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T Cells in Asthma

T Cells in Asthma

Asthma is a chronic inflammatory respiratory disorder (Khan, 2020). Asthma is characterized by variable airflow limitation and airway hyperresponsiveness, both due to the exaggeration of the contractile response of the airways to antigen stimuli. The diseases affect the airways, resulting in intermittent and reversible blockage. The blocking or narrowing of the airways causes the patient to experience tightening of the chest and rib cage, wheezing, coughing, and shortness of breath. Clinical research on Asthma has increasingly made it clearer that it’s a heterogeneous inflammatory disorder of the airways in relation to immunopathology and clinical phenotypes (Kuruvilla et al., 2019). Asthma has a strong genetic association based on the role of RNA in the regulation of T-cell function (Huang & Xiong, 2020). However, substantial evidence portrays atopic Asthma as an immune-mediated disease (Kaur & Chupp, 2019). The body’s immune responses to environmental, aeroallergens and other pathogenic and non-pathogenic elements in inhaled air are associated with the inflammatory response leading to Asthma. Besides other cellular elements that may contribute to asthmatic reactions to inhaled aeroallergens, it is majorly suggested that T cells have a vital role in the development of inflammatory responses in asthma (Wiest et al., 2018). The diverse array of T cell phenotypes in the lungs and the airways and the response of the T cells to exposure to allergens and infections are responsible for the broad-ranging inflammatory reactions leading to the various endotypes of Asthma and the need for diverse asthma treatments (Kuruvilla et al., 2019). Due to asthma’s heterogeneity, over 339 people globally suffer from one type of asthma endotype and phenotype (León & Ballesteros-Tato, 2021).

Recent clinical research focused on the T-cells’ role in Asthma and has contributed to understanding the complex inflammatory processes involved in the development of Asthma. These clinical studies contribute to developing and improving therapeutic approaches and the prevention of Asthma. This paper reviews T-cells in Asthma. The review will cover the role T-cells play in the development of allergic Asthma. The review will also expound on how T-cells contribute to the exacerbation of pathophysiological features of Asthma.

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Role of T-Cell Response in the Pathophysiology of Asthma

The pathogenesis of asthma is predominantly characterized by an elevated action of T cells, mainly the CD4+ Th2 cells’ response to antigens. The major pathophysiological features of Asthma include inflammation of the airway and airway remodelling, secretion of mucus and airway hyperresponsiveness (AHR). These pathophysiological features of Asthma are associated with the underlying immunopathological factors of Asthma.

T cells are a type of lymphocyte critical to the human immune system and activate an adaptive immune response in case of an infection. T cells have a T-cell receptor on their cell that makes it a distinguishing feature from other lymphocytes. The T cells produce a number of cytokines that play a role in exacerbating asthmatic symptoms and inflammation during Asthma (Bryant & Muehling, 2022). The foreign antigens, including allergens, pathogens, and other particulate matter that enter the lung airways, are picked up by the antigen-presenting cells (APC). The APC processes the antigens and provides accessory signals that control the activation and response of the T cells towards cognate peptide-major histocompatibility complex (MHC II complex) molecules. The innate and adaptative immune responses are activated through exposure to allergens, APC action, and eosinophilic airway inflammation. The eosinophilic airway inflammation and the MHC II complex further activate allergen-specific T cells and increase their presence in the airways. The activated T cell subsets include the T-helper-1 (Th1) and T-helper-2 (Th2). These Th2 cells are central in antigen response and initiate the asthmatic inflammatory response (Kuruvilla et al., 2019).

The availability of sufficient co-stimulatory signals supports the cognate interaction between the allergen-specific T cells with the peptide-MHC II complex on APC that mediates the activation of the Th2 cells. The Th2 cells have a significant role in the pathogenesis of atopic Asthma, including the generation and infiltration of innate lymphoid cells (ILC2s) into the airways. ILC2s constitute a group of lineage-negative innate lymphocytes (ILs) that differ from T and B cells (Kuruvilla et al., 2019). The ILC2s are not involved in the activation of the allergen-specific T cells. However, the ILC2s are responsible for producing the ILs that mediate the Th2-mediated allergic reaction and asthmatic inflammation, including IL-3, IL-4, IL-5, IL-13, and IL-33 (Khan, 2020). Further, the T cells incite the production of immunoglobulin (Ig) E antibody by B-lymphocytes, which also play a role in allergic asthma pathophysiology.

T Cells- and Th2-Mediated Asthmatic Inflammation and Pathophysiological Features of Asthma

Allergen-induced immune response activates the Th1 and Th2. The Th1 plays an immunosuppression role. The Th2 cells, central to the immune response, induce an allergic inflammation to counter the allergens. In allergic inflammation, the Th1-type cells act as immunosuppressors during immune responses, while Th2-type cells are essential in allergic inflammation. During Asthma, the immune response is mostly unregulated and creates an unbalanced homeostatic function. The Th1 subset type cells secrete regulatory cytokines, such as IL-10 and TGF-βare, which regulate the immune response of the Th2 type cytokines, thereby maintaining tolerance during asthma inflammation (Khan, 2020).

As noted earlier, the clinical manifestations of atopic asthmatic inflammation include airway inflammation, mucus secretion, and airway hyperresponsiveness (AHR). Asthma’s pathophysiological features manifest as a result of T cells and Th2 type-mediated immune response processes. From a pathological view, asthma progression includes airway epithelium hyperplasia, metaplasia of the mucus cell, increased airway smooth muscle mass, and increased deposition of extracellular matrix proteins (Khan, 2020).

