Anaesthesia and Immune Response
Thomas H. M. Stewart, E. Frederick Wheelock in Cellular Immune Mechanisms and Tumor Dormancy, 2017
Memory and specificity are the key components of adaptive immunity and in all vertebrates the small lymphocyte plays a major role in it. On an anatomical and functional basis, lymphocytes are classified into either thymus dependent or T-lymphocytes, or bursa dependent B-lymphocytes.17 The specificity of the adaptive immune system is based on the specificity of the antibodies and lymphocytes. Antigen binds to a small number of cells which recognise it and induces them to proliferate. This occurs both for the B-lymphocytes which mature into antibody producing cells, and for the T-lymphocytes which transform into lymphoblasts, undergo proliferation, and perform functions that depend upon their subclass. Thus, we have the dichotomy of the specific immunity into cellular or humoral components.
Myeloproliferative Neoplasms (MPN)
Dongyou Liu in Tumors and Cancers, 2017
Lymphocytes evolve from lymphoblasts (a type of blood stem cell in the bone marrow) and represent the main cells in lymphoid tissue, which is distributed in the lymph nodes, thymus gland, spleen, tonsils, and adenoids, as well as the digestive and respiratory systems and bone marrow. Lymphocytes comprise two major populations: B lymphocytes (B cells) and T lymphocytes (T cells). Lymphocytes help regulate the immune system and protect the body from invading microbes. Specifically, T cells migrate to the thymus, differentiate further under the influence of thymic hormones, and have either helper (CD4) or cytotoxic (CD8) immunological functions (cellular immunity); B cells migrate directly to organs without undergoing modification in the thymus, become sensitized after exposure to antigen, and differentiate into plasma cells for antibody production (humoral immunity). Further, there is another class of large granular lymphocytes (distinct from T cells and B cells) called natural killer cells, which produce inflammatory cytokines and spontaneously kill malignant, infected, or “stressed” cells without prior sensitization.
Leukemias
Pat Price, Karol Sikora in Treatment of Cancer, 2020
The recognition of structural chromosomal and genetic abnormalities in the majority of lymphoblasts has contributed enormously to understanding the molecular pathogenesis and prognosis of ALL. These abnormalities include changes in chromosome numbers (aneuploidy) and chromosomal translocations and rearrangements, which probably constitute the initiating events, followed by somatic mutations and DNA copy number alterations.33 The ALL genome contains about 10–20 mutations at diagnosis. These mutations impact multiple cellular processes, including transcription, lymphoid development and differentiation, and cell-cycle regulation. Figure 28.6 depicts the unfolding cytogenetic and genomic landscape of ALL of both B- and T- lineages. About 10% of all ALL currently remains unclassifiable. Adolescents and adults have an usually high prevalence of poor-risk subtypes, such as BCR-ABL1 and MLL rearrangement, and a lower risk of the favorable subtypes, such as ETV6-RUNX1 and high hyperdiploidy.
T-cell lymphoblastic lymphoma involving the ocular adnexa: report of two cases and review of the current literature
Published in Orbit, 2019
Lucy Sun, Alan H. Friedman, Rand Rodgers, Matthew Schear, Giovanni Greaves, Kathryn B. Freidl
The diagnosis of T-LBL relies on histological and immunophenotypic analysis of the extramedullary tissue biopsy, peripheral blood, or BM. Immunohistochemical or flow cytometry of neoplastic cells will demonstrate markers T-cell lineage in arrested maturation. Markers of non-lineage specific blastic differentiation include cluster of differentiation (CD)1a, CD10, CD34, CD99, and deoxynucleotidyltransferase (TdT). In T-LBL, 95% of lymphoblasts express TdT. 16 T-cell lineage markers include CD2, CD3, CD4, CD5, CD7, and CD8. Depending on the stage of arrested maturation, immature lymphoblasts variably express T-cell lineage antigens. The earliest marker of T-cell lineage is CD7, but the most specific marker is CD3. 5,6,17 Imunohistochemical staining of the lymph node biopsy from our first patient was positive for markers TdT, CD2-5, CD7, and CD8, with a similar profile in the BM biopsy. Immunohistochemical staining of the orbital mass from our second patient was positive for markers CD3, CD5, CD99, MIB-1, and TdT, with a similar profile in the BM biopsy as well. MIB-1 is a marker for cellular proliferation.
Treatment response and outcome of children with T-cell acute lymphoblastic leukemia expressing the gamma-delta T-cell receptor
Published in OncoImmunology, 2019
Ching-Hon Pui, Deqing Pei, Cheng Cheng, Suzanne L. Tomchuck, Scarlett N. Evans, Hiroto Inaba, Sima Jeha, Susana C. Raimondi, John K. Choi, Paul G. Thomas, Mari Hashitate Dallas
The V-(D)-J gene rearrangement for the TRG and TRD loci expressed by the lymphoblast was identified using single-cell PCR as previously described.38,39 Appropriate consents and samples were available for 9 of the 12 patients with γδ T-ALL (Table 3). A dominant clonal population of lymphoblast was identified for all patients. A biclonal population was observed in one patient where one TRDV region paired with two unique TRGV regions. The combinatory diversity of the TRG genes showed a bias toward TRGJ segments from the distal region 2 (JP2 and J2) (89%) joining to the terminal constant region (TRGC2). The use of the proximal region 1 (TRGJ1 and TRGC1) was rare. The TRGV regions detected were TRGV9 (33%), TRGV5 (33%), TRGV4 (20%), TRGV2 (10%), and TRGV8 (10%). Despite variability in the TRGV regions the CDR3γ regions were similar. The CDR3γ region contained an average of 14.2 ± 2.2 amino acids and each patient had an average of 3.3 ± 2.6 unique amino acids and shared an average of 11 ± 0.5 amino acids (88%). In contrast, the TRDV regions expressed were predominantly TRDV1 (67%). Non-TRDV1 included TRDV3 (11%), TRDV5 (11%), and TRDV8 (11%). All in frame sequences used the TRDJ1 segment.
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].
Related Knowledge Centers
- Cluster of Differentiation
- Immunostaining
- Myeloblast
- White Blood Cell
- Cellular Differentiation
- Lymphocyte
- Acute Lymphoblastic Leukemia
- Cluster of Differentiation