Chronic obstructive pulmonary disease is a common respiratory disease characterized by persistent respiratory symptoms with incompletely reversible airflow limitation. Currently available treatments include oral or inhaled bronchodilators, oxygen therapy and surgery. However, these treatments are not effective enough in most cases, so it is clinically important to explore the mechanism of action and therapeutic strategies of chronic obstructive pulmonary disease in depth. The phosphatidylinositol 3-kinase/protein kinase B signaling pathway can play an important role in the occurrence and development of chronic obstructive pulmonary disease by regulating the release of inflammatory mediators and oxidative stress. Traditional Chinese medicine is characterized by holistic and comprehensive treatment of diseases, and has achieved good results in the prevention and treatment of chronic obstructive pulmonary disease in recent years. Traditional Chinese medicine monomers, active ingredients and their combinations can directly or indirectly regulate the phosphatidylinositol 3-kinase/protein kinase B signaling pathway by inhibiting the inflammatory response of the airway and alleviating oxidative stress, and play a protective role against chronic obstructive pulmonary disease with their multi-targeting, multi-component, and multi-pathway biologic advantages. Analyzing the research progress of traditional Chinese medicine at home and abroad in recent years, this article reviews the preventive role and mechanism of traditional Chinese medicine in regulating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway in chronic obstructive pulmonary disease, and provides further theoretical basis for the study of the mechanism of clinical prevention and treatment of chronic obstructive pulmonary disease by traditional Chinese medicine.
Objectives: To investigate the anti‐inflammatory and anti‐oxidative effects of anthocyanins from cherries on Freund's adjuvant‐induced arthritis (AIA) in rats.
The interaction of SIRPα with CD47 represents a major mechanism for preventing macrophage phagocytosis. However, CD47-independent mechanisms are poorly defined. Here, we report a critical role of SLAM family receptors (SFRs), ubiquitously expressed on hematopoietic cells and forming homotypic interactions, in constraining macrophage phagocytosis. We found that SFR deficiency triggered macrophage phagocytosis of hematopoietic cells, leading to severe rejection of donor hematopoietic graft in recipient mice. Specific SFR members, mainly SLAMF3 and SLAMF4, were identified as "don't eat me" receptors on macrophages. These receptors inhibited "eat me" signals, such as LRP1-mediated activation of mTOR and Syk, through SH2 domain-containing phosphatases. SFRs combined with, but were independent of, CD47 to mitigate macrophage phagocytosis, and the combined deletion of SFRs and CD47 resulted in hematopoietic cytopenia in mice. This SFR-mediated tolerance was compromised in patients with hemophagocytic lymphohistiocytosis, a syndrome characterized by inappropriate phagocytosis toward hematopoietic cells. Loss of SFRs potently elicited macrophage rejection of hematopoietic tumors. Deletion of SFRs also significantly enhanced the phagocytosis of CD19-positive hematopoietic targets by the macrophages expressing the chimeric CD19 antigen receptor. Therefore, SFR-mediated inhibition of macrophage phagocytosis is critical to hematopoietic homeostasis, and SFRs may represent previously unknown targets for tumor immunotherapy.
Granuloma faciale (GF) is a rare chronic inflammatory dermatosis in clinical practice. The etiology is not yet clear, and it often occurs on the face. The progression of skin lesions is slow and persistent, with almost no self regression and a risk of recurrence, which may lead to disfigurement. We reported a 61-year-old male with GF who had poor reaction with topical corticosteroids and calcineurin inhibitors, but the lesions were significantly improved after systematic application of minocycline. This report describes the good clinical effect of minocycline on GF.
The serine/threonine/tyrosine kinase 1 (STYK1) is a receptor protein-tyrosine kinase (RPTK)-like molecule that is detected in several human organs. STYK1 plays an important role in promoting tumorigenesis and metastasis in various cancers. By analyzing the expression of RTKs in immune cells in the database of 2013 Immunological Genome Project, we found that STYK1 was principally expressed in NK cells. In order to investigate the function of STYK1, we used CRISPR/Cas9 technology to generate STYK1-deleted mice, we found STYK1 deletion mice have normal number, development, and function of NK cells in spleen and bone marrow in tumor-free resting state. To examine the tumor surveillance of STYK1 in vivo, we utilized a variety of tumor models, including NK cell-specific target cell (ß2M and RMA-S) clearance experiments in vivo, subcutaneous and intravenous injection of B16F10 melanoma model, and the spontaneous breast cancer model MMTV-PyMT. Surprisingly, we discovered that deletion of the oncogenic STYK1 promoted the four-model tumor progression, and we observed a reduction of NK cell accumulation in the tumor tissues of STYK1 deletion mice compared to WT mice. In order to study the mechanism of STYK1 in NK, RNA sequence of STYK1−/− and WT NK have unveiled a disparity in the signaling pathways linked to migration and adhesion in STYK1−/− NK cells. Further analysis of chemokine receptors associated with NK cell migration revealed that STYK1-deficient NK cells exhibited a significant reduction in CCR2 expression. The STYK1 expression was negatively associated with tumor progression in glioma patients. Overall, our study found the expression of STYK1 in NK cell mediates NK cell anti-tumor response through regulating CCR2 and infiltrating into tumor tissue.
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