Immune response eosinophils

Decreases the production of lymphocytes and eosinophils in the blood by causing atrophy of the thymus gland blocks the release of cytokines, resulting in a decreased performance of T and B monocytes in the immune response. (This action, coupled with the anti-inflammatory action, makes the corticosteroids useful in delaying organ rejection in patients with transplants.)... 

A large number of cells are involved in the immune response and all are derived fiom the multipotential stem cells of the bone marrow. The predominant cell is the lymphocyte but monocytes-macrophages, endothelial cells, eosinophils and mast cells are also involved with certain immune responses. The two types of immunity (humoral and cell-mediated) are dependent on two distinct populations of lymphocytes, the B cells and the T cells respectively. Both the humoral and the cell-mediated systems interact to achieve an effective immune response. 

The development of respiratory hypersensitivity requires an induction phase where exposures to the sensitizer lead to an interaction with immune cells and the eventual development of specific effecter immune molecules (e.g., antibodies) and cells (e.g., T lymphocytes) [5], The induction phase can require months to years of exposure before there is a detectable immune response and/or onset of symptoms typical of respiratory hypersensitivity, including asthma. Classic IgE mediated responses have been described as Th2 cell dominant responses. A subset of CD4+ T cells known as Th2 cells push the immune response to the development of IgE and IgG4 antibodies in humans along with secretion of cytokines that attract and activate inflammatory cells such as eosinophils. 

Immune responses are mediated through the lymphocytes called B cells and T cells. Lymphocytes are a particular type of white blood cell. White blood cells (leukocytes) are divided into granulocytes (neutrophils, 55-70% eosinophils, 1-3% and basophils, 0.5-1%) and agranulocytes (lymphocytes [B and T cells], 20-40% and monocytes, 1-6%). There are 5000-10,000 white blood cells per milliliter of blood, compared with five million red blood cells in the same volume. 

Basophils and Eosinophils. These two types of granulocyte represent only a small proportion of the circulating leukocytes. The basophil possesses receptors specific for the Fc portion of IgE molecules. It is involved in allergic reactions and can play a role in the clinical state of anaphylaxis, which is a life-threatening allergic response. Eosinophils are involved with the immune reactivity of drug allergies and with the body s immune response to parasitic infestations such as worms (see chapter 9). 

Endogenous histamine has a modulating role in a variety of inflammatory and immune responses. Upon injury to a tissue, released histamine causes local vasodilation and leakage of plasma-containing mediators of acute inflammation (complement, C-reactive protein) and antibodies. Histamine has an active chemotactic attraction for inflammatory cells (neutrophils, eosinophils, basophils, monocytes, and lymphocytes). Histamine inhibits the release of lysosome contents and several T- and B-lymphocyte functions. Most of these actions are mediated by H2 or H4 receptors. Release of peptides from nerves in response to inflammation is also probably modulated by histamine, in this case acting through presynaptic H3 receptors. 

This type of immune response is unlike the other three in that antibodies are not involved, the response being initiated by sensitized TH1 cells. These are activated by contact with APCs. This stimulates them to secrete cytokines, which recruit macrophages, neutrophils, and eosinophils causing inflammation at the site of exposure. The cytokines also recruit and activate cytotoxic T cells, which can destroy the cell such as when an altered cell membrane is the antigen (Fig. 6.34). 

Type II, or cytotoxic immune, responses can be complement-independent or complement-dependent in nature. In the former case, IgG antibodies bind to antigens attached to the surface of normal cells (e.g., erythrocytes, platelets, etc.). Cytotoxic cells (macrophages, neutrophils, and eosinophils) then attach to the crystallizable fragment (Fc) portion of the antigen, release cytotoxic granules, and lyse the cell. 

CeU recruitment to the site of damage (monocytes that infiltrate tissues to become macrophages, neutrophils, antigen-presenting dendritic cells, lymphocytes including B- and T-ceUs (leading to an adaptive immune response), natural killer cells (an effector cell in innate immunity) and eosinophils). 

The pathophysiology of VKC is derived from a combination of type I and IV hypersensitivity reactions.This allergic response involves IgE,Th-2 lymphocytes, eosinophils, mast cells, basophils, neutrophils, macrophages, proin-flammatory cytokines, interleukins, histamine, and other associated mediators. Also involved in this immune response are hormonal and neuroendocrine influences. This immune response results in the clinical manifestations of photophobia, itching, redness, tearing, papillae, corneal vascularization, mucous discharge, and plaque formation. 

The adrenal corticosteroids have been extensively used to suppress many different aspects of the immune response. AU of the corticosteroids have similar mechanisms of action. They bind to specific corticosteroid binding proteins in the cytoplasm. These complexes are then transported into the nucleus where they bind to discrete portions of the cell s DNA. This binding results in derepression of regulatory genes and the subsequent transcription of new mRNA (Rhen and Cidlowski, 2005). Steroids inhibit the consequences of the immune response. They have several different actions in this regard. One of their most important effects is to transiently alter the number of circulating leukocytes. There is a rapid increase in the number of neutrophils and a concomitant decrease in the number of lymphocytes, monocytes, eosinophils and basophils (Krensky et al, 2005). 

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