1. I.Tillie-Leblond, et al.2005, They studied about acute asthma and reviled that substances like allergens, irritants, viruses and some triggers can induce severe acute asthma etc., which induce inflammation and provoke acute bronchoconstriction. Activated eosinophils and neutrophils are some inflammatory cells identified in the sputum and bronchial lavage (BAL or BALF ) of children and adults who attacked by severe acute asthma and shows increased levels of IL-5, IL-8, and of pro-inï¬‚ammatory mediators. These inflammatory mediators are responsible for the bronchial inï¬‚ammation, which involve small and large airways. Activated T cells are having important role in the development of severe asthma. The cytotoxic CD 4+ T lymphocyte response is associated with Asthma and CD 8+ T cells in COPD. The epithelial damage, other abnormalities of epithelial and endothelial permeability and the extensive mucus plugging which are associated with severe acute asthma are due to the persistence of inï¬‚ammatory cells in bronchi, particularly neutrophils, which are poorly respond to corticosteroids. In asthmatics, the persistence of neutrophils and of substantial pro-inï¬‚ammatory activity in bronchial fluids associated with abnormally high bronchial and epithelial permeability may cause the high level of airway resistance under mechanical ventilation.
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2. Tore Seternes et al 2001, They explain lipopolysaccharides as an important component of the cell envelope of gram-negative bacteria. The lipopolysaccharide (LPS) molecules are having three structural units; O-polysaccharide, a lipophilic lipid A component and core oligosaccharide. The lipid A portion is responsible for the typical endotoxin effects observed in mammals, such as haemodynamic changes, fever, and inflammatory intravascular coagulation and shock and represents the endotoxic component of LPS and. In several mammalian species, LPS was found to trigger macrophages to produce powerful inflammatory mediators like tumour necrosis factor alpha (TNFα), IL-1a, IL-1b and IL-6. The LPS is highly toxic and the increased production of these mediators is believed to be the direct cause of LPS toxicity.
3. A. Todo Bom et al 2006, they studied about dipeptidyl peptidase IV (DPP-IV-CD26) which is a multifunctional molecule with enzymatic and proinflammatory activities. The T-cell activation antigen CD26 is recognized as the cellular marker of DPP-IV, a membrane peptidase. DPP-IV is a multifunctional molecule which, beside enzymatic activity, exhibits several important functions. Asthmatic patients demonstrated an increased expression of DPP-IV compared to normal control subjects. This elevated level of CD26/DPP-IV in the asthma patients can result from cell activation during the inflammatory process. DPP-IV can be involved in the catabolism of peptides implicated in asthma pathology.
4. Ingrid De Meester et al 1999, they studied the costimulatory properties of CD26 extensively and sagest complex nature of this molecule. In general, the activation of T cells requires at least two signals. The first signal is provided by stimulation of the common T-cell receptor (TCR) complex by specific peptide antigen. The second is delivered by triggering co-stimulatory surface molecules (eg: CD26). The nature of its substrates, together with its regulated expression and non-enzymatic interactions characterize active participation of CD26 in the immune, nerve and endocrine networks in human physiology.
5. Roger Yazbeck et al 2009, DPP-IV is expressed in immune cells and represent novel pharmacological targets for inflammatory diseases. DPP-IV has a number of regulatory functions, including the hydrolysis of several peptide hormones and chemokines and a co-stimulatory effect on T-cell activation via its signaling function. The emergency of synthetic inhibitors if DPP activity has provided a novel therapeutic option for several human diseases, including type 2 diabetes, arthritis and IBD. The approval of the DPP-IV selective inhibitors Januvia and Galvus for therapeutic use in patients with type 2 diabetes highlights the safety, tolerability and efficiency of this class of drugs.
