Allergen Induced Treg Response On The Peripheral Blood Mononuclear Cells ( Pbmcs ) Of Patients With Nasal Polyposis

It was important to discuss with Lisa during consultation family history that could provide additional support for my final diagnostic conclusion .Going thru such topic area Lisa explain that her husband James dad was suffering with atopic eczema since childhood .This was quite an important piece of information as such conditions like atopic eczema ( dermatitis ) are hereditary conditions often (National Eczema Society ,2011).Atopic dermatitis or eczema is a chronic skin disorder inflammatory with pruritic skin that appears mostly on the face ,neck ,bends of the arms or legs caused by the malfunction in the skin barrier( NICE,2013).

B.J.was exposed to cats, thus causing an acute asthma attack. Patient being exposed to cat fur is what caused his allergic reaction. IgE antibodies cause allergic reactions, these cells are mainly attached to mast cells that lie in the lung interstitium in close association with the bronchioles and small bronchi. Once BJ breathes in the fur, to which he is sensitive to, the pollen reacts with these mast cells and thus causing these cells to release histamine. Which causes localized edema in the bronchioles as well as thick mucus. This causes the spams in the bronchilar smooth muscle which cause airway resistance. In return causing an acute asthma attack.

The ironic thing about allergens is that most aren’t harmful to the body, but this doesn’t stop the immune system for mistaking them for foreign bodies, which is why it decides to fight back. Our immune systems are amazing things. They create proteins to fight disease, which are known as antibodies. These antibodies try to battle it out against the antigens. Once our immune system creates certain antibodies, they’ll recognize the same intruders again and protect our bodies automatically year in year

Based on the patient’s culture and other characteristics, the physician should avoid using medical or technical terms like “allergic”. This is because it caused problems between the physician and the interpreter.

The specific cause of Atopic dermatitis is not known. However, the disease is said to be associated with people from families with a history of allergies such a family with people suffering from

Atopy: Type I hypersensitivity. Atopy is caused by allergens which cause the production of IgE to be high to defence against the allergens. The allergens have the ability to stimulate type I hypersensitivity reaction in all of the sensitized individuals when it is inhaled or ingested. Therefore since there is a production of IgE and allergens caused the response, it is type I

Allergic Asthma is a chronic disorder that can impact the patient quality of life. This diagnosis is made through a

There are three main players in the development of allergies: immunoglobulin E (IgE), mast cells and histamine. IgE is a specific type of antibody that has a significant role in the development of allergies; IgE is able to bind to both allergens and to mast cells, cells that mediate inflammatory responses such as hypersensitivity and allergic reactions (3). Once IgE binds to an allergen, the allergen releases T cells to stimulate B cells, developing into plasma cells that produce and release more antibodies (4). Once

The pathology of asthmatic symptoms is quite complex, and includes the effects of mast cells, eusinophils, T cell lymphocytes, mactrophages, neutrophila, and epithelial cells, which collectively lead to inflammation. Pathologic qualities of asthma include goblet cell hyperplasia leading to mucus overproduction, basement membrane thickening with subepithelial fibrosis, desquamation of the airway epithelium, bronchial smooth muscle hyperplasia, and cellular infiltration with lymphocytes, neutrophils, and eosinophils. Airflow obstruction is caused by the smooth muscle constriction around airways, leading to wheezing, coughing, and chest tightness. Exposure to allergens, irritants (eg smoke), and viral infections can also

Although the role of the sex hormones is unclear, there is research suggesting females that have early menarche, have a higher incidence of developing asthma (Grossman & Mattson Porth, 2014). In regards to ethnicity, African Americans and Puerto Ricans have the highest incidence of asthma. This trend is resultant of genetic disposition and/or socioeconomic factors influencing a higher rate in these populations (American Lung Association [ALA], 2010). A child with a parent having asthma is three to six times more likely to develop asthma (Benaroch,

Allergic rhinitis” is very comnon disease affects about 5-22% from world population with about 9% of all visits to physicians” for the allergic diseases [1].

Over the last thirty to forty years, the incidence of atopic diseases has increased. Atopic diseases are considered the “classic allergic” diseases like dermatitis, allergic rhinitis (hay fever) and asthma. Atopy is considered the ability to produce IgE (Immunoglobulin E, which is a type of antibody that can be found in small amounts in the body but plays a major role in allergic diseases) in response to common environmental proteins like house dust mites, grass pollen, and food allergens. This increase in diseases led to research into what may be the cause. Genetic predisposition is a key factor in one’s susceptibility to atopic diseases. However, researchers concluded that this particular increase had occurred in too short of a time frame

A single mast cell can be coated with different types of IgE antibodies, each of which bind to a different allergen.1 When an allergen trigger enters the body it is detected by the IgE antibodies, which then triggers the release of histamine from the mast cells.1 In addition to histamine, a slow reactive substance of anaphylaxis (SRS-A) is also released, which “induces prolonged and profound contraction of smooth muscle, especially of the respiratory airways”.1 Hence, the mast cells release chemicals that characterise the immediate hypersensitivity

Levels may continue to rise over many months of maintenance immunotherapy, and elevated levels may persist for many years after immunotherapy is discontinued. The generation of allergen-specific regulatory T and B cells (Tregs and Bregs) and suppression of allergen-specific effector T cell subsets and innate lymphoid cells (ILCs). During allergen immunotherapy, allergen-specific Treg cells are generated, which produce IL-10 and transforming growth factor-beta (TGF-beta), cytotoxic T lymphocyte antigen 4 (CTLA-4), and program death molecule 1 (PD1). These cytokines suppress proliferative and cytokine responses against major allergens. IL-10 reduces proinflammatory cytokine release from mast cells, eosinophils, and T cells, and elicits tolerance in T cells by means of selective inhibition of the CD28 costimulatory pathway. The transcription factor forkhead box protein 3 (FOXP3) is required for the development and function of naturally occurring T regulatory cells, and its expression is sufficient to convert nonregulatory CD4+CD25+ T cells into T cells with regulatory activity. FOXP3 expression negatively correlates with levels of IgE, eosinophilia,

Chronic rhinosinusitis with or without nasal polyps is an inflammatory disorder of the nose and the paranasal sinuses characterized by two or more symptoms of nasal congestion or anterior/posterior nasal discharge with either facial pain or reduced/absent sense of smell, lasting more than 12 weeks and either endoscopic signs of polyps, mucopurulent discharge and/or edema primarily in middle meatus or computed tomography (CT) changes with mucosal changes within the osteomeatal complex and/or