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The Non-Hodgkin’s Lymphomas and Plasma Cell Dyscrasias
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Lynne V. Abruzzo, L. Jeffrey Medeiros
The T-cell and NK-cell subtypes of LGLL are distinguished by immunophenotypic studies. The major difference between these subtypes is that T-cell LGLL express the CD3 antigen and T-cell receptors (usually the α/β TCR, rarely the γ/δ TCR) on their surface. NK-cell LGLL lack CD3 and T-cell receptors. Both subtypes express T-cell antigens, such as CD2, and have a CD4-CD8+ immunophenotype. Natural killer cell-associated antigens, such as CD16 and CD57, may be expressed by both subtypes. NK-cell LGLL also may be CD56-positive. Both subtypes of LGLL are negative for TdT, the CD1 and CD25 antigens, Ig, and B-cell antigens.
Inflammation in Psoriasis and Psoriatic Arthritis
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
NK cells constitute 5%–8% of the cellular infiltrate in psoriasis, more so in the mid- and papillary dermis. Some recent studies have shown lower CD57 expression in NK cells in patients, suggesting skewing to an immature phenotype. Immature NK cells produce more cytokines (IFN-γ) and have a heightened response to IL-2 stimulation. They also exhibit a higher degranulation capacity and greater turnover, lending support to their possible active participation in the ongoing inflammation in psoriasis [12].
Abnormal Immunoregulation and the Tumor Dormant State in Human Cancer
Published in Thomas H. M. Stewart, E. Frederick Wheelock, Cellular Immune Mechanisms and Tumor Dormancy, 2017
Jules E. Harris, Donald P. Braun
Although the adherent cells used in these studies were greater than 95% positive for latex ingestion and macrophage morphology, the possibility that a minor contaminating cell population was downregulating the response to the macrophage activators was considered. Accordingly, adherent macrophage cultures were treated with antibodies against Τ cells (anti-CD3+) or NK cells (anti-CD56 and anti-CD57) + complement to remove any residual adherent lymphocytes that may have influenced the development of cytotoxicity in the tumor-associated macrophages. Our initial studies were conducted with AM from lung cancer patients (Table 3) . In those studies, we found that treatment of AM cultures with anti-CD3 antibodies + complement prior to the addition of IFN + LPS significantly augmented the development of cytotoxicity in these otherwise, poorly-cytotoxic macrophages. In contrast, treatment with anti-CD56 or anti-CD57 antibodies failed to do so. Initially, we interpreted this result to indicate that a CD3+ cell was inhibiting the development of cytotoxicity in AM from lung cancer patients. However, as shown in Table 3, control cultures revealed that complement was not needed for the augmentation of cytotoxicity by anti-CD3 monoclonal antibodies nor was stimlation with η-IFN. Thus, it appeared that the elimination of a CD3+ cell might not have been responsible for the augmentation of tumoricidal function seen in anti-CD3-treated macrophages, and additional studies were needed.
The prognostic role of NK cells and their ligands in squamous cell carcinoma of the head and neck: a systematic review and meta-analysis
Published in OncoImmunology, 2020
Sangeeta K. Bisheshar, Emma J. De Ruiter, Lot A. Devriese, Stefan M. Willems
NK cells are an essential component of the innate immune system as an early line of defense against tumor cells and act by killing them. They could, therefore, function as a prognostic biomarker in HNSCC. NK cell subpopulations can be defined based on CD56 expression on the surface of the cells, in which CD56bright cells express a relatively high density of CD56 and CD56dim cells express the relatively low density of CD56. Classically, NK cells are divided in CD56bright CD57− immune regulatory cells and CD56dim CD57+ cytotoxic cells.20 In most studies CD56 is the archetypal phenotypic marker of NK cells.21 Another marker, CD57, is a marker of differentiated and highly cytotoxic NK cells and is often used in studies, as it has been described as a phenotypically stable NK cell marker.22
NK cells in pancreatic cancer demonstrate impaired cytotoxicity and a regulatory IL-10 phenotype
Published in OncoImmunology, 2020
Francesca Marcon, Jianmin Zuo, Hayden Pearce, Samantha Nicol, Sandra Margielewska-Davies, Mustafa Farhat, Brinder Mahon, Gary Middleton, Rachel Brown, Keith J. Roberts, Paul Moss
We next went on to assess the expression of markers associated with NK cell differentiation and activation on peripheral NK cells. CD57 expression is expressed on late differentiated cells and associated with high cytotoxic activity.31 Of note, CD57 was expressed on 50% of cells in the patient group compared to only 44% within healthy donors (p = .04) (Figure 2a). The major activatory protein CD16 was also increased in patients, expressed on 88% compared to 77% of controls (p = .0002) (Figure 2a). A trend toward increased expression of NKG2C (Figure 2a) was also seen in the patient group (NKG2C: 4.8% vs 5.2% for HD vs PDAC, p = .68). Overall this profile reveals a somewhat more differentiated profile of peripheral NK cells within the patient group.
NK cell activation and recovery of NK cell subsets in lymphoma patients after obinutuzumab and lenalidomide treatment
Published in OncoImmunology, 2018
Dang-Nghiem Vo, Catherine Alexia, Nerea Allende-Vega, Franck Morschhauser, Roch Houot, Cedric Menard, Karin Tarte, Guillaume Cartron, Martin Villalba
During in vivo maturation CD56bright cells become CD56dimCD62L+CD57− cells that produce perforin, while maintaining high IFN-γ production in response to cytokines28,33. On the other hand, CD56dimCD62L−CD57+ cells show low response to cytokines and higher cytotoxic capacity28,34. CD62L was slightly increased in patients and the treatment decreased the expression (Fig. 2B). In contrast CD57 was lower in patients and remained unchanged by the treatment (Fig. 2B). This suggests that at the end of treatment the NK cells show decreased expression of an immature marker, i.e. CD62L. When NK cells reach fully mature CD56dimCD16+ status, they gain full expression of killer inhibitory receptors (KIRs) receptors. KIR expression in patients before and after treatment was variable and expression of the 3 KIRs taken together was similar in patients and healthy donors (Fig. 2C).