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Gene Rearrangement in Leukemias and Lymphomas
Published in John T. Kemshead, Pediatric Tumors: Immunological and Molecular Markers, 2020
A consistent karyotypic abnormality known as the Philadelphia chromosome (Ph) characterizes chronic myeloid leukemia (CML). Cytogenetic and enzymatic studies have indicated the clonal nature of the disease, which is derived from the transformation of a progenitor cell.33 The overproduction of granulocytes marks the chronic phase of the disease which usually progresses to an acute period, the blast crisis. Approximately one third of patients enter a lymphoid blast crisis in which the neoplastic cells generally express Tdt and CD 10 and possess rearranged IgH genes.34,36,37 In all cases of myeloid blast crisis examined, only germline configurations of immunoglobulin genes have been identified.34,36,37 Two cases of “mixed” blast crises have been analyzed and the CDlO-positive cells, which displayed myeloid antigens, were shown to have germline Ig genes.37,38 The analysis of two separate episodes of blast crisis in one patient has revealed that, although both clones possessed the same IgH gene configuration, their light chain genes differed.37 This data has been interpreted as indicating a common lymphoid progenitor cell for both clones which had not undergone light chain gene rearrangement at transformation. It is suggested that the blast crisis represent the expansion of subclones derived from the progenitor neoplastic cell which has undergone further Ig gene rearrangement. Distinguishing between patients with lymphoid rather than myeloid blast crises has obvious clinical consequences.
The Thymus and Immunotherapy, Reconstructive Vs. Stimulatory or Suppressive Conceptions
Published in Marek P. Dabrowski, Barbara K. Dabrowska-Bernstein, Immunoregulatory Role of Thymus, 2019
Marek P. Dabrowski, Barbara K. Dabrowska-Bernstein
There is common agreement on the primary role of lymphoid progenitor cell defect responsible for the impairment of both T and B cell lineage development and maturation in patients with severe combined immunodeficiency disease (SCID). In some cases, however, B cells are present in periphery,66 and moreover, coculturing of these cells with normal T lymphocytes results in elaboration of antibody.360 Bach postulates that such cases of SCID may involve pathogenic elements related to disturbed development of the thymus.66 Thus, in SCID, the defects of immunogenesis may comprise a different quantitative combination of a qualitative disfunction at the pre-T, pre-B, and thymic levels.
Leptin’s Immune Action: A Review Beyond Satiety
Published in Immunological Investigations, 2023
Alice Abend Bardagi, Clarissa dos Santos Paschoal, Giovanna Ganem Favero, Luisa Riccetto, Maria Luisa Alexandrino Dias, Gil Guerra Junior, Giovanna Degasperi
The bone marrow is one of the largest tissues in the body. Protected by the bones, it is found within the central cavities of axial and long bones and is the main physiological site for hematopoiesis in adults, being responsible for the production of erythrocytes, granulocytes, monocytes, lymphocytes, and platelets (Lucas 2021). HSCs are responsible for the generation and renewal of erythroid, myeloid, and lymphoid progenitor cell lineages. HSCs reside in specialized microenvironments known as “niches”, which promote essential elements for the self-renewal ability and generation of cell diversity (Pinho and Frenette 2019). Megakaryocytes, erythrocytes, basophils, neutrophils, eosinophils, and monocytes arise from the myeloid progenitor, while B lymphocytes, T lymphocytes, and natural killer (NK) cells originate from lymphoid progenitors (Zhang et al. 2018).
An immunologist’s guide to immunosenescence and its treatment
Published in Expert Review of Clinical Immunology, 2022
Calogero Caruso, Mattia Emanuela Ligotti, Giulia Accardi, Anna Aiello, Giuseppina Candore
This profound and complex change in innate and acquired immunity is probably the result of epigenetic and metabolic modifications affecting immune cells at different levels, from HSCs to terminally differentiated cells. In younger people, HSCs provide a balanced output of myeloid and lymphoid progenitor cells. The shift from lymphoid to myeloid differentiation that occurs with aging determines a bias of aged HSCs toward differentiation into common myeloid progenitor cells and a concomitant reduction in common lymphoid progenitor cell [CLP] frequencies; this is followed by a reduction in B and T cell production with aging [54]. The reduction of naïve T lymphocytes is further linked to thymic involution. It is not completely clear why thymic involution occurs, but it is believed to be an evolutionary reason. In fact, at puberty individuals have encountered almost all pathogens living in their environment and continuing to educate T lymphocytes for cells that will never be of any use would be a waste of energy. After puberty, exposure to new pathogens is, indeed, less likely, and immune memory for local pathogens is critical. Resources are concentrated on maintaining defense against environmental pathogens because immune memory can be very long-lasting [55,56].