Immune response cytokine

Cytokines and antagonists (2—4), intercellular proteins produced by immune cells, play an important role in the regulation of immune responses. Cytokines are present in a variety of tissues under normal conditions. Through insufficient or excessive production, these macromolecules can mediate chronic inflammatory diseases. An inability to respond to cytokines, eg, interleukin 1 (IL-1) or interleukin 2 (IL-2), may lead to an immunosuppressive state, whereas over-production can result in severe shock, autoimmune disease, or immunopathological conditions, such as leukemia and rheumatoid arthritis (RA). Specific communications between immune cells are constantly modulated by naturally occurring inhibitors. 

Histamine receptors variously mediate the bronchoconstrictant, inflammatory, irritant, vasodilator, gastric pepsin secretion and immune suppression actions of histamine. Associated with the immune response, cytokines cause release of histamine from mast cells. Histamine acts via HI, H2, H3 and H4 GPCRs. HI and H2 receptors couple via both Gas (elevating cAMP) and Gaq (elevating Ca2+ in a pertussis toxin-insensitive fashion) and H3 couples via Gai (decreasing cAMP). 

In addition to thek role in coordinating immune system functions, cytokines mediate communication betw een the peripheral immune system and the central and peripheral nervous system (Plata-Salaman, 1991). During an innate immune response, cytokines released by macrophages, vascular endothelial cells, and other cells activate the HPA axis, resulting in the release of ackenal glucocorticoids (Silverman et al., 2005). 

Cytokines play an important role in the control of switching of antibody isotypes in humans away from IgM during the evolution of the immune response. Cytokines which play a role in this process may be classified as follows. 

Cytokine responses to infection or tumors are thought phylogenetically to be the most ancient form of immune response. Cytokines are generated in response to antigen challenge and now have a large impact in the clinical management of many diseases. However, unlike antibodies, cytokine responses are nonspecific, and their principal... 

Garcia, V. E., Chuluyan, H. E. SLAM and CD31 signaling molecules involved in