The Thoracic Lymphatic System and Lymph Nodes, and the Spread of Tumours within the Lungs, the Tracheobronchial Tree and the Mediastinum.
Fred W Wright in Radiology of the Chest and Related Conditions, 2022
Lymphocytes are the basic cells of the lymphoid system and are of three main types - B, T and Null (i.e. not B or T). B lymphocytes when stimulated by antigens differentiate into plasma-cells which in turn produce antibodies. T lymphocytes are of several types: - (i) T-helper cells which produce cytokines and assist B lymphocytes, macrophages and granulocytes, (ii) T-cytoxic cells which destroy cells infected with viruses and tumour cells, and (iii) T-suppressor cells which turn down an immune response. Null cells destroy cells coated with antibodies. T cells are particularly produced in the thymus. Lymphocytes circulate in the blood, rapidly detect antigens (many are specific to certain antigens) and stimulate the production of more lymphocytes in nodes etc. to cause the immune response.
The Host Response to Grafts and Transplantation Immunology
Julius P. Kreier in Infection, Resistance, and Immunity, 2022
The level and types of cytokines that a recipient produces are important to the survival of the graft. One type of T-helper cell can become predominant over the other and over the immune response to a particular antigen because of the immunoregulatory ability of certain cytokines. Interferon-y (a Th1 cytokine) suppresses the activation of Th2 lymphocytes, whereas interleukin-10 (a Th2 cytokine) suppresses the activation of Th1 lymphocytes. When this happens the response is said to have become polarized toward a cellular or a humoral response. Th1-like cytokines activate cell-mediated mechanisms of acute rejection. In contrast, Th2-like cytokines are involved in the activation and proliferation of B lymphocytes, thereby promoting humoral mechanisms of rejection. Th2 cells also produce transforming growth factor β (TGF-β) and granulocyte-macrophage colony-stimulating growth factor, cytokines that are involved in the activation of T-suppressor cells. Therefore, a Th2 response favors the establishment of anergy or tolerance. However, one of these same cytokines, TGF-β, may contribute to the pathology of chronic rejection.
The Lymphatic/Immune System and Its Disorders
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss in Understanding Medical Terms, 2020
Thymic lymphocytes (also called thvmus-dependent lymphocytes or T-cells) are so named because they are formed in the thymus, pass through it, or are influenced by it on their way to the tissue. T-lymphocytes are components of cellular or cell-mediated immunity. T-lymphocytes fall into two categories: T-suppressor cells inhibit the stimulation of antibody production and serve a regulatory function in immunity; T-helper cells (also called CD4+ cells because of the CD4" receptor site on their surface) assist such stimulation. T-lymphocytes also can attach to and kill large antigenic cells such as cancer cells and transplant cells, so they are involved in the process of transplant rejection.
Direct Engagement of TLR9 Ligand with T Helper Cells Leads to Cell Proliferation & Up-regulation of Cytokines
Published in Immunological Investigations, 2019
Ravi Kumar Sharma, Shobha Sehgal, Naresh Sachdeva, Rajendra Kumar, Amod Gupta
T helper cells are classically and predominantly involved in adaptive immune response. A few reports indicate that certain subsets of T lymphocytes expressed TLR9, however, its precise role in CD4+CD25- T helper(TH) cells has been equivocal (Babu et al., 2006; Hammond et al., 2010; Klonowska-Szymczyk et al., 2014; Landrigan et al., 2011). TLR9 ligands have been shown to co-stimulate CD4 cells without involvement of MyD88 or TLR9 (Landrigan et al., 2011). Reports indicate apoptotic signalling or suppression of apoptosis after engagement with TLR9 (Funderburg et al., 2008; Zheng et al., 2008). Here, we observed that purified CD4+T cells consistently bind to the TLR9 ligand ODN 2216 and increase cellular proliferation and cytokine expression, particularly TGF-β. This prompted us to elucidate further the sequence of events in purified TH cells after engagement with the ligand and its significance in immune activation and cytokine up regulation.
Immune to addiction: how immunotherapies can be used to combat methamphetamine addiction
Published in Expert Review of Vaccines, 2021
Md Kamal Hossain, Majid Hassanzadeganroudsari, Erica Kypreos, Jack Feehan, Vasso Apostolopoulos
METH conjugated vaccines are administered via parenteral route to avoid gastrointestinal denaturation and lysis. After administration, the anti-METH vaccine is either processed via T cell dependent pathway or T cell independent pathway. In the T cell dependent pathway, the anti-METH vaccine conjugate is taken up by antigen presenting cells which is processed and presented on the surface in complex with the major histocompatibility complex class II (and/or class I). This causes T helper cells to be activated which help stimulate B cells to mature into plasma cells to produce antibodies. After vaccination, once an individual uses METH, their body’s immune system can then recognize the drug as a threat and the anti-METH antibodies would bind to the METH molecules and potentially reduce their entry to the CNS, reducing the dopamine release and associated consequences [18,42] (Figure 4(a)). A number of anti-METH vaccines have been developed through hapten design and investigated in animal models as a means of active immunization. Most of the anti-METH vaccines demonstrate excellent antibody titers and prevent METH induced hyper locomotor activity and self-administration [18,42,43].
HIV TB coinfection - perspectives from India
Published in Expert Review of Respiratory Medicine, 2021
Bharat Bhushan Rewari, Amitabh Kumar, Partha Pratim Mandal, Anoop Kumar Puri
Infection with HIV elicits both innate and adaptive immunity, including cellular and humoral response. However, HIV persists as a chronic infection due to genomic integration of the virus, cellular latency, and genetic variability, leading to immune escape. Cluster Determinant (CD)8+lymphocytes have a key role in initial control of viremia but eventually immune system becomes exhausted and dysfunctional [14]. A persistent antigenic stimulation leads to dysfunction of T cells; however, the hallmark of HIV infection is the depletion of CD4+T helper cells. The CD 4+T helper cells confer Cell Mediated Immunity (CMI) and primarily provide the defense against TB infection [15]. Consequently, there can be a reactivation of TB, re-infection by exogenous TB bacteria or development of progressive primary disease in HIV infection.
