Immune response natural killer cells

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). 

Immune Defense. Figure 2 Cytokines involved in the development of adaptive immune responses in secondary lympoid tissues such as the lymph nodes or spleen. Abbreviations B B-lymphocyte, IFN interferon, Ig immunoglobulin, IL interleukin, NK natural killer cell, TE T-effector (cytotoxic) lymphocyte, TH T-helper lymphocyte... 

Syk and ZAP-70 are early intermediates in the transduction of signals from immune receptors, including the B- and T-cell recqrtors for antigen, activatory natural killer-cell receptors, the mast cell and basophil receptor for IgE, and the widely distributed receptors for the Fc portion of IgG. Immune receptors control checkpoints in lymphocyte development and serve to integrate the responses of innate and acquired immunity. 

The sterols and sterolins in rice bran are potent immunomodulators. The best response was obtained with a 100 1 sterol/sterolin mixture that demonstrated T-cell proliferation from 20% to 920% and active cell antigens after four weeks in human subjects (Bouic et al, 1996). Another in vitro experimental study with sterol/sterolins, demonstrated a significant increase in cytokinines, interleukin-2 and y-interferon between 17% and 41 % in addition to an increase in natural killer cell activity. These experiments (Bouic et al, 1996) prove that sterol/sterolins are potent immunomodulators with important implications for the treatment of immune dysfunction. Rice bran products are excellent dietary supplements for the improvement of immune function. It is probable that the effects of rice bran on diabetes, CVD and cancer all result from improved immune function. 

Immunotoxicity. The data in humans are limited to a few studies of immune function in lead workers and a study of firearm instructors. In both type of studies, inhalation is assumed to be the primary route of exposure. One study reported significant suppression of IgA levels (Ewers et al. 1982). Another study indicated that serum immunoglobulin levels were not significantly altered (Alomran and Shleamoon 1988). Another large study examined several parameters of immune function (serum immunoglobulins, PHA response, and natural killer cell activity) and found no differences in exposed workers and controls (Kimber et al. 1986b). The study of firearm instructors found functional impairment of cell-mediated immunity in subjects with PbB levels >25 pg/dL (Fischbein et al. 1993). A recent study that evaluated a... 

FIGURE 9.2 Regulation of Immunity by lnterleukin-2 (IL-2). IL-2 production by T cells and DCs supports the proliferation of T cells, B cells, T reg cells, and NK cells, in addition to establishing a bias towards a Type 1 T cell response. IL-2 can also activate monocytes and NK cells, resulting in increased cytotoxicity. DC dendritic cell IL-2 interleukin-2 NK natural killer cell. 

Based upon recent controlled studies, there is considerable evidence that opioids such as morphine induce substantial effects on immune status. For example, it has been shown that morphine administration is associated with alterations in a number of immune parameters, such as natural-killer cell activity [12,13], proliferation of lymphocytes, [13, 14] antibody production [15,16], and the production of interferon [17]. Studies in our laboratory have shown that acute morphine treatment in rats suppresses splenic lymphocyte proliferative responses to both T- and B-cell mitogens, splenic natural-killer cell activity, blood lymphocyte mitogenic responsiveness to T-cell mitogens, and the in vitro production of the cytokines interleukin-2 and interferon-y [18-22], Furthermore, the immune alterations induced by morphine are dose-dependent and antagonized by the opioid-receptor antagonist, naltrexone (e.g., [22]). 

Other Cells with a Possible Regulatory Function It has been clearly demonstrated that natural killer cells, epithelial cells, macrophages, glial cells, etc., express suppressor cytokines such as IL-10 and TGF-(3. Although their role has not been coined as professional regulatory cells, these cells may efficiently contribute to the generation and maintenance of a regulatory/suppressor type immune response [121-126]. The expression of suppressor cytokines in resident tissue cells may additionally contribute to this process (table 1). 

The cells are called natural killer cells since they kill without a requirement for MHC class I or class II proteins. This characteristic is sometimes termed the MHC-independent immune response. Their principal role is in defence against virnses and other intracellular microorganisms that is, they kill host cells infected with a vims or other pathogen. They also kill tumour cells. Thus they have a role in the process of immune surveillance for tumour cells. 

Bacillus Calmette-Guerin (BCG) is a viable attenuated strain of Mycobacterium bovis. Nonviable strains of the bacterium also have been shown to augment the immune response. The smallest active compound derived from BCG thus far has been identified as muramyl dipeptide. The T cell is a principal target for BCG. It also appears to stimulate natural killer cells, which in turn can kill malignant cells. It has been suggested that BCG cross-reacts immunologically with tumor cell antigens. 

The opioids modulate the immune system by effects on lymphocyte proliferation, antibody production, and chemotaxis. In addition, leucocytes migrate to the site of tissue injury and release opioid peptides, which in turn help counter inflammatory pain. However, natural killer cell cytolytic activity and lymphocyte proliferative responses to mitogens are usually inhibited by opioids. Although the mechanisms involved are complex, activation of central opioid receptors could... 

An additional line of defense is provided by natural killer cells (NK cells), a type of circulating lymphoid cell able to kill cancer cells, to participate in antiviral defenses, and to help control immune responses.273 -276 NK cells, which utilize their own signaling pathways, are also able to use MHC class I molecules to recognize and to spare the lives of normal, healthy cells.277/277a b Partial deprivation of a night s sleep can reduce NK cell activity, damaging the cellular immune response.278... 

Harish A, Hohana G, Fishman P, Amon O, Bar-Yehuda S (2003) A adenosine receptor agonist potentiates natural killer cell activity. Int J Oncol 23(4) 1245-1249 Hart DN (1997) Dendritic cells unique leukocyte populations which control the primary immune response. Blood 90(9) 3245-3287... 

Surprisingly, no difference in immune function as measured by spleen cell counts, in vitro lymphocyte proliferation responses to mitogens, and in vitro and in vivo plaque-forming cell responses to antigens was observed (30). However, human studies have shown changes in natural killer cell activity after TSD and during RS (31,32). 

Conneely, 2001). LF has the ability to bind to the surface of several types of immune cells, which suggests that it can modulate immune functions. Both stimulatory and inhibitory effects of LF on lymphocyte proliferation have been described in the literature. LF has been reported to induce in vitro maturation of T- and B-lymphocytes, to modulate the activity of natural killer cells and to enhance the phagocytic activity of neutrophils. In mice, bovine LF has been shown to induce both mucosal and systemic immune responses (Debbabi et al., 1998). Cell-culture studies have demonstrated that LF and peptides derived from LF influence the production of various cytokines which regulate the immune and inflammatory responses of the body (Crouch et al., 1992 Shinoda et al., 1996). 

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