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The Role of the Macrophage in Immunity
Published in Richard C. Niemtzow, Transmembrane Potentials and Characteristics of Immune and Tumor Cell, 2020
Only a small percentage of macrophages are I-region-positive cells capable of presenting antigen to lymphocytes.128 In fact, some antigen presenting cells are not true macrophages at all. A cell commonly found accompanying macrophages is the adherent but nonphagocytic dendritic cell. Although this cell represents a minor portion of adherent cells, it has a high concentration of I-region antigens,129 and some investigators have suggested that the dendritic cell is the principal cell responsible for antigen presentation to lymphocytes. Dendritic cells are described as nonphagocytic, adherent, bone-marrow-derived cells which are mobile, have stellate morphology with little membrane ruffling, and have plentiful mitochondria but are lacking in vacuoles and lysosomes.130 This cell is a potent stimulator of the mixed lymphocyte reaction and might play a role in graft rejection.131 The dendritic cell has the ability to act as an accessory cell for lymphocyte activation, and eventually it will be clear as to how much of that responsibility it carries.
Toward More Selective Therapies to Block Autoimmunity
Published in George S. Eisenbarth, Immunotherapy of Diabetes and Selected Autoimmune Diseases, 2019
Terry B. Strom, Vicki E. Kelley
Therefore, accessory cell activation is required for support of full T cell activation. Direct cell to cell contact between antigen-activated T cells and macrophages, or stimulation of macrophages by soluble T cell products, causes macrophage activation resulting in signal transduction, probably via formation of intracellular second messengers. These as yet unidentified second messengers, in turn, activate the tumor necrosis factor (TNF) and IL-1 genes. Transcription of IL-1 encoding mRNA proceeds, and translation of large alpha and beta pro IL-1 molecules occurs.36 Precursor IL-1 molecules are cleaved intracellularly, and the considerably smaller mature forms of IL-1 are secreted. Powerfully T cell stimulatory membrane bound forms of IL-1 also exist. TNF is also translated as a propeptide with a 76 amino acid appendage at the N-terminus of the human peptide.37 Both of these monokines may be directly involved in islet cell destruction. IL-1 and TNF are pleiotropic molecules with overlapping function. Both are directly cytotoxic to some cell types. IL-1 has been demonstrated to directly destroy islet cells.38 TNF potentiates these islet cell cytodestructive effects.39
Tissue Distribution And Cellular Expression Of Ia Antigens
Published in Soldano Ferrone, Chella S. David, Ia Antigens, 2019
There is currently some controversy concerning the relative contributions of dendritic cells and classical macrophages to antigen presentation and accessory cell function for proliferative responses.53-61 All groups agree that the cells involved in antigen presentation and accessory cell function express Ia Antigens. Whether the dendritic and mac-rophage interconvert, represent common descendents of a single precursor, or represent lineally distinct cell populations is not certain. A detailed discourse on the similarities and differences between these two populations is beyond the scope of this review.
Expanded NK cells from umbilical cord blood and adult peripheral blood combined with daratumumab are effective against tumor cells from multiple myeloma patients
Published in OncoImmunology, 2021
Chantal Reina-Ortiz, Michael Constantinides, Alexis Fayd-Herbe-de-Maudave, Jessy Présumey, Javier Hernandez, Guillaume Cartron, David Giraldos, Rosana Díez, Isabel Izquierdo, Gemma Azaceta, Luis Palomera, Isabel Marzo, Javier Naval, Alberto Anel, Martín Villalba
NK cells were expanded using two different protocols. UCB NK cells, due to their need for both KIR and KAR signals to reach a mature phenotype, were cultured with PLH, an EBV-transformed HLA-I+ B lymphoblastoid cell line which works as an accessory cell with both required signals.7 Conversely, PB NKs are fully mature and need only activating signals thus the EBV+ HLA-I negative cell line 721.221 was employed.43 As a first step, T cells and NKT cells were depleted from the cultures using anti-CD3 mAb, to favor NK cell expansion (see Figure 1(a), d 0). Each protocol required different ratios of accessory cells, while IL-2 and IL-15 were added at the same concentrations. UCB NKs were treated with accessory cells and cytokines every 3 d and benefited from little manipulation. PB NKs were sustained for 5–6 d before culture renewal and withstood daily manipulation seen in Figure 1. By d 20, almost all cells from both sources present in the culture were CD56+CD3− NK cells (see Figure 1(a,b)). The purity of NK cells was 94.28 ± 2.08% for UCB and 95.8 ± 1.46% as an average (see Suppl. Figure 1 and Suppl. Table I). The CD3+ fraction, which was successfully depleted at d 0, did not overtake the CD56+ population, allowing for successful expansion of NK cells (Figure 1(a,b)). Beginning with 1E6 NKs in each expansion, PB NKs reached an average of 240E6 cells by d 20 and UCB NKs averaged a 700-fold expansion (Suppl. Fig 2).
Ex vivo Stimulation of Lymphocytes with IL-10 Mimics Sepsis-Induced Intrinsic T-Cell Alterations
Published in Immunological Investigations, 2018
Fanny Poujol, Guillaume Monneret, Emmanuelle Gallet-Gorius, Alexandre Pachot, Julien Textoris, Fabienne Venet
It should be noted that our results do not exclude an indirect role of IL-10 on T cells, for example, through the alteration of the monocyte accessory cell function. Indeed, indirect mechanisms involved in the induction of a sepsis-like decrease in T-cell proliferative response through impairment of monocyte functionality have been described in previous works by Wolk et al. (2000) and our team (Poujol et al., 2015). Hence, IL-10 priming of PBMCs may recapitulate, ex vivo, both direct and indirect mechanisms involved in the sepsis-induced decrease in T-cell proliferative response.