China
Africa
Explore chapters and articles related to this topic
The Inducible Defense System: The Induction and Development of the Inducible Defence
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Michael A. Hickey, Diane Wallace Taylor
Naive CD4 T cells are referred to as Th0 cells. Based on the differentiation signals they receive, Th0 T helper cells will differentiate into either T helper 1 (Th1) or T helper 2 (Th2). A number of factors influence whether the cell becomes a Th1 or Th2 cell. For example, low quantities of soluble antigen tend to stimulate the production of Th2 cells, whereas large amounts of insoluble particulate antigen induce production of Th1 cells, in addition, AFC have an effect on differentiation of Th0 cells. Antigens presented by macrophages tend to cause Th0 to differentiate into Th1 cells, whereas when presented by B cells, antigens tend to induce Th2 cells. As discussed below, cytokines also influence Th1/Th2 production. T helper 1 and 2 cells are referred to as effector cells because they have the ability to secrete cytokines that activate other cell types.
Toxoplasma gondii
Published in Peter D. Walzer, Robert M. Genta, Parasitic Infections in the Compromised Host, 2020
Effector cell dysfunction has also been reported in AIDS patients. Monocytes from AIDS patients are able to effectively kill T, gondii, and killing by monocyte-derived macrophages from AIDS patients can be enhanced with gammainterferon (283). Thus, the severe immune abnormalities in patients with AIDS have complicated both the serological diagnosis of toxoplasma infection and the ability to control the infection with chemotherapeutic agents.
Use of Fluorescence as a Voltage Indicator in Mononuclear Cells*
Published in Richard C. Niemtzow, Transmembrane Potentials and Characteristics of Immune and Tumor Cell, 2020
Jeffrey L. Rossio, Richard C. Niemtzow
Knowing that these subpopulations exist and that they exhibit distinct membrane surface structures, we can ask whether the activation of each of these cell populations occurs in a similar way, using changes in transmembrane potential as a measure of activation. The fluorescence activated flow cytometer can choose to look at cells bearing only certain membrane receptors, and the changes in transmembrane potential of these cells can be monitored in the presence of various activating stimuli. This type of study may provide new insights into the ways in which cells interact during immunological reactions to regulate themselves and to produce effector cells which carry out the terminal immunological functions of direct killing of invaders, activation of the phagocytes for increased clearance, production of antibody, etc. Little is known concerning the differences in activation requirements for individual lymphocyte subpopulations. The use of fluorescence methodology and transmembrane potential measurement may quickly change this situation.
The tumor microenvironment and triple-negative breast cancer aggressiveness: shedding light on mechanisms and targeting
Published in Expert Opinion on Therapeutic Targets, 2022
Natsuki Furukawa, Vered Stearns, Cesar A. Santa-Maria, Aleksander S. Popel
Once naive T cells encounter antigens binding to their T cell receptor (TCR), they differentiate into effector T cells or memory T cells. Effector cells have been functionally classified into CD4+ Th1 cells, CD4+ Th2 cells, CD4+ Th17 cells, CD4+ T follicular helper cells (Tfh), CD4+ Tregs, and CD8+ cytotoxic T cells (Figure 1). Th1 cells produce IFN-γ and TNF-α, which directly act on cancer cells to suppress growth. These cytokines activate cellular immunity and strengthen anti-tumoral immunity. On the other hand, Th2 cells secrete cytokines that activate humoral immunity such as IL-4, IL-5, and IL-13. Th2 cells promote the growth of cancer cells, and suppress anti-tumoral immunity. Th17 cells produce IL-17 to induce inflammation and are reported to facilitate cancer progression by promoting inflammation [60,61]. Tfh cells are a relatively recently discovered subtype, which promote B cell proliferation and maturation [62]. Tregs suppress immune reactions by multiple mechanisms such as the induction of apoptosis of effector T cells, production of immunosuppressive cytokines, and expression of immune checkpoint molecules [63].
Yin and yang of immunological memory in controlling infections: Overriding self defence mechanisms
Published in International Reviews of Immunology, 2022
Roshan Kumar Roy, Rakhi Yadav, Aklank Jain, Vishwas Tripathi, Manju Jain, Sandhya Singh, Hridayesh Prakash
Vaccination works on the principle of developing the immunological memory against specific pathogens. Vaccination of Poxvirus infected patients with T cell epitope generated a strong T cell response and maintained both B and T cell memory for 8–12 years [91] with antibody titres up to 75 years after secondary vaccination [95]. This indicated interdependency of memory cell formation and neutralizing antibodies for generating T and B cell memory and long-lived plasma cells in infected patients. In small pox vaccination, homeostatic maintenance of memory cells is influenced by the presence of IL-7, IL- 15, presentation of antigens by follicular dendritic cells for extended period of time, activating B cell receptor, bystander activation of TLR activation which maintains the repertoire of memory cells [96]. Further, re-stimulation of memory cells that elicit robust immunity against chronic infections is believed to inhibit/eliminate exhausted effector cells and likely to control disease more strongly [9]. Memory cells that are generated during secondary or tertiary infections over primary infection are more cytotoxic in nature. These cells express high titre of Granzyme B and have longer shelf life [97]. The finding indicates the importance of booster doses that maintain the effectiveness of vaccine for longer period.
Tracing the origins of extracellular DNA in bacterial biofilms: story of death and predation to community benefit
Published in Biofouling, 2021
Davide Campoccia, Lucio Montanaro, Carla Renata Arciola
However, in the presence of an excess of inflammatory response, tissue disruption and cellular damage can also derive from the disproportionate activation of effector cells of the immune system. This can be triggered either by the presence of foreign bodies such as implant materials and their wear debris or by unresolved biofilm-associated chronic infections. Both of these conditions can determine frustrated leukocyte phagocytosis and release into the outer space of potentially harmful chemicals, normally confined within phagosomes (Arciola et al. 2018). Thus, the large arsenal of molecules usually exploited to contain invading microorganisms or generally directed against foreign bodies poses a risk of collateral damage to surrounding tissues (Kzhyshkowska et al. 2015). Under normal conditions, the successful resolution of acute inflammation is characterized by the apoptosis of neutrophil cells and their engulfment by macrophages. Conversely, in chronic bacterial infections, neutrophil cells are thought to undergo necrosis rather than apoptosis (Cox et al. 1995).