Hematopoietic Organs and Blood
George W. Casarett in Radiation Histopathology, 2019
Lymphatic nodules are dense accumulations of lymphocytes usually resulting from lymphocytopoietic activity concentrated in small regions in the lymphoid tissue. These nodules appear and reveal intense lymphocytopoiesis by proliferation of lymphocytes and to a lesser extent by transformation of primitive reticular cells, and then they may disappear. When the nodule is fully developed, it consists of a pale germinal center, often surrounding a small nutrient artery, in which medium-sized lymphocytes predominate and proliferation of lymphocytes is occurring. This central area is surrounded by a darker corona of small lymphocytes partly produced by the germinal center which was at first bare and without a corona. After proliferation in the germinal center has ceased, medium-sized lymphocytes in the germinal center become small lymphocytes or disappear, and the active center gradually becomes depleted of lymphocytes and resembles in some respects some of the stages of the reaction centers seen in certain infectious diseases. When completely at rest, the center has been reduced or has disappeared and the lymphatic nodule consists chiefly of closely packed small lymphocytes. Considerable degeneration of small lymphocytes may also be seen during intense lymphopoiesis.
Dopamine in the Immune and Hematopoietic Systems
Nira Ben-Jonathan in Dopamine, 2020
T cells are created by lymphopoiesis from a common lymphoid progenitor in the bone marrow. The newly generated cells migrate to the thymus where they undergo extensive maturation and screening. Through a combination of positive and negative selection processes, the cells are differentiated, yielding a repertoire of mature T cells that tolerate self-antigens and are capable of mounting strong responses to foreign antigens. Within the thymus, T cells undergo a V(D)J recombination, a unique mechanism of genetic recombination that occurs only in developing lymphocytes during maturation. It involves somatic recombination that results in a highly diverse assortment of the TCRs. Cell selection in the thymus is accompanied by an extensive cell death by apoptosis and phagocytosis, with only a very small percent of the cells surviving the selection process, and these are exported to extra-thymic sites.
Myeloproliferative Neoplasms (MPN)
Dongyou Liu in Tumors and Cancers, 2017
Lodged within the bone marrow, blood stem cells (also known as hematopoietic stem cells, HSC, or hematopoietic stem and progenitor cells, HSPC) are divided into myeloid and lymphoid stem cells. Myeloid stem cells give rise to myeloid lineage cells (i.e., red blood cells [erythrocytes], white blood cells [eosinophil, basophil, neutrophil, mast cell, and monocyte, but not lymphocyte], and platelets) in a process known as hematopoiesis (or hemapoiesis). Lymphoid stem cells differentiate into lymphoid lineage cells (T- and B-lymphocytes as well as natural killer cells) in a process known as lymphopoiesis (lymphocytopoiesis or lymphoid hematopoiesis) (Figure 13.1).
Therapy-related acute lymphoblastic leukemia following treatment for multiple myeloma – diagnostic and therapeutic dilemma
Published in Acta Oncologica, 2022
Alicja Sadowska-Klasa, Mary Abba, Justyna Gajkowska-Kulik, Jan Maciej Zaucha
Secondary acute leukemia refers to patients with either therapy-related or disease progressing from an antecedent hematologic disorder typically a myelodysplastic syndrome or a myeloproliferative neoplasm. Neither MM is considered a typical neoplasm that leads to secondary hematopoietic neoplasms nor ALL is a typical secondary hematopoietic malignancy. Lymphoblasts and plasmocytes are cells both originating from lymphopoiesis; however, their proliferating potential is very different. Plasma cells represent the final differentiation stage, nevertheless, there are hypotheses that somatic mutations occurring in younger precursors affect further stages of lymphopoiesis, and the final oncogenic events take place in secondary lymphoid organs [19,20]. The hereditary component of MM susceptibility was reported many years ago; however, increased risk for other B-cell originating neoplasms was also noticed in MM-risk families [1,8]. Interestingly tr-ALL, which accounts for up to 9% of all ALL, occurs mainly in women after chemotherapy for breast cancer [21]. Regardless, the second most common cause of tr-ALL is MM [22].
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 immune system is composed of many different tissues. The primary (or central) lymphoid organs, destined to generate lymphocytes from immature progenitor cells, are the thymus that is involved in T-cell lymphopoiesis, and the bone marrow that hosts both B-cell and T-cell precursors. Spleen and lymph nodes are secondary (peripheral) lymphoid organs, where B and T-cells are activated after being exposed to antigens, giving birth to mature immune cells that enter the bloodstream to reach the target tissues. During pathological processes, e.g., chronic inflammation or autoimmune conditions, the ‘tertiary lymphoid structures’ (TLS) appear. These are abnormal ‘lymph node-like’ structures that emerge within the affected organs/tissues and are characterized by active germinal centers surrounded by follicular dendritic cells (5). B-cell follicles, T-cell zones are often evident within TLS. Specialized vessels known as high endothelial venules (HEVs) are also present, but TLS do not have afferent lymphatic vessels (6). Within them, both B and T-cell responses can be developed, just like in lymph nodes.
Melanoma induced immunosuppression is mediated by hematopoietic dysregulation
Published in OncoImmunology, 2018
Neha Kamran, Youping Li, Maria Sierra, Mahmoud S. Alghamri, Padma Kadiyala, Henry D. Appelman, Marta Edwards, Pedro R. Lowenstein, Maria G. Castro
A central observation of our study is the decreased proportion of mature B cells. A model proposed by Takizawa et al. suggests that myelopoiesis and lymphopoiesis compete for the same developmental resources and under conditions of systemic infection, reduced lymphoid supportive growth and retention signals lead to lymphocyte mobilization thus creating a vacant niche space for enhanced myelopoiesis.15 Furthermore, CLPs have been shown to be reprogrammed to generate DCs and pathogens and TLR ligands are capable of suppressing the differentiation of Pre pro B cells.31 Since CLP frequency was not altered, the decrease in mature B cells in the bone marrow and blood of tumor bearing mice observed in our study could result from enhanced mobilization of immature B cells or increased apoptosis of pro B cells, thereby limiting the pool available for further development. In fact, it has been demonstrated that during alum/infection or PAMPs induced emergency granulopoiesis, cytokines such as IL-1, IL-3, IL-6, G-CSF and GM-CSF cause BM mobilization of lymphocytes to lymphoid organs such as the spleen.15 Our experiments using the IL-3 antibody interestingly show a trend of decreased CD19+ B cells in the BM with no effect on the B cell progenitors, suggesting an increase in the egress of B cells from the bone marrow. Nevertheless, it is evident that melanoma growth resulted in a decrease in the peripheral B cell pool.
Related Knowledge Centers
- Haematopoiesis
- Lymphoproliferative Disorders
- Myeloid Tissue
- White Blood Cell
- Lymphatic System
- Bone Marrow
- Lymphocyte
- Red Blood Cell
- Lymphoma
- Lymphoid Leukemia