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The Human Immune System Seen from a Biomedical Engineering Viewpoint
Published in Robert B. Northrop, Endogenous and Exogenous Regulation and Control of Physiological Systems, 2020
Let us go back and examine the role and importance of the chemokine receptor cofactors for HIV binding and entry. Macrophages carry several chemokine receptors, some of which have affinity for part of the HIV’s gp120 molecule. The macrophage CCR5 chemokine receptor normally binds with RANTES (which stands for regulated on activation, normal T-cell expressed and secreted, the ultimate acronym). Macrophage CCR5 also binds with an HIV1 gp120 site. Helper T-cells carry a chemokine receptor called CXCR4 which normally binds to stromal cell-derived factor 1 (SDF-1). The CXCR4 receptor also has an affinity to HIVl’s gp120. An HIV virion is called M-tropic or T-tropic depending on whether the v3 loop of gp120 has an affinity for macrophage CCR5 or T-cell CXCR4, respectively. What controls this tropism switch is not known.
Machine Learning Approach to Overcome the Challenges in Theranostics
Published in Shampa Sen, Leonid Datta, Sayak Mitra, Machine Learning and IoT, 2018
Bishwambhar Mishra, Sayak Mitra, Karthikeya Srinivasa Varma Gottimukkala, Shampa Sen
CXCR4 is a member of the chemokine receptor subfamily of seven transmembrane domain, G-protein coupled receptors, whose sole known natural ligand is CXCL12/SDF-1. CXCR4 is an unusual chemokine receptor by virtue of having expanded roles beyond leukocyte recruitment, including fundamental processes such as the development of the hematopoietic, cardiovascular, and nervous systems during embryogenesis. The receptor was first discovered as one of the coreceptors for HIV, and thereafter was also found to be expressed by multiple cancers including breast, prostate, lung, colon, and multiple myeloma.
Static electric field exposure decreases white blood cell count in peripheral blood through activating hypothalamic–pituitary–adrenal axis
Published in International Journal of Environmental Health Research, 2022
Jiahong Wu, Li Dong, Junli Xiang, Guoqing Di
Following the activation of HPA axis, the increased CORT in peripheral blood diffuses into cells and binds to the glucocorticoid receptor (GR), resulting in the rise of concentration of intracellular CORT-GR complex (Bekhbat et al. 2017). The CORT-GR complex then translocates from cytoplasm to nucleus and binds to glucocorticoid response elements in the target gene’s promoter, which can promote the expression of target gene such as C-X-C motif chemokine receptor 4 (CXCR4) (Shimba and Ikuta 2020). The interaction between CXCR4 and its specific ligand CXCL12 plays a pivotal role in guiding cells into specific locations in vivo (Cesare et al. 2007). Previous studies demonstrated that the CORT-GR complex could significantly upregulate the expression of CXCR4 gene in lymphocytes (Besedovsky et al. 2014; Cain et al. 2020), which could induce lymphocytes to migrate from peripheral blood to the tissues with high CXCL12 levels (e.g. bone marrow, spleen and lung) (Engler et al. 2004). On the basis of the analysis above, it is concluded that one critical reason for the decrease of total WBC count and lymphocyte count in this study is that HPA axis is activated after the SEF exposure of 7d and 14d. CORT, the end-product of HPA axis, induces lymphocytes to migrate out of peripheral blood by upregulating CXCR4 gene expression. To more clearly present the process in which the SEF exposure of 7d and 14d induces the migration of lymphocytes, the discussion above is visually summarized in Figure 4(a).
Dendrimer as a promising nanocarrier for the delivery of doxorubicin as an anticancer therapeutics
Published in Journal of Biomaterials Science, Polymer Edition, 2021
Vanshikha Singh, Prashant Kesharwani
Breast cancer is undoubtedly one of the very commonly diagnosed cancer in women, in which cells in different region of breast starts uncontrolled differentiation. This invasive cancer is characterized by additional property of metastasis in which the malignant cancer cells advances toward other regions of body including liver, bones, brain, lungs, lymph nodes, etc. C-X-C chemokine receptor type 4 (CXCR4) along with its ligand CXCL12 plays vital role in the process of metastasis of different types of cancer. The high level of CXCL12 in these organs serves as chemoattractant to drive CXCR4 positive primary tumor cell toward secondary metastatic sites. CXCR4 are highly expressed only in cancerous tissue and the normal cells usually stay devoid of them, this characteristic of CXCR4 can be used to deliver anticancer drug targeted at the tumor site [107].
Peptide-enabled receptor-binding-quantum dots for enhanced detection and migration inhibition of cancer cells
Published in Journal of Biomaterials Science, Polymer Edition, 2020
Ruijuan Zu, Xiaocui Fang, Yuchen Lin, Shilin Xu, Jie Meng, Haiyan Xu, Yanlian Yang, Chen Wang
Dedicated efforts have been reported on studying chemokine receptor CXCR4 as a potential therapeutic target for cancer diagnosis and treatment [10]. One small molecule antagonist named as plerixafor (also termed as AMD3100) has been approved by the U.S. Food and Drug Administration (FDA) for non-Hodgkin’s lymphoma and multiple myeloma treatment [11,12]. Several other CXCR4 antagonist candidates are currently being evaluated in various stages of clinical development. In our previous study, we selected a series of potential peptide antagonists with designated sequences in our original experiments according to the extracellular domain of CXCR4. The binding strengths between peptide antagonists and CXCR4 were examined using flow cytometry, surface plasmon resonance (SPR), and confocal microscopy methods. Our results demonstrated that, peptide E5 (GGRSFFLLRRIQGCRFRNTVDD) shows high binding affinity and selectivity towards CXCR4-overexpressed cancer cells [13]. E5 was observed to inhibit the migration and adhesion of cancer cells, and increase the sensitivity of cancer cells to chemotherapeutic agents by antagonizing CXCR4/CXCL12 chemokine axis [13–15].