T Cells
Miroslav Holub in Immunology of Nude Mice, 2020
Since the earliest days of the discovery of “athymia”, or, more exactly, thymic dysgenesis in the nude mouse, it has been known that the animal is not entirely devoid of the T-lineage cells. There are many more nu/nu spleen and lymph node cells, which are positive for the brain-derived antigen. The thymus epithelial stroma seems to need few fully competent T-cell progenitors to be primed for its normal development and it has been suggested for human thymic dysgenesis that it may be caused by the failure of T-cell progenitors to populate the epithelial anlage: the same may be true for the earliest development of the nude thymus. In addition, there may be an abnormal specificity repertoire and an abnormal distribution of T-cell clones in nude mice. There is the logical possibility that few maturing T cells may fill the peripheral compartments by clonal expansion even without antigenic stimulation.
Hematopoietic Stem Cell Transplantation as Treatment for Type 1 Diabetes
Richard K. Burt, Alberto M. Marmont in Stem Cell Therapy for Autoimmune Disease, 2019
Type 1 diabetes mellitus is an autoimmune disease associated with B cell derived antibodies and T cell proliferative responses to a variety of islet cell peptides. Near normalization of blood sugar levels as monitored by glycosylated hemoglobin (HgbAlC) diminishes diabetic secondary complications. Insulin, while prolonging life, is not a cure and intensive insulin therapy to control blood sugar is not always practical, especially in lower economic classes or developing countries. Even in developed countries, serious sequela and mortality still occur. 1-5 In America, diabetes remains the most common cause of blindness and renal failure, and the sixth leading cause of death. Hematopoietic stem cell transplantation in early onset diabetes, and in established diabetes when combined with either pancreas or islet cell transplantation, offers hope of curing diabetes by reintroduction of islet cell tolerance.
B Lymphocyte Development and Immunoglobulin Genes
Julius M. Cruse MD PhD, Robert E. Lewis in Atlas of Immunology, 2004
T cells but is absent or of low density on γδ T cells. It has been discovered on many murine B cell lymphomas as well as on endothelial cells of blood vessels in the pregnant sheep uterus. CD72 on B cells is one of its three ligands. CD5 is present on thymocytes and most peripheral T cells. It is believed to be significant for the activation of T cells and possibly B1 cells. CD5 is also present on a subpopulation of B cells termed B1 cells that synthesize polyreactive and autoreactive antibodies as well as the “natural antibodies” present in normal serum. Human chronic lymphocytic leukemia cells express CD5, which points to their derivation from this particular B cell subpopulation.
T-cell-specific mTOR deletion in mice ameliorated CD4
Published in Virulence, 2019
Hao Wang, Guangxu Bai, Na Cui, Wen Han, Yun Long
ABSTRACT The mammalian target of rapamycin (mTOR) pathway can mediate T-cell survival; however, the role of this pathway in T-cell survival during fungal sepsis is unclear. Here, we investigated the role of the mTOR pathway in CD4+ T-cell survival in a mouse model of rapidly progressive lethal sepsis induced by severe invasive candidiasis and explored the possible mechanism. The decrease in CD4+ T-cell survival following fungal sepsis was ameliorated in mice with a T-cell-specific mTOR deletion, whereas it was exacerbated in mice with a T-cell-specific tuberous sclerosis complex (TSC)1 deletion. To explore the mechanism further, we measured expression of autophagy proteins light chain 3B and p62/sequestosome 1 in CD4+ T cells. Both proteins were increased in T-cell-specific mTOR knockout mice but lower in T-cell-specific TSC1 knockout mice. Transmission electron microscopy revealed that T-cell-specific mTOR knockout mice had more autophagosomes than wild-type mice following fungal sepsis. CD4+ T-cell mTOR knockout decreased CD4+ T-cell apoptosis in fungal sepsis. Most notably, the T-cell-specific mTOR deletion mice had an increased survival rate after fungal sepsis. These results suggest that the mTOR pathway plays a vital role in CD4+ T-cell survival during fungal sepsis, partly through the autophagy–apoptosis pathway.
Immunophenotypic and Gene Rearrangement Analysis in Null- or T-Cell Neoplasias: Study of 16 Cases
Published in Leukemia & Lymphoma, 1991
M. Santos, C. Rivas, G. Echezarreta, M. Bernacer, A. Santon, M. Robledo, J. Benitez
Immunophenotypic and molecular studies were performed in sixteen cases of T-cell lymphoproliferative disorders. These included eleven patients with peripheral T-cell lymphoma, two thymic lymphomas and three patients with T-gamma lymphocytosis. Peripheral T-cell lymphomas were of both low and high grades. There was one case of Sezary's syndrome, two of small T-cell pleomorphic type, two medium sized T-cell pleomorphic lymphomas, two large T-cell pleomorphic type and four large cell anaplastic T cell lymphomas with activated T cell markers. Two patients had lymphoblastic lymphoma of thymic origin. In this report we attempted to correlate immunophenotypic and molecular characteristics. Rearrangements of the T-cell receptor (TCR) genes were observed in all cases, including those lacking any immunophenotypic markers, and unusual rearrangements of both the TCR and Ig genes were evident in thymic and peripheral T-cell lymphomas. In the cases of T-gamma lymphocytosis, a lymphoproliferative disorder that is not always clearly defined monoclonality was seen in one. The use of the genotypic approach for refining the characterization and diagnosis of some T-cell neoplasias is emphasized. The problems and pitfalls arising from the application of these methods are also discussed.
Long noncoding RNA Malat1 is not essential for T cell development and response to LCMV infection
Published in RNA Biology, 2018
Yingpeng Yao, Wenhui Guo, Jingjing Chen, Pingting Guo, Guotao Yu, Juanjuan Liu, Fang Wang, Jingjing Liu, Menghao You, Tianyan Zhao, Youmin Kang, Xi Ma, Shuyang Yu
ABSTRACT Long noncoding RNAs (lncRNAs) are emerging as critical mediators of various biological processes in the immune system. The current data showed that the lncRNA Malat1 is highly expressed in T cell subsets, but the function of Malat1 in T cell remains unclear. In this study, we detected the T cell development and both CD8+ and CD4+ T cell response to LCMV infection using Malat1−/- mice model. To our surprise, there were no significant defects in thymocytes at different developmental stages and the peripheral T cell pool with ablation of Malat1. During LCMV infection, Malat1−/- mice exhibited normal effector and memory CD8+ T cells as well as TFH cells differentiation. Our results indicated that Malat1 is not essential for T cell development and T cell-mediated antiviral response though it expresses at very high level in different T cell populations.
Related Knowledge Centers
- Lymphocyte
- B Cell
- Cell-Mediated Immunity
- White Blood Cell
- Thymus
- T-Cell Receptor
- Natural Killer Cell