vaccine Hesitancy
Michelle A. Linterman
Combining immune checkpoint blockade with ErbB targeted therapies for cancer treatment
Zhida Liu, Chuanhui Han, Yang-Xin Fu
The Emerging Role of Mitophagy in Kidney Diseases
Divya Bhatia, Mary E. Choi
Regulation and New Treatment Strategies in Breast Cancer
Rosa-Maria Ferraiuolo, Kay-Uwe Wagner
Epigenetic Regulation of Cardiac Development and Disease through DNA Methylation
Yahui Lan and Todd Evans
Kinases: The "Indispensables"of the DNA Damage Response Cascade
Vijay Menon and M. Michael Dcona
Metabolic adaptations to glutamine deprivation in pancreatic cancer
Ying Yang, Mari B. Ishak Gabra, and Mei Kong
JoLS, Journal of Life Sciences, a Postdoc Community Initiative
Nimrat Chatterjee, and Theo van den Broek
Road to HIV cure; from Berlin to London and beyond
Theo van den Broek
12

Author(s)
Kathrin Bohn-Wippert and Roy D. Dar

Institute
University of Illinois at Urbana-Champaign
Address

1406 West GreenStreet, Urbana, IL 61801, USA, 1206W Gregory Drive,Urbana, Illinois 61801, USA.

Abstract:

Human immunodeficiency virus (HIV) preferentially infects T-lymphocytes by integrating into host DNA and forming a latent transcriptionally silent provirus.  As previously shown, HIV-1 alters migration modes of T-lymphocytes by co-regulating viral gene expression with human C-X-C chemokine receptor-4 (CXCR4). Here, we show that motility of infected T-lymphocytes is cell size dependent. In cell migration assays, migrating cells are consistently larger than non-migrating cells. This effect is drug-treatment independent. The cell size dependent motility observed in a previously generated Jurkat latency model correlates with the motility of primary human CD4+ T-cells containing a modified HIV-1 full-length construct JLatd2GFP. In addition, large migrating T-cells, latently infected with HIV, show a slightly decreased rate of reactivation from latency. these results demonstrate that HIV reactivation is cell migration-dependent, where host cell size acts as a catalyst for altered migration velocity. We believe that host cell size controlled migration uncovers an additional mechanism of cellular controlled viral fate determination important for virus dissemination and reactivation from latency. This observation may provide more insights into viral-host interactions regulating cell migration and reactivation from latency and helps in the design and implementation of novel therapeutic strategies.


Author(s)
Michelle A. Linterman

Institute
Babraham Institute
Address

Laboratory of Lymphocyte Signalling andDevelopment, Babraham Institute, Cambridge, UK.


Abstract:

Vaccination has been one of the most successful medical interventions to date, reducing the morbidity and mortality of vaccine-preventable infectious disease by over 90% in countries where vaccines are readily available. Despite its success, the uptake of vaccines worldwide is declining; so much so that in 2019 the World Health Organisation declared that vaccine hesitancy, the reluctance or refusal to vaccinate despite the availability of vaccines, is one of the top ten threats to Global Health in 2019. The reasons for decreased vaccination uptake are complex, but it is becoming increasingly clear that solutions to counter this trend are required as vaccine-preventable illness and death are increasing worldwide.


Author(s)
Zhida Liu, Chuanhui Han, Yang-Xin Fu

Institute
UT Southwestern Medical Center, Dallas, TX 75235, USA.
Address

Departments of Pathology and Immunology, UT Southwestern Medical Center, Dallas, TX 75235, USA.


Abstract:

Aberrant EGFR family signaling pathways are well known as oncogenic drivers and account for several types of cancer with their functions in abnormally promoting cell proliferation and preventing cell apoptosis. Accumulating evidence has indicated that EGFR family signaling could facilitate tumor cells to escape from immunological surveillance by reducing tumor mutation burden and inducing immunosuppressive tumor microenvironment. Therefore, ErbB driven cancers are sensitive to ErbB targeted therapies and resistant to immune checkpoint blockade (ICB). Whether combining ErbB targeted therapies and ICB can actually benefit cancer patients is still controversial. Here, we review the correlation between EGFR family signaling and cancer, summarize the recent findings in the immune related mechanisms of ErbB targeted therapies and the potential reasons why ErbB driven cancers are resistant to ICB, and further discuss the potential strategies of combining ErbB targeted therapies and ICB.  


Author(s)
Divya Bhatia, Mary E. Choi

Institute
Weill Cornell Medicine
Address

Division of Nephrology and Hypertension, Joanand Sanford I. Weill Department of Medicine, NewYork-Presbyterian Hospital,Weill Cornell Medicine, New York, NY, USA.


Abstract:

Mitochondria fulfill the high metabolic energy demands of the kidney and are regularly exposed to oxidative stress causing mitochondrial damage. The selective removal of damaged and dysfunctional mitochondria through a process known as mitophagy is essential in maintaining cellular homeostasis and physiological function. Mitochondrial quality control by mitophagy is particularly crucial for an organ such as the kidney, which is rich in mitochondria. The role of mitophagy in the pathogenesis of kidney diseases has lately gained significant attention. In this review, we summarize the current understanding of the implications of mitophagy during pathological conditions of the kidney, including acute and chronic kidney diseases.


Author(s)
Rosa-Maria Ferraiuolo, Kay-Uwe Wagner

Institute
Wayne State University School of Medicine
Address

Karmanos Cancer Institute at WayneState University School of Medicine, Detroit, MI 48202.


Abstract:

Breast cancer classifications are based on the presence or absence of estrogen receptor and progesterone receptor along with the overexpression or amplification of the Her2 receptor. Although the overall 5-year survival rate of breast cancer patients has increased due to the use of targeted therapies, a subset of patients can acquire resistance over time or are unresponsive when presented in the clinic. Novel therapies focusing on molecular pathways and cell cycle regulation currently being used in the clinic may lead to increased response in this subset of patients.

 
 
     
 
 
top
 
btm

 
footer