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Major Histocompatibility Complex and Autoimmune Disease
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Ursula Holzer, Gerald T. Nepom
For inflammatory bowel disease, such as Crohn’s disease and ulcerative colitis, a genetic predisposition is strongly supposed.45 The genes in the HLA region are candidate genes contributing to susceptibility for these diseases as they encode functionally relevant gene products in the gut epithelium and they colocalize to a linkage region on chromosome 6.46,47 The association with HLA-DRB1*0103 and extensive ulcerative colitis has been widely replicated.46,48,49 For Crohn’s disease, an association with DR7, DRB3*0301 and DQ4 were found.49 Nevertheless, the contribution of HLA-DQ genes is less clear-cut in these diseases and the association of HLA-DR molecules in the pathogenesis of ulcerative colitis may be threefold larger compared with Crohn’s disease.49 Non-HLA genes, such as NOD2 (a family of cytosolic proteins that regulate the host response to pathogens), are known to be contributory in this disease, as are environmental agents and bacterial gut flora, so the exact role for HLA genes in disease initiation or progression is not clear.
Major Histocompatibility Complex Binding and Various Health Parameters Analysis
Published in Adwitiya Sinha, Megha Rathi, Smart Healthcare Systems, 2019
Abhinav Gautam, Arjun Singh Chauhan, Ayush Srivastava, Chetan Jadon, Megha Rathi
Stabilized matrix method (SMM) is the key algorithm that is being used for predicting the bond length between the peptide and the MHC. SMM is one of the most sought after immunology analysis algorithm, because it compares its result by using data from 14 human MHC Human Leukocyte Antigen – DR isotype (HLA-DR) and 3 Mouse Alleles (H2-IA). It has been proved to be better than other algorithms like Gibbs Sampler, Support Vector Machine - Regression (SVR)MHC, and Major Histocompatibility Prediction (MHCpred) methods (Nielsen et al., 2007). SMM has been trained and tested for the largest data set on HLA-DR and H2-IA (Nielsen et al., 2007). The SMM method generates quantitative models of sequence specificity of biological processes, which in turn can be used to predict and understand these processes (Peters & Sette, 2005). SMM can eventually help in better understanding and finding the exact epitopes of a given pathogen, thereby leading to a faster development of the vaccine.
Cellular Biology in Tissue Engineering
Published in Joseph W. Freeman, Debabrata Banerjee, Building Tissues, 2018
Joseph W. Freeman, Debabrata Banerjee
Histocompatibility antigens responsible for the most vigorous allograft rejection reactions are located on the major histocompatibility complex (MHC). They are inherited as haplotypes or two half sets (one from each parent). This makes a person half identical to each of his or her parents with respect to the MHC complex. Every person expresses 6 MHC1 alleles (HLA-A, HLA-B, HLA-C—one from each parent) and at least 6 MHC2 alleles (HLA-DQ, HLA-DP, HLA-DR—one from each parent). The MHC molecules are divided into two classes. The class I molecules are normally expressed on all nucleated cells, whereas the class II molecules are expressed only on the professional antigen-presenting cells (APCs), such as dendritic cells, activated macrophages, and B cells. The physiological function of the MHC molecules is to present antigenic peptides to T cells. The class I molecules are responsible for presenting antigenic peptides from within the cell (e.g., antigens from the intracellular viruses, tumor antigens, self-antigens) to CD8 T cells. The class II molecules present extracellular antigens such as extracellular bacteria to CD4 T cells. The activation of T cells is dependent on two essential signals. In addition to the bond formed by the MHC and the TCR, there is also the need for a secondary co-stimulatory response. This secondary response occurs when a bond is formed between the molecule B7 and CD28 on APCs and Helper T cells, respectively.
Magnetic stimulation of the angiogenic potential of mesenchymal stromal cells in vascular tissue engineering
Published in Science and Technology of Advanced Materials, 2021
Ana C. Manjua, Joaquim M. S. Cabral, Carla A. M. Portugal, Frederico Castelo Ferreira
For immunophenotypic characterization, cells were tested by flow cytometry after 5 days, with and without magnetic exposure, for expression of cell surface markers indicative of MSC using a panel of mouse anti-human monoclonal antibodies (PE-conjugated) against: CD73+, CD90+, CD105+, CD14−, and human leukocyte antigen HLA-DR− (all from Biolegend, California, U.S.). The cells were incubated with the monoclonal antibodies for 15 min in the dark at room temperature. Then, cells were washed with PBS and fixed with 4% paraformaldehyde (Sigma-Aldrich). Appropriate isotype controls (IgGy1 and IgGy2b) were also prepared. A minimum of 7,000 events were collected for each sample, and Cell Quest (Becton Dickinson, New Jersey, U.S.) and FlowJo® (LLC) software were used for acquisition and analysis, respectively.