6. Jutta Schade et al 2008, The expression of DPP-IV/CD26 alter T cell recruitment to airways and lungs in an experimental rat asthma model. The gene of the structural homologous DPP-10 is having a susceptibility locus for asthma in humans. Result also shows the increased DPP-IV enzymatic activity in the bronchoalveolar lavage fluid and parenchyma. The increased expression of DPP-IV, primarily found in the bronchial epithelium of the asthmatic's airways. From the study they also found increased DPP-IV- like activities in the lung and BAL fluid of murines, an elevated number of activated T-cells after asthma induction. They defined asthma as a disease of the airways which require, a site-specific expression and regulation of DPP-IV and the DPP-IV-like peptidases in the whole lung and especially in the bronchi.
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7. C. Kruschinski et al .2005. they describe that by the modulation of cell adhesion and T cell activation the CD26 truncates several chemokines as well as neuropeptides and inï¬‚uences immune responses. They suggesting an involvement of CD26 in asthmatic and airway inflammation. Therefore, Fischer 344, Brown Norway and Lewis rat strains, which differ in their CD26-like enzymatic activity, were studied and compared using an asthma model. They included additionally two CD26-deï¬cient mutant F344 rat sub strains and compared to the wild-type F344 sub strain. CD26 is an important molecule necessary for constituting a full-grown T cell component in response to antigens such as OVA. CD26 is an important activation marker for T lymphocytes, they found decrease in T cell recruitment in CD26 deficient rats. There for significant differences in inflammatory cell numbers occurred in their study.
8. K. Ohnuma et al 2005. Meanwhile, recombinant soluble CD26/DPP-IV molecule up-regulates expression of CD86 on antigen presenting cells (APC), leading to greater APC-T cell interaction and enhanced T cell proliferation, with important implications for immunoregulation . T-cell differentiation antigen, CD26 is preferentially expressed on a specific population of T lymphocytes, the subset of CD4+, CD8+ memory T cells, and is up-regulated after T cell activation. Its expression on activated T cells, and various other evidence have studied to demonstrate that CD26 is functionally related with T cell signal transduction processes, which are essential of transmitting signals relating to T cell activation. CD26 is also serves as a functional collagen receptor having an important role in T cell activation, as well as having a potential role in thymic ontogeny. The enzymatic activity of CD26 appears to be very important in enhancing cellular responses to external stimuli.
9. Robert A et al 2002. They found the polymorphonuclear leukocyte- neutrophils, which are having key role in the secondary host defense system actively participate in the pathogenesis of chronic lung disease. The neutrophil also shows significant participation in the experimentally induced COPD and can reproduce many of the features of patients with this syndrome. For instance, the aerosol administration of LPS to murine can produce extensive epithelial damage. The neutrophil is short-lived and transient cells which are recruited from the circulation to the airways in the lung during inflammation (in the absence of pneumonia or interstitial lung disease). Pathological studies have indicated the elevated number of neutrophils in the bronchial tissue of patients with COPD and reveled the role of these cells relates to the severity of airflow obstruction. Furthermore, neutrophils are found to be increased in the airways of smokers and patients with COPD, chronic bronchitis etc. The neutrophils are playing major role in many of the features of COPD. The neutrophils are the only cells that have been shown directly to cause all of the pathological features of COPD. The individual pathological features of COPD can be determine by the site of neutrophil recruitment occurs.
10, Saint-Mezard P et al 2004 says that hapten specific T cells mediates delayed-type hypersensitivity reactions like allergic contact dermatitis (ACD) and contact hypersensitivity (CHS). The skin dendritic cells expose haptenated peptides during the sensitisation phases which intern activates both CD4+ and CD8+ T cell precursors in the draining lymph nodes. Subsequent hapten skin exposure induces the recruitment of T cells at the site of challenge. This induces apoptosis and inflammatory signals of epidermal cells, causes the development of a skin inflammatory infiltrate and of clinical symptoms.
11, S.L. Seneviratne et al 2006 Higher percentages of T cells expressed the skin homing marker dermatitis patients compared with non-atopic healthy controls. In addition, CD4+ and CD8+ T cells from our patients showed increased expression of markers of activation, adhesion and apoptosis, and preferential chemokine receptor usage. Levels of expression of differentiation markers differed between dermatitis patients and healthy controls.