China
Africa
Explore chapters and articles related to this topic
Comparative Immunology
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Although birds are commonly considered not to possess lymph nodes, they do possess structures that can be considered to be their functional equivalent. These avian lymph nodes consist of a central sinus that is the main lumen of a lymphatic vessel. It is surrounded by a sheath of lymphoid tissue that contains germinal centers. Avian lymph nodes have no external capsule.
Inherited Defects in Immune Defenses Leading to Pulmonary Disease
Published in Stephen D. Litwin, Genetic Determinants of Pulmonary Disease, 2020
Lymphatic tissue fails to show germinal centers; plasma cells are missing from the bone marrow, intestinal tract, and lymph nodes. Circulating blood lymphocytes do not include Β lymphocytes with surface Ig. Τ lymphocytes are quantitatively and functionally normal.
Immune Reconstitution after Hematopoietic Stem Cell Transplantation
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Andreas Thiel, Tobias Alexander, Christian A. Schmidt, Falk Hiepe, Renate Arnold, Andreas Radbruch, Larissa Verda, Richard K. Burt
B cells undergo further affinity maturation within lymph node germinal centers by a process of somatic hypermutation (SHM), gene conversion, and class switching recombination (CSR) (Fig. 4). SHM is the term for insertion of point mutations in the vicinity of the variable region exon (Fig. 4) and results in generation of antigen specific high affinity antibodies. Gene conversion is the transfer of a pseudovariable (ipV)gene sequence into the variable region exon (Fig. 4). Both SHM and gene conversion alters the antigen binding site of the immunoglobulin.71-72 CSR involves switching the constant region heavy change (e.g., IgM to IgG) that alters the effector function of the antibody (Fig. 4). The mechanisms involved in DNA SHM, gene conversion, and CSR although incompletely understood probably involve common mechanisms of DNA recognition, targeting, cleavage, and repair.73 The enzyme activation-induced cytidine deaminase (AID) is involved in all three reactions by helping to create the DNA cut or cleavage.65,74-75
Cellular mechanisms and clinical applications for phenocopies of inborn errors of immunity: infectious susceptibility due to cytokine autoantibodies
Published in Expert Review of Clinical Immunology, 2023
Rui Sun, Yating Wang, Hassan Abolhassani
Abnormal GC presents without immunization and detectable pathogen invasion [30–32]. The role of abnormal GC formation has been described in several autoimmune diseases including the defective exclusion of autoreactive B cells that are supposed to be anergic after BCR stimulation during the early stage of GC [33] and major blood B cell subset alterations (e.g. reduction of mature B cell and increased frequency of pre-GC B cells in the blood of children) [34] in system lupus erythematosus (SLE) patients, ectopic GC, and B cell-T cell aggregations that lacks FDC in the synovial tissues in rheumatoid arthritis patients (RA) [35,36], Fas mutation-related lymphocyte apoptosis deficiency in autoimmune lymphoproliferative syndrome (ALPS) [37,38], the ectopic GC in the salivary gland and subsequent development in the spleen in Sjogren’s syndrome (SS) [39,40], and ectopic expression of neuromuscular molecules in MG-type thymoma [41]. In current acute COVID-19 cases, extrafollicular B cell responses are also reported. Together with mounted Bcl-6 expressing T follicular helper cell loss, absence of germinal centers, and the expanded plasmablasts. Also, the autoantibody profiles and the B cell responses resemble SLE flares [42]. The abnormal germinal center formation may relate to the limited durability of humoral immunity [43]. Though we can not exclude abnormal germinal center formation as a potential factor in IEI phenocopy autoAbs generation, limiting evidence supports the aberrant germinal center formation contributed to anti-cytokine autoantibodies in IEI phenocopies and still requires further demonstration.
Immune-based therapies in diffuse large B-cell lymphoma
Published in Expert Opinion on Investigational Drugs, 2023
Dustin McCurry, Christopher R. Flowers, Casey Bermack
Diffuse large B-cell lymphoma (DLBCL) is an aggressive and clinically heterogeneous malignancy with up to 40% of patients experiencing primary refractory disease or relapse after first-line treatment [1]. DLBCL originates from B-cells developing through humoral immune responses. Upon initial germinal center (GC) formation, B-cells undergo somatic hypermutation and proliferation in GC dark zones prior to selection and activation in GC light zones, potentially repeating this cycle between GC dark and light zones for affinity maturation of B-cell receptors. Upon sufficient maturation, activated B-cells leave GCs and may develop into memory B-cells or terminally differentiate into plasma cells [2]. In the early 2000s, transcriptomic analyses subdivided DLBCL into at least two biologic classes, a group of tumors that are transcriptionally similar to germinal center B-cells (GCB) and another with similarities to activated B-cells (ABC), which confers poor prognosis [2,3].
Tertiary Lymphoid Structures, Immune Response, and Prognostic Relevance in Non-Small Cell Lung Cancer
Published in Cancer Investigation, 2023
Alexandra Giatromanolaki, Paschalis Chatzipantelis, Constantinos A. Contrafouris, Michael I. Koukourakis
The density of TLS was assessed in the tumor periphery and the inner tumor area, in hematoxylin–eosin tissue sections, in all available optical fields. As ‘tumor periphery’ was defined the area comprised by the first ×200 optical field containing tumor invading front and normal lung adjacent to this front. TLSs were identified in the stroma of the invading tumor and in the normal lung infiltrated by the tumor. Inner tumor areas refer to all available ×200 optical fields of the tumoral tissue section, immediately below the optical filed that defined the tumor periphery. TLSs were identified in the stroma areas. Necrotic areas were excluded. All tertiary lymphoid structures with or without identifiable germinal centers were recorded. The whole tissue section was analyzed at ×200 magnification power. The number of TLS in normal lung across the tumor periphery was recorded and divided by the number of optical fields to provide the peritumoral ‘pTLS-score’. A similar procedure was applied within the tumor body, where after counting the TLS number in all ×200 optical fields, we produced the inner tumor area ‘iTLS-score’, by dividing the total TLS number with the number of optical fields.