Metabolomics approach to biomarkers of dry eye disease using 1H-NMR in rats
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Jung Dae Lee, Hyang Yeon Kim, Jin Ju Park, Soo Bean Oh, Hyeyoon Goo, Kyong Jin Cho, Suhkmann Kim, Kyu-Bong Kim
Inflammation of the ocular surface and increased osmotic pressure of the tear film play an important role in DED development (Li et al. 2017; Research Subcommittee of the International Dry Eye WorkShop 2007). In general, DED is diagnosed based upon ocular surface staining, noninvasive tear breakup time (TBUT) evaluation, and osmotic pressure measurement (Inomata et al. 2018). In addition, the common features of DED include inflammation of the surface of the eye and major tear glands. Previous investigators noted that inflammatory markers such as human leukocyte antigen-DR isotype (HLA-DR) and interleukin (IL)-1β were detected in the conjunctiva (Brignole et al. 2000; Narayanan, Miller, and McDermott 2006). DED is attributed to the death of conjunctival epithelial cells due to apoptosis or cytotoxicity (Baudouin 2001; Rivas et al. 1992; Stern and Pflugfelder 2004). Various investigators reported increased tear osmotic pressure induced overexpression of pro-inflammatory cytokines and chemokines such as tumor necrosis factor-alpha (TNF-α), IL-1, and IL-6 (Li et al. 2004, 2006, 2017; Yoon et al. 2007). However, the diagnosis and treatment of DED is difficult because the correlation between reported symptoms and clinical signs is not clear (Sullivan et al. 2014).
Head Transplantation: The Immune System, Phantom Sensations, and the Integrated Mind
Published in The New Bioethics, 2018
In the vocabulary of immunology, the expressions ‘self’ and ‘non-self’ may be thrown about with such abandon that these expressions are easily used to conflate issues in the broader language of personhood. It is important, therefore, to remember that when these expressions are used in immunology they are concerned with molecular recognition. The immune system consists of a network of molecular and cellular systems that undertake the critical function of differentiating that which is described in immunological terms as ‘self’ from that which is ‘non-self’ and imposes a level of identity on cells and tissues that must be considered in any transplant operation. These systems are typically grouped under the general headings ‘innate immunity’ and ‘adaptive immunity’ and involve more than 1600 genes (Abbas et al. 2005). Underpinning the adaptive responses are protein complexes brought together under the general heading the ‘major histocompatibility complex’ (MHC), also referred to as ‘human leukocyte antigens’ (HLA) when specific human MHC proteins are being referenced. MHC antigens are grouped into a number of classes, which, in broad terms, might be said to share function, insofar as they may, for example, process proteins into small chunks that are then presented to the T-cell receptor (TcR) on T-cells (La Gruta et al. 2018). They do, however, differ structurally from each other and serve different specific tasks. One of these, MHC class I (MHC-I, of which HLA-A, HLA-B, and HLA-C are members), is normally present on all nucleated cells, and subclasses of this are expressed within the first three days of the life of a human embryo (Wang et al. 2009). The absence MHC-I expression on cells leaves them vulnerable to destruction through the action of the MHC-I-sensing ‘killer cell immunoglobulin-like receptor’ (KIR), present on subpopulations of immune cells known as Natural Killer (NK) cells and subsets of T-cells. An important exception to this is the red blood cell population. Red cells do not express MHC-I, instead escaping destruction by NK cells through the expression of another protein, CD47 (Wang et al. 2010). Alongside the MHC-I, the expression of MHC class II (MHC-II, comprising HLA-DP HLA-DQ and HLA-DR in humans) and minor histocompatibility antigens (MiHA) like the male-specific H-Y antigen. The result of this is that, by the 8-cell stage of the embryo, the embryo is immunologically reactive with respect to the mother and its continued development requires the induction of immunological tolerance within the womb to prevent fetal rejection and miscarriage (Fernandez et al. 1999; Larsen et al. 2013; Colucci 2017).