In vitro Testing for Adverse Drug Reactions
Kirsti Kauppinen, Kristiina Alanko, Matti Hannuksela, Howard Maibach in Skin Reactions to Drugs, 2020
Brender et al.16 have studied the T-lymphocyte responses in penicillin allergy in a more detailed fashion. The data indicated a heterogeneous response. The response could be elicited with both penicillin G itself and penicillin G coupled with human serum albumin. Both CD4 and CD8 T-cells were stimulated with penicillin G, but only CD4 T-cells with the albumin-coupled drug. The penicillin G-speeific clones were human leukocyte antigen (HLA) class I or class II restricted and the albumin-coupled drug had to undergo antigen processing prior to antigen presentation. Various cell types could serve as antigen presenting cells. The cytokine pattern secreted was also heterogeneous, most T-cell clones producing large amounts of interleukin-2, interferon-gamma, and tumor necrosis factor-alpha, and variable amounts of interleukin-4 and -5. The immunological heterogeneity may explain the variety of clinical pictures in penicillin allergy.
Dermal Hypersensitivity: Immunologic Principles and Current Methods of Assessment
David W. Hobson in Dermal and Ocular Toxicology, 2020
The two major arms of the immune system are humoral immunity and cell-mediated immunity. Specific antibodies from B lymphocytes mediate humoral immunity, whereas specifically sensitized T lymphocytes produce cell-mediated immunity. Various cells (macrophages) in the mononuclear phagocytic system (MPS) process and present antigens on their surface membranes in context with class II major histocompatibility (MHC) antigens. These antigen-presenting cells enable specific lymphocytes to recognize the foreign antigen and to generate an immune response against the antigenic substance. The cell in the skin with this antigen presentation role is primarily the Langerhans’ cell.25 T lymphocytes function as two main subpopulations which express different surface markers, the helper/effector T cells (TH) and the suppressor T cells (Ts). Human TH cells express CD4+ and Ts cells express CD8+ surface antigens.17
The Challenge of Parasite Control
Eric S. Loker, Bruce V. Hofkin in Parasitology, 2015
Other issues can hamstring the development of effective vaccines. One concern is the route through which a vaccine is administered. To effectively stimulate a protective immune response, the key antigenic peptides in the vaccine must be presented to CD4+ T cells by antigen-presenting cells. Because of the need to prevent proteolysis of the antigens before they reach the antigen-presenting cells, many vaccines are given by injection rather than orally to avoid the low pH of the stomach and proteases found there. Vaccine administration via injection may not be of concern if the vaccine is designed to protect against a pathogen normally found in the blood or the lymphatic fluid. For other parasites, for example, those of intestinal lumen or those inhabiting the lungs, this route of administration may reduce vaccine efficacy because it does not produce the necessary mucosal immunity. Ideally, a vaccine will mimic a normal infection as closely as possible, and inducing immunity at the normal portal of entry for the parasite is an important consideration.
Epstein–Barr virus-positive diffuse large B-cell lymphoma features disrupted antigen capture/presentation and hijacked T-cell suppression
Published in OncoImmunology, 2020
Xiang-Nan Jiang, Bao-Hua Yu, Wan-Hui Yan, Jimmy Lee, Xiao-Yan Zhou, Xiao-Qiu Li
B cells may modulate immune function through various means. They may function as antigen-presenting cells by capturing antigens via the BCR and presenting them to T cells through MHC II.4 Antigen capturing also triggers the BCR signaling cascade to help maintain B cell survival and differentiation. In addition to antigen presentation, B cells can also express PD-L1 to suppress T cell function and maintain immune homeostasis5 These immune-regulatory properties may be retained during B cell transformation and hijacked by the malignant cells as a survival mechanism. In particular, B cell infected with EBV often show disrupted function and differentiation, such as abnormal plasmacytic differentiation and aberrant expression of latent membrane protein 1 (LMP1).6,7 We hypothesize that EBV infection may also cause changes in the immunomodulatory activities of transformed B-cells, including antigen capture, antigen presentation, and T-cell suppression in EBV+ DLBCL, leading to the aggressive phenotype observed clinically. Here we compare tissue samples from EBV+ and EBV- DLBCL patients to determine if EBV+ DLBCL has altered BCR activity or aberrant expression of MHC II and PD-L1.
The immunophenotyping of different stages of BK virus allograft nephropathy
Published in Renal Failure, 2019
Ping Li, Dongrui Cheng, Jiqiu Wen, Xuefeng Ni, Xue Li, Kenan Xie, Jinsong Chen
Virus-specific T cells can recognize cells presenting viral epitopes on the cell surface via major histocompatibility complex (MHC) molecules [38]. Classically, CD8+ T cells recognize and destroy infected cells displaying viral peptides presented by MHC class I molecules, whereas CD4+ T cells scan viral epitopes presented by MHC class II molecules on antigen-presenting cells such as macrophages, B lymphocytes and dendritic cells. On the other hand, activated T lymphocytes regulate the proliferation, differentiation and immune function of B lymphocytes and macrophages by secreting a variety of cytokines to control viral infection, such as IL-2 and IFN-γ. Therefore, T lymphocyte-, B lymphocyte- and mononuclear macrophage-mediated immune responses are involved during BKV infection in renal allografts and these immune components interact intimately.
Axicabtagene ciloleucel for the treatment of relapsed or refractory follicular lymphoma
Published in Expert Review of Anticancer Therapy, 2022
CD4+ and CD8 + T-cells are predominantly responsible for the process of immunosurveillance of cancer cells. A hallmark of tumorigenesis is immunoediting, a process of tumor cell selection by the immune system for clones capable of escaping immune pressure. Immune escape includes genetic and epigenetic changes that result in (1) alterations in tumor antigen expression, (2) production of factors that negatively regulate T-cells, (3) changes to the tumor microenvironment to upregulate immune cells such as regulatory T-cells and myeloid-derived suppressor cells and (4) downregulation of MHC molecules [45–47]. CD8+ and CD4+ lymphocytes require MHC class I and II, respectively, to recognize tumor antigens in the same fashion as they would foreign peptides by antigen presenting cells.
Related Knowledge Centers
- Antigen Presentation
- Antigen Processing
- B Cell
- Major Histocompatibility Complex
- Dendritic Cell
- T Cell
- Antigen
- Macrophage
- Cell
- T-Cell Receptor