China
Africa
Explore chapters and articles related to this topic
Innate Immune System in Cardiovascular Diseases
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Benjamin J. Kopecky, Kory J. Lavine
Monocytes are produced in the bone marrow from hematopoietic precursors, most proximally from the common myeloid progenitor [10]. In mice, monocytes can be distinguished on the basis of their expression of Ly6C. Classical monocytes are identified as Ly6chigh CCR2+ CX3CR1low CD62Lhigh cells [10], while non-classical monocytes are defined as Ly6clow CCR2− CX3CR1high CD62Llow cells [11, 12]. Classical (Ly6Chigh) monocytes can differentiate into macrophages or non-classical monocytes via Nr4a1 [13, 14]. In humans, classical monocytes are identified as CD14+CD16− cells, and nonclassical monocytes are defined as CD16+CD14dim cells [15]. Humans also contain intermediate monocytes (CD14+CD16+) that harbor functional and phenotypic characteristics of both classical and non-classical monocyte populations. In steady state, mouse monocytes have a life span of 1–2 days, whereas human classical monocytes live for about 3 days [16].
Inflammation and Infection
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Judith Hall, Christopher K. Harding
Newly recruited Ly6C+ macrophages produce TNF.TNF stimulates resident macrophages to secrete CXCL2.CXCL2 induces circulatory neutrophils to produce metalloproteinases, which allows them to penetrate basement membranes and move transepithelially.
Role of dendritic cells in integrating immune responses to luminal antigens
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Brian L. Kelsall, Maria Rescigno
Myeloid populations are now more clearly defined on the basis of ontogeny (Figure 12.2). According to this scheme, the three primary circulating myeloid precursors, monocytes, pre-cDCs, and pDCs, differentiate from hematopoietic stem cells in the bone marrow. In mice, monocytes can be further distinguished by their expression of Ly6C. In the steady state, circulating Ly6Chi monocytes give rise to CD11c+ and CD11c− mature intestinal macrophages in a process in which expression of Ly6C is lost and expression of MHC II, CX3CR1, F4/80, and CD64 is increased. A population of resident self-renewing macrophages that are not dependent on blood precursors also has been identified that expresses CD4 and Tim-4 (see later and Chapter 13).
Spotlight on liver macrophages for halting liver disease progression and injury
Published in Expert Opinion on Therapeutic Targets, 2022
Amit Khurana, Umashanker Navik, Prince Allawadhi, Poonam Yadav, Ralf Weiskirchen
Differential expression of certain cell surface markers helps identify KCs and MoMFs. CD11blow, F4/80hi, C-type lectin domain family 4 member F, CD68+, and CX3C chemokine receptor 1 are considered to be the characteristics of KCs [27]. Further, mouse MoMFs express CD11b+, F4/80+, Ly6C+, and macrophage colony-stimulating factor 1 receptor (CSF1R)+. In contrast to mice, KCs of humans are not as well-characterized and normally identified as CD68+ cells whereas MoMFs are normally identified as CD14+, CC-chemokine receptor 2 cells [27–29]. Furthermore, apart from M1 and M2 macrophages, distinct Ly6c expression has been widely utilized to describe the populations of circulating monocytes and macrophages in disease. Ly6c is a cell surface glycoprotein which is used to differentiate several populations of circulating monocytes such as Ly6c+ and Ly6c−and evidence suggests that recruited Ly6chigh monocytes are the source of the Ly6chigh and Ly6clow macrophage subsets [30]. Ly6chigh macrophages are assumed to be pro-inflammatory and mimic the M1 macrophage phenotype whereas Ly6clow macrophages acquire a M2-like phenotype, which can play an anti-inflammatory function during liver injury [31].
Neutrophils, as “Trojan horses”, participate in the delivery of therapeutical PLGA nanoparticles into a tumor based on the chemotactic effect
Published in Drug Delivery, 2020
Jifu Hao, Junlan Chen, Meixiang Wang, Jing Zhao, Jianze Wang, Xingrong Wang, Yuhong Li, Hua Tang
Then, blood leukocytes were incubated with a 2 μg/mL anti-Fcγ RIII/II receptor mAb (2.4 G2) (eBioscience) to block the Fcγ RIII/II receptors at 4 °C. After being washed with PBS, the cells were incubated for 15 min in PBS with cell-surface antibodies, then washed with PBS again and incubated for 15 min in PBS with Live cell/Dead cell Discrimination. Subsequently, the stained cells were analyzed on an LSRII (BD Biosciences), and the flow cytometry data was performed with Flow Jo software (Tree Star Inc.). The following antibodies were used in the experiments and purchased from eBioscience: anti-Ly6C (clone HK1.4), anti-Ly6G (clone 1A8).
B cell lymphoma progression promotes the accumulation of circulating Ly6Clo monocytes with immunosuppressive activity
Published in OncoImmunology, 2018
Sara J. McKee, Zewen K. Tuong, Takumi Kobayashi, Brianna L. Doff, Megan SF Soon, Michael Nissen, Pui Yeng Lam, Colm Keane, Frank Vari, Davide Moi, Roberta Mazzieri, Graham Leggatt, Maher K. Gandhi, Stephen R. Mattarollo
The accumulation of Ly6Clo monocytes in circulation may be a consequence of increased Ly6Chi to Ly6Clo conversion, preferential expansion/survival of the Ly6Clo subset, or altered migration of monocyte subsets and differentiation into macrophages. Monocyte adoptive transfer experiments revealed that in tumor-bearing hosts the recovery of transferred Ly6Clo monocytes from blood was higher than for Ly6Chi cells, whereas in healthy hosts the recovery of subsets was equivalent. This implies that the tumor microenvironment preferentially supports the survival of Ly6Clo cells, or alternatively promotes migration of Ly6Chi cells out of circulation. Furthermore, the majority of recovered monocytes (>80%) in tumor-bearing hosts were of the Ly6Clo phenotype, regardless of their phenotype upon transfer. Conversely, in healthy mice, the initial Ly6C expression phenotype was maintained upon recovery. This strongly suggests that signals from the tumor environment leads to increased conversion of Ly6Chi to Ly6Clo monocytes. Recently it has been shown that signals from endothelial cells convert Ly6Chi to Ly6Clo monocytes, in a Notch ligand-dependent manner.42 Previous reports have described pro-angiogenic behavior in aggressive B cell lymphoma which is associated with a poor clinical outcome.43,44 Further studies are required to determine whether dysregulated angiogenesis and an increase in endothelial cells in Eµ-myc lymphoma promotes conversion of mobilized Ly6Chi monocytes to long-lived Ly6Clo monocytes. Identifying whether circulating immunosuppressive monocytes in B cell lymphoma hosts are precursors cells or a reservoir for equivalent populations in the malignant lymphoid tissues, will allow us to potentially target these cells with systemic treatment.