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The Etiopathogenesis of Autoimmunity
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Howard Amital, Yehuda Shoenfeld
Both CD4+ and CD8+ T cells secrete cytokines, but the CD4+ cell subtype may be subdivided according to patterns of cytokines secretion into Th1 cells that produce interleukin (IL)-2 and interferon (IFN)-y that are critical for cell-mediated immunity and acute allograft rejection, whereas Th2 cells produce IL-4, IL-5, IL-6, IL-9 and IL-10 that promotes antibody production and humoral immunity.54 IFN-γ and IL-12 are potent enhancers of Th1 cell differentiation, while IL-4 is a potent inducer of Th2 cells and is crucial for their maturation. IL-10 suppresses the synthesis of Th1 cytokines.55-56
Vaccines
Published in Nduka Okafor, Benedict C. Okeke, Modern Industrial Microbiology and Biotechnology, 2017
Nduka Okafor, Benedict C. Okeke
Specific immunity has two components, humoral and cell-mediated immunity which are mediated by white blood cells known as lymphocytes. Humoral immunity is mediated by B-Lymphocytes, while cell-mediated immunity is brought about by T-Lymphocytes. White blood cells including lymphocytes and red blood cells are produced from stem cells in the bone marrow. The B-lymphocytes remain in the bone marrow until mature, while T-lymphocytes mature in the thymus, a small organ located above the heart.
In Vivo
Published in Nihal Engin Vrana, Biomaterials and Immune Response, 2018
T-cells are a subset of lymphocytes with a central role in the adaptive immune response. “T” stands for thymus, the organ in which the final stage of their development occurs. T-cells are especially important in cell-mediated immunity, which is the defence against tumour cells and pathogenic organisms. There are several different kinds of T-cells, which can be divided into two different general classifications: killer T-cells and helper T-cells.
Mechanistic links between vitamin deficiencies and diabetes mellitus: a review
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Tajudeen O. Yahaya, AbdulRahman B. Yusuf, Jamilu K. Danjuma, Bello M. Usman, Yahaya M. Ishiaku
Owing to the regulatory role of vitamin A on immune functions, particularly T-cell-mediated immunity, some scientists suggest that impaired vitamin A metabolism can cause autoimmunity and T1DM [19,25]. In a study, vitamin A and its derivative (all-trans retinoic acid) significantly boosted the immune system and prevented islet inflammation and TIDM by inhibiting Teff cells and increasing Treg cells mass [26]. Similarly, diabetic mice treated with 4-IU vitamin A for 16 weeks showed a significantly reduced fat mass, lipid profile, and malonaldehyde as well as increased superoxide dismutase, glutathione peroxidase, and catalase compared to the control [27]. These suggest that vitamin A supplementation may protect tissues from free radical damage and thus may reduce or prevent DM complications [27]. Vitamin A may also contribute to the synthesis of insulin and glucagon [26]. The mechanistic links between vitamin A deficiency and DM are summarized in Figure 1.
Inhibitory effect of particulate matter on toll-like receptor 9 stimulated dendritic cells by downregulating mitogen-activated protein kinase and NF-κB pathway
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Madeeha Arooj, Irshad Ali, Hee Kyoung Kang, Jin Won Hyun, Young-Sang Koh
Innate immune cells such as dendritic cells (DCs) and macrophages are key endogenous components to counteract pathogens and serve as a link between innate and adaptive immunity. Antigen-presenting cells (APCs) recognize pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) (Akira and Takeda 2004; Koo et al. 2012). Toll-like receptors (TLRs) interaction with PAMPs activates major signal transduction pathways including mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and induces cytokine production which serves as a trigger to initiate T-cell-mediated immunity (Akira and Takeda 2004). MAPKs including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 kinase play a key role in apoptosis, cell survival, proliferation, differentiation, and inflammation. NF-κB is a rapid-acting transcription factor that aids in the expression of cytokines and cell survival. Under quiescent conditions, NF-κB, a transcription factor within cytosol is coupled with specific inhibitor nuclear factor of kappa light polypeptide gene enhancer in B-cells, alpha (IκBα). Upon TLR stimulation, IκBα is phosphorylated and ubiquitinated, which leads to proteasomal degradation and translocation of NF-κB into the nucleus where it regulates transcription of various inflammatory genes including cytokines (Akira and Takeda 2004; Blasius and Beutler 2010; Koo et al. 2012).
Recommendations to maintain immune health in athletes
Published in European Journal of Sport Science, 2018
Laboratory studies where core temperature remains within 2°C of normal baseline indicate a rather limited effect of either hot or cold environments on immune function; the only possible exception is T-cell-mediated immunity that has been reported to decrease when heat is superimposed onto exercise (Severs, Brenner, Shek, & Shephard, 1996). As such, most of the available evidence from laboratory studies does not support the contention that exercising in the heat or cold poses a greater threat to immune function compared with thermoneutral conditions (Walsh et al., 2011a). It is worth noting that individuals exercising in environmental extremes (e.g. hot vs. temperate or hypoxia vs. normoxia) tend to fatigue sooner or reduce their work rate so their exposure to exercise stress in the heat (or hypoxia) tends to be self-limiting.