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Mucosal B cells and their function
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Jo Spencer, Edward N. Janoff, Per Brandtzaeg
A constant flow of lymph from the gut into the thoracic duct contains immunoblast precursors of plasma cells derived from Peyer's patches. Nevertheless, when this lymph flow is interrupted in rats, following an initial decline, the intestinal IgA+ plasma cell density is remarkably well maintained, perhaps implying sideways migration of precursor cells from GALT structures. Similar observations of highly localized B-cell responses to topically applied antigen have been made in a multiple-intestinal-loop model in lambs. Production of IgA antibodies in the gut lamina propria, therefore, probably depends on the potential of GALT to generate a continuous supply of plasma cell precursors, both laterally and by homing through lymph and peripheral blood. The cells at the periphery of GALT illustrated in Figure 10.2 may be involved in this process of lateral migration prior to differentiation.
B Cells and Humoral Immunity
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Following the antigen-independent phase of B cell development, we enter the antigen-dependent phase. These are the developmental stages following the encounter of the B cell with stimuli leading to antibody secretion. The first visible event in activation is blast transformation. The B cell enlarges and begins to divide. While resting mature B lymphocytes are relatively small, only 7–9 μ in diameter, the rapidly dividing B lymphoblast or immunoblast is much larger, about 15 μ.
Marginal Zone Lymphoma
Published in Wojciech Gorczyca, Atlas of Differential Diagnosis in Neoplastic Hematopathology, 2014
The lymphoid cells are mostly small to occasionally medium in size with variable admixture of large B cells with prominent nucleoli (immunoblast-like). Cellular pleomorphism (variable shape and size of neoplastic cells) is seen in the majority of cases, and only a subset of lymphomas is composed of predominantly small cells with occasional, scattered intermediate-sized cells. Large cell component, usually <20% of the infiltrate, can be identified in many cases [9]. Rare cases may show up to 50% large cells, but none of the nodal MZLs has >50% large cells or sheets of large cells [9]. MZL with an increased number of large cells (20%–50%) does not behave more aggressively [3]. In contrast to follicular lymphoma (FL), there are no defined criteria for grading of MZL. Transformation to diffuse large B-cell lymphoma (DLBCL) is currently diagnosed only in the presence of sheets of large cells.
Papillary thyroid carcinoma in Struma Ovarii
Published in Gynecological Endocrinology, 2020
Khatuna Khatchapuridze, Nino Kekelidze, Zaza Tsitsishvili, Maia Mchedlishvili, Dimitri Kordzaia
In the right ovary, there were observed the co-existence of the micro-, macro-, normo-follicular structures, lined by monomorphic thyroid cells, without atypia. The follicles were filled by eosinophilic, in some places swollen colloid. The stroma was infiltrated with lymphocytes composing lymphoid follicles. Immunoblast-type cells were observed at the germ cell center of the follicle. Focally, there was observed ‘pouring’ the colloid into the interfacial spaces, which are predominantly represented by a scarce fibrovascular stroma. The infiltration of the stroma with lymphocytes that produce lymphoid follicles was detected. Immunoblast-type cells were observed at the germ cell center of the follicle, predominated by capillary blood vessels. The mantle zone was poorly distinguishable. The marginal zone was hyperplastic. The follicular and papillary structures lined by relatively large thyrocytes were found in the area of the nodal structure sized up to 2 cm. The overlapping cells had ‘optically luminous’ nuclei with the incisions and insertions. The aforementioned cytologic triad corresponds to papillary carcinoma (Figure 1).
Clinicopathologic features and prognostic significance of CD30 expression in de novo diffuse large B-cell lymphoma (DLBCL): results in a homogeneous series from a single institution
Published in Biomarkers, 2020
María Queralt Salas, Fina Climent, Gustavo Tapia, Eva DomingoDomènech, Santiago Mercadal, Ana Carla Oliveira, Carmen Aguilera, García Olga, Miriam Moreno Velázquez, Marcio Andrade-Campos, Maite Encuentra, Alberto Fernández de Sevilla, Anna Sureda, Juan Manuel Sancho, Eva González-Barca
CD30 is a member of the tumour necrosis factor receptor (TNFR) superfamily (Falini et al.1995). It is an activation marker inducible in vitro by mitogenic signals, and it is expressed by T and B immunoblast in the parafollicular region and the peripheral rim of germinal centres (Schneider and Hubinger 2002). CD30 overexpression in tumour cells results in increased cell proliferation and survival and in the inhibition of apoptosis by nuclear translocation of proteins NK-kB and MAPK family (Schneider and Hubinger 2002). CD30 can be expressed in a variety of malignancies such as Hodgkin Lymphoma, different subtypes of T- and B-cell NHL, anaplastic large cell lymphoma, Epstein-Barr virus (EBV)–driven clonal lymphoproliferative disorders, and also in some DLBCL (Noorduyn et al.1994, Hartley et al.2017).
Progress in the development of novel therapies for choroideremia
Published in Expert Review of Ophthalmology, 2019
Jasmina Cehajic Kapetanovic, Maria I Patrício, Robert E MacLaren
In addition to a characteristic phenotype and X-linked family history, genetic diagnosis of choroideremia is essential in the current era of gene therapy. There are 346 unique DNA variants in CHM reported to date (Leiden Open Variation Database, LOVD3, www.lovd.nl/CHM), most of which are functionally null either through deletions or nonsense sequence variations. Deletion varies in size from a few kilobases to the entire gene deletion, leading to loss of function or complete absence of REP1. Nonsense variations result in premature stop codons and termination of protein translation. Unlike most retinal degenerations, the missense variants that result in pathological protein misfolding are rarely found in choroideremia [25]. Any missense change, therefore, needs to be interpreted with caution to ensure a true pathogenic effect, rather than a simple mistake in the sequence readout. In cases of strong clinical suspicion and no identified genetic variant or in the case of a variant of uncertain pathogenicity, it is important to follow several additional steps to confirm the diagnosis. Further genetic testing can be requested to include sequencing of a recently reported novel deep intronic variant [26] and a variant in the promoter region of CHM [27] that are not routinely included in the panel. Several rare phenotypes that can mimic choroideremia such as, gyrate atrophy of the choroid [28], progressive bifocal chorioretinal atrophy [28], Oliver-McFarlane syndrome [29] and a phenotype associated with-dominant RPE65 variants [30,31] need to be excluded. Although choroideremia is by far the most prevalent (1:50,000) of those masquerading conditions, it is helpful to examine a female relative to confirm the specific carrier phenotype. Lastly, functional in-vitro immunoblast assay to check for the absence, reduced levels or absent/reduced prenylation activity of REP1 in peripheral blood mononuclear cells can aid the clinical diagnosis [17].