Monocyte Chemotactic Disorder

Last update 08 May 2025

Basic Info

Synonyms

MONOCYTE CHEMOTACTIC DISORDER, Monocyte Chemotactic Disorder, 单核细胞趋化性疾病

Introduction-

Clinical Trials associated with Monocyte Chemotactic Disorder

NCT01161745

/ CompletedNot ApplicableIIT

PD-1/PD-L1 Pathway in T Lymphocyte Apoptosis and Monocyte Dysfunction in Septic Patients

The investigators want to identify that whether PD-1/PD-L1 pathway will change in human sepsis, and whether PD-1/PD-L1 pathway play an important role in sepsis induced immunosuppression.

Start Date01 Dec 2008

Sponsor / Collaborator

Changhai Hospital of Shanghai

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100 Clinical Results associated with Monocyte Chemotactic Disorder

100 Translational Medicine associated with Monocyte Chemotactic Disorder

0 Patents (Medical) associated with Monocyte Chemotactic Disorder

113

Literatures (Medical) associated with Monocyte Chemotactic Disorder

21 Jan 2025·Proceedings of the National Academy of Sciences

CFTR dictates monocyte adhesion by facilitating integrin clustering but not activation

Article

Author: Zhou, Beiyan ; Vella, Anthony T. ; Younis, Doulathunnisa Ahamed ; Cao, Ziming ; Bruscia, Emanuela M. ; Fan, Zhichao ; Liu, Wei ; Gan, Wenqi ; Pulikkot, Sunitha ; Marosvari, Mason ; Chen, Yunfeng ; McArdle, Sara ; Hu, Liang ; Yu, Ji

Monocytes are critical in controlling tissue infections and inflammation. Monocyte dysfunction contributes to the inflammatory pathogenesis of cystic fibrosis (CF) caused by CF transmembrane conductance regulator (CFTR) mutations, making CF a clinically relevant disease model for studying the contribution of monocytes to inflammation. Although CF monocytes exhibited adhesion defects, the precise mechanism is unclear. Herein, superresolution microscopy showed that an integrin clustering but not an integrin activation defect determines the adhesion defect in CFTR-deficient monocytes, challenging the existing paradigm emphasizing an integrin activation defect in CF patient monocytes. We further found that the clustering defect is accompanied by defects in CORO1A membrane recruitment, actin cortex formation, and CORO1A engagement with integrins. Complementing canonical studies of leukocyte adhesion focusing on integrin activation, we highlight the importance of integrin clustering in cell adhesion and report that integrin clustering and activation are distinctly regulated, warranting further investigation for selective targeting in therapeutic strategy design involving leukocyte-dependent inflammation.

01 Jan 2025·Journal of Hepatology

Circulating monocytes upregulate CD52 and sustain innate immune function in cirrhosis unless acute decompensation emerges

Article

Author: Cheng, Hung-Wei ; Matter, Matthias S ; McPhail, Mark J W ; Soysal, Savas ; Weston, Chris J ; Brenig, Robert G ; Lütge, Mechthild ; Bernsmeier, Christine ; Wendon, Julia ; Meier, Marie-Anne ; Semela, David ; Pop, Oltin T ; Lussier, Paul O G ; Ludewig, Burkhard ; Künzler-Heule, Patrizia ; Heim, Markus ; Roux, Julien ; Flint, Emilio E ; Geng, Anne

BACKGROUND & AIMSThe susceptibility of patients with cirrhosis to infection, a major determinant of prognosis, relates to the development of immuneparesis, a complex interplay of different immunosuppressive cells and soluble factors. The mechanisms underlying the dynamics of immuneparesis of innate immunity remain unclear. We aimed to dissect the heterogeneity of circulating monocyte states in different stages of cirrhosis, and to determine the function of selected differentially expressed genes.METHODSWe systematically investigated circulating monocytes in health and compensated/non-acutely decompensated cirrhosis using single-cell RNA sequencing. Selective genes were confirmed by flow cytometry and diverse functional assays on monocytes ex vivo.RESULTSWe partitioned monocytes into seven clusters. Their abundances varied between cirrhosis stages, confirming previously reported changes, i.e. the reduction in CD14^lowCD16⁺⁺ and emergence of monocytic myeloid-derived suppressor cells in advanced stages. Differentially expressed genes between health and disease and among stages were detected, including CD52 for the first time. CD52 expression on monocytes significantly increased through compensated and non-acutely decompensated cirrhosis. In patients with cirrhosis, CD52^highCD14⁺CD16^highHLA-DR^high monocytes had a functional phenotype of active phagocytes, with enhanced migratory potential and increased cytokine production capacity but limited ability to activate T cells. Following acute decompensation, CD52 was cleaved by elevated PLC, and soluble CD52 was detected in the circulation. Inhibition and cleavage of CD52 significantly suppressed monocyte functions ex vivo and in vitro, while the predominance of immunosuppressive CD52^low circulating monocytes in patients with acute decompensation was associated with infection and low transplant-free survival.CONCLUSIONCD52 may represent a biologically relevant target for future immunotherapy. Stabilising CD52 may enhance monocyte functions and infection control in the context of cirrhosis, guided by soluble CD52/PLC as biomarkers of immuneparesis.IMPACT AND IMPLICATIONSMonocyte dysfunction substantially contributes to infection susceptibility, which is a major determinant of the prognosis of patients with cirrhosis and represents a major unmet therapeutic need. Its underlying mechanisms remain poorly understood, although, among hepatologists, it is thought that the therapeutic reconstitution of monocyte function could enhance defence against infection and thus reduce morbidity and mortality of patients with cirrhosis. By systematically delineating the heterogeneity and function of circulating monocytes ex vivo, we identified that the absence of CD52 expression on monocytes represented a distinct biomarker of monocyte dysfunction in patients with cirrhosis, discriminating patients at substantial risk of infectious complications. Otherwise, given the beneficial antimicrobial functions of CD52-expressing monocytes, CD52 stablisation may also represent a therapeutic approach worth exploring.

01 Dec 2024·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Multiple myeloma exosomal miRNAs suppress cGAS-STING antiviral immunity

Article

Author: Wang, Liwen ; Li, Xin ; Xie, Linzhi ; Cheng, Qian ; Chen, Xin ; Yan, Yuhan ; Tang, Yishu ; Deng, Zuqun

DNA virus infection is a significant cause of morbidity and mortality in patients with multiple myeloma (MM). Monocyte dysfunction in MM patients plays a central role in infectious complications, but the precise molecular mechanism underlying the reduced resistance of monocytes to viruses in MM patients remains to be elucidated. Here, we found that MM cells were able to transfer microRNAs (miRNAs) to host monocytes/macrophages via MM cell-derived exosomes, resulting in the inhibition of innate antiviral immune responses. The screening of miRNAs enriched in exosomes derived from the bone marrow (BM) of MM patients revealed five miRNAs that negatively regulate the cGAS-STING antiviral immune response. Notably, silencing these miRNAs with antagomiRs in MM-bearing C57BL/KaLwRijHsd mice markedly reduced viral replication. These findings identify a novel mechanism whereby MM cells possess the capacity to inhibit the innate immune response of the host, thereby rendering patients susceptible to viral infection. Consequently, targeting the aberrant expression patterns of characteristic miRNAs in MM patients is a promising avenue for therapeutic intervention. Considering the miRNA score and relevant clinical factors, we formulated a practical and efficient model for the optimal assessment of susceptibility to DNA viral infection in patients with MM.

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Monocyte Chemotactic Disorder

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