Contact Hypersensitivity

Allergic contact dermatitis occurs when a person’s body immune system is sensitive to a substance, it causes an immune skin reaction. These substances include poison ivy, antibiotics, nickel (up to 10% of women are allergic to it) etc. allergic contact dermatitis develops over a period and once the person is allergic to a substance, the slightest contact amount causes reaction.

binds with the surface IgE and mediators are released (Story, 2012). TH2 cells are involved

The function of the epidermis to prevent entry of pathogens is disturbed, which leads in dry skin. The dermatopathological signs associated with Atopic dermatitis include spongiosis, hyperkeratosis, exocytosis, parakeratosis, eosinophilis and lymphocytic infiltrates (Williams, 2005). People with the Atopic dermatitis condition produce immunoglobin E even with just trigger from low amounts of allergens. Rhinoconjunctivitis and asthma are some of the symptoms associated with Atopic dermatitis. In infancy, an individual may develop a desquamation that is yellow in color on the scalp (Darsow et al., 2010). The rashes spread to the face of the individual and later to the

Contact dermatitis: Type IV hypersensitivity. Contact dermatitis occurs when a substance like soaps, plants etc. comes into contact with the skin. This causes a red, itchy rash. When the allergen chemical gets absorbed into the skin, an immune response occur. The allergens are recognized by the antigen presenting cells of the epidermis which are then presented to T cells for proliferation and clonal expansion. Thus resulting in an immune response. The immune response occurs within 48 hours after exposure. Therefore since contact dermatitis is cell mediated and not antibody mediated it is a type IV hypersensitivity.

Treatment of allergic diseases represents a vast source of global healthcare costs. Allergies affect hundreds of millions of people worldwide with the number of cases continuing to increase at an alarming rate. The study of allergies and how genes and environmental factors affect them are ongoing. Currently, allergen immunotherapy is one of the few viable forms of treatment recognized. However, an alternative method of therapy utilizing microbes may be on the horizon.

The APC’s, when activated, migrate to the lymph nodes and interact with T and B cells to initiate the immune response. Antigens gets broken down to peptide fragments and presented on the cell surface by major histocompatibility complex 2 molecules (MHC-II) to T cell receptors. For this reaction to be significant, a co-stimulatory signal is also needed to increase interleukin-2 (IL-2) production. IL-2 is a T cell growth factor that is necessary for T cell activation. When T cells are activated the Th2 cytokines are produced. In particular, IL-4 causes CD4+ cells to adopt Th2 properties and stimulates B and T cell proliferation, along with the upregulation of MHC-II expression. IL-4 also causes B cells to undergo class switching and produce IgE that is specific to the allergen. The IgE binds to the Fc receptors on mast cells and basophils and upon re-exposure to the allergen, mediators, mainly histamine, leukotrienes, and cytokines, are released from preformed granules in the cell.4 Another cytokine, IL-5, activates eosinophils and has a stimulatory role on B cell growth. Eosinophils, along with neutrophils, basophils, T cells, and macrophages produce more cytokines and inflammatory mediators, which keeps the inflammatory response active. This is known as the late phase of an allergic reaction, which is responsible for the persistent chronic symptoms of allergies. Chronic symptoms include swelling of the nasal

Allergen immunotherapy alters the immune system's reaction to causative allergens and induces long-lasting tolerance to these allergens. Subcutaneous immunotherapy has been in

Human TCMs are CD45RO+ memory cells that constitutively express CCR7 and CD62L , two receptors that are also characteristic of naïve T cells, which are required for cell extravasation through high endothelial venules (HEV) and migration to T cell areas of secondary lymphoid organs (Campbell et al., 1998). When compared with naïve T cells, TCMs have higher sensitivity to antigenic stimulation thus providing more effective stimulatory feedback to dendritic cells (DCs) and B cells (Forster et al., 1999). Following TCR triggering, TCMs produce mainly IL-2, but after proliferation they differentiate to effector cells and produce large amounts of IL-4 of IFN-γ (Lanzavecchia and Sallusto, 2000).

Jamora C. (2010). Development of atopic dermatitis-like skin disease from the chronic loss of epidermal caspase-8. Proceedings Of The National Academy Of Sciences Of The United States Of America, 107(51), 22249-54. doi:10.1073/pnas.1009751108

Its pathogenesis may include disrupted epidermal barrier function, immune dysregulation, and IgE-mediated sensitization to food and environmental allergens. The centre point of research on the mechanisms of AD has been the adaptive immune system with an emphasis on the T-helper 1 (Th1)-Th2 paradigm. Recently, the conceptual focus has largely shifted to include a primary defect in the epithelial barrier as an initial event in AD, pointing to a complex secondary interplay of environmental and immunological squeal with barrier disruption.5 Various evidences suggests that AD is a cutaneous manifestation of a systemic disorder that also gives rise to other atopic conditions therefore optimal management of AD requires a multifaceted approach aimed at healing and protecting the skin barrier and addressing complex immunopathogenesis of this

In order to fight off exposure to a new pathogen, specific clones of B and T cells are created, they then have to activate and expand; this process can take up to a week or more before the responses are effective. For example, “a single bacterium with a doubling time of one hour can produce almost 20 million progeny, a full-blown infection, in a single day.” As a result, we rely on our innate immune system to protect us from infection during the first critical hours and days of exposure to a new pathogen [2]. Although the function of adaptive immunity is to destroy invading pathogens or toxins, there are cases when the system reacts destructively against the host’s own molecules. Adaptive immune responses are destructive, so as a result, it is essential that the responses be made only in response to foreign molecules. A major aspect of adaptive immunity is distinguishing what molecules are foreign and what are self. When the system fails to make the distinction, the adaptive immune system reacts destructively against the host’s own molecules, and thus fatal diseases such as autoimmune diseases are created.

In 2009 a study carried out by scientists at the University of Edinburgh concluded that the defects in a particular gene known as the filaggrin gene are linked to a considerably amplified risk of developing allergic disorders such as eczema, rhinitis, and asthma (Varanasi, 2000 in Hedge et.al, 2010). The typical locations of eczema include the face (scalp and around the eyes), the

Fibroblasts, the major cell type of the dermis, produce and maintain most of the ECM proteins. Indeed, they produce collagen, elastic fibres, and glycosaminoglycan [93]. The dermal fibroblasts are differentiated from the mesenchymal cells and appear as thin spindle-shaped cells. The dermis includes other types of cell such histiocytes, mast cells and dermal dendritic cells. Histiocytes are star-shaped cells with a small

Diseases that stem from allergies have increased worldwide the past couple decades. Many genetic and environmental influences have been associated with the development and prolongation of food allergies. In some cases, food allergies often show unprompted

Within skin, mast cells are distributed throughout the dermis with significant regional variations observed between different cutaneous sites (Weber, BJD, 2003; Grimbaldeston, BJD, 2003; Tong et al. JID 2014). In mice, this regional variation results in altered physiological response to allergen for example, in a model of passive cutaneous anaphylaxis the ear skin exhibited enhanced vascular permeability when compared to back skin (Tong, 2014). This enhanced vascular leakage closely mirrored the higher density of mast cells found in the murine ear skin. Using fluorochrome labelled avidin, Galli and colleagues have visualised the release of secretory granules from mast cells in a murine model for contact hypersensitivity. The presence of negatively charged proteoglycans along with low pH resulted in long term