According to Khan (2020), inflammation of the airways during asthmatic inflammation is mediated by the overproduction of the Th2-type cells, IgE, and eosinophils. During the immune response, the Th2 cells proactively generate a high number of IL-4, IL-5, and IL-13 (Kuruvilla et al., 2019). For instance, IL-5 production favours and initiates the maturation of the eosinophils within the bone marrow and the eventual release of the eosinophils into the bloodstream to counter antigens in the lungs and airways. The release and activation of a large number of eosinophils within the lung induce bronchial hyperresponsiveness and enhanced differentiation of the goblet cells, leading to increased mucus secretion. The airway macrovascular remodelling process is a complex mediated by the T and B cells, macrophages, eosinophils, and other accessory fragments mediated inflammation that induces tissue injury and extracellular matrix (ECM) proteins (Persson, 2019). The ECM proteins also available in specific asthmatic airways contribute to the hyper-responsiveness of the airways and modulate specific airway remodelling (Ito et al., 2019). Airway macrovascular remodelling eventually impairs the functioning of the lung airway system, aiding the progression of Asthma (Hough et al., 2020). The over-expression of cytokines such as IL-1, IL-5, IL-13, and IL-4 within the airways leads to the resistance to asthma medications available today, including inhaled corticosteroids (ICS) (León & Ballesteros-Tato, 2021).


Asthma is among the most common inflammatory chronic diseases. Extensive primary research agrees that Asthma is a Th2 cell-associated inflammatory disease. The research also provides deeper insights into the role of Th2-type cytokines, including IL-4, IL-5 and IL-13, in the pathogenesis of Asthma. The immune response involving T cells due to the entry of allergens into the lung airways causes inflammation in the airways, leading to narrowing airways. Based on existing literature, the immune response of the T cells and the immune suppression of the T cells functions by the T-reg cells plays a part in the progression of atopic Asthma. However, the multiple T cell phenotypes associated with Asthma make it hard to develop a single treatment regimen for the disease. There is a need to focus on future research to determine whether immunosuppression of the T cell responses aids in regulating asthmatic inflammation or in the progression of the disease. Further, the association between Asthma and extrinsic allergens and the role of the T cells subset, Th2, in Asthmatic inflammation and disease progression is well documented. However, research has described Asthma as largely heterogeneous, with multiple phenotypes and endotypes (Kaur & Chupp, 2019; Kuruvilla et al., 2019). With some evidence available on the role of other T cells besides the Th2 subset in the development of Asthma, there is a need to expand the knowledge and identify the other unconventional T cells that contribute to the development of Asthma. Bryant and Muehling (2022) recommend the study of unconventional T-cell types, including gd T, iNKT, and MAIT cells and their role in the progression of Asthma. In conclusion, as Asthma is notoriously heterogeneous, expanding knowledge of the various phenotypes and endotypes of Asthma can help develop efficient medications.


Bryant, N., & Muehling, L. M. (2022). T-cell responses in asthma exacerbations. Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology.

Hough, K. P., Curtiss, M. L., Blain, T. J., Liu, R. M., Trevor, J., Deshane, J. S., & Thannickal, V. J. (2020). Airway Remodeling in Asthma. Frontiers in Medicine, 7, 191.

Huang, Z.-L., & Xiong, W.-N. (2020). [Research progress of non-coding RNA in regulating the function of T cells in Asthma]. Sheng Li Xue Bao : [Acta Physiologica Sinica], 72(5), 586–596.

Ito, J. T., Lourenço, J. D., Righetti, R. F., Tibério, I. F. L. C., Prado, C. M., & Lopes, F. D. T. Q. S. (2019). Extracellular Matrix Component Remodeling in Respiratory Diseases: What Has Been Found in Clinical and Experimental Studies? Cells 2019, Vol. 8, Page 342, 8(4), 342.

Kaur, R., & Chupp, G. (2019). Phenotypes and endotypes of adult asthma: Moving toward precision medicine. Journal of Allergy and Clinical Immunology, 144(1), 1–12.

Khan, M. A. (2020). Regulatory T cells mediated immunomodulation during Asthma: a therapeutic standpoint. Journal of Translational Medicine 2020 18:1, 18(1), 1–8.

Kuruvilla, M. E., Lee, F. E. H., & Lee, G. B. (2019). Understanding Asthma Phenotypes, Endotypes, and Mechanisms of Disease. Clinical Reviews in Allergy & Immunology, 56(2), 219.

León, B., & Ballesteros-Tato, A. (2021). Modulating Th2 Cell Immunity for the Treatment of Asthma. Frontiers in Immunology, 12, 268.

Persson, C. (2019). Airways exudation of plasma macromolecules: Innate defence, epithelial regeneration, and Asthma. The Journal of Allergy and Clinical Immunology, 143(4), 1271–1286.

Wiest, M., Upchurch, K., Yin, W., Ellis, J., Xue, Y., Lanier, B., Millard, M., Joo, H. M., & Oh, S. K. (2018). Clinical implications of CD4+ T cell subsets in adult atopic asthma patients. Allergy, Asthma and Clinical Immunology, 14(1), 1–14.


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