Immune response initiation

The authors suggested that lamotrigine may have exacerbated a mild immune response initially induced by valproate, without clinical evidence of systemic disease. 

In recent years it has become clear that the nature of the immune response initiated by CD4 T lymphocytes is at least partly dependent on the selection or preferential activation of particular subsets of CD4 T lymphocytes which secrete defined patterns of cytokines (Table 2.3). These patterns of cytokine release result in the initiation and propagation of distinct immune effector mechanisms. Initial studies of mouse CD4 T lymphocyte clones revealed that these could be divided into two basic fiinaional subsets termed ThI and Th2. ThI T lymphocytes were characterized by the predominant secretion of IL-2, interferon y (IFNy) and tumour necrosis factor 8 (TNF/3), while Th2 cells characteristically... 

We assumed that IC31 - that is, the combination of KLKL5KLK and ODNla - would result in an effective adjuvant, and we are currently investigating the potency of IC31 on the induction of adaptive immune responses. Initial results indicate that peptide-specific type 1 cellular immune responses and protein-specific mixed type 1/ type 2 cellular and humoral immune responses are induced. This implies that... 

Chemokines are chemotactic cytokines that induce directional sensing and motile responses (defined as chemotaxis) in cells expressing the corresponding chemokine receptors. Chemokines are small (approx. lOkDa), mostly secreted proteins that were initially implicated in the regulation ofblood cell trafficking during host defense and immune responses initiated by pathogens. The first molecule with chemotactic properties (IL-8) was identified in 1987 [1] and since then the chemokine family has expanded rapidly to its current size. The family now consists in humans of 53 chemokines and 23 chemokine receptors (for an overview, seehttp //cytokine.medic. kumamoto-u.ac.jp/CFC/CK/Chemokine.html) [2]. 

The innate immune response is initiated once the host detects the presence of foreign pathogens. This recognition step is performed by specialized cells of... 

Type I allergic reactions are inappropriate immune responses to an allergen with preferential synthesis of immunoglobulin E (IgE), a special antibody class, which binds to mast cells and basophilic granulocytes via Fee receptors. Binding of the allergen to the cell-bound IgE initiates the rapid release of allergic mediators, most prominently histamine, and the de novo synthesis of arachidonic acid metabolites and cytokines, which are responsible for the clinical symptoms. 

Both vaccines and toxoids are administered to stimulate the immune response within the body to specific antigens or toxins. These agents must be administered before exposure to the pathogenic organism. The initiation of the immune response, in turn, produces resistance to a specific infectious disease. The immunity produced in this manner is active immunity. Display 54-5 gives examples of indications for use of toxoids and vaccines. 

Hepatitis B Hepatitis B vaccines provide another illustration of how drug products have advanced vdth increasing technical capability. Vaccination against hepatitis B is common pradice for health workers, travellers and others who may be at risk of exposure to the virus. The initial vaccines contained inactivated virus to promote the immune response necessary to proted against future infection by the live virus. However, there was always some concern in case there was not complete inactivation of the virus used for vaccination. Further research into the virus identified the surface proteins against which the immune response is raised. The genetic... 

Describe the roles of the antigen-presenting cells in initiating the immune response. 

O T cells are the chief components initiating the immune response against the allograft. The activity of T cells is mediated largely through the synthesis and release of interleukin-2 (IL-2). 

Psoriasis is a T-lymphocyte-mediated inflammatory disease that results from a complex interplay between multiple genetic factors and environmental influences. Genetic predisposition coupled with some precipitating factor triggers an abnormal immune response, resulting in the initial psoriatic skin lesions. Keratinocyte proliferation is central to the clinical presentation of psoriasis. 

Topical therapy is the initial drug treatment strategy for patients with mild to moderate psoriasis. It is estimated that approximately 70% to 80% of all patients with psoriasis can he treated adequately with use of topical therapy.1 Topical therapies include corticosteroids, coal tar products, anthralin, vitamin D3 analogues such as calcipotriol, retinoids such as tazarotene, and topical immunomodulators such as tacrolimus and pime-crolimus.18 Vitamin D3 analogues and topical retinoids all affect keratinocyte functions and the immune response. Currently, these are in wider use than is either anthralin or coal tar preparations. 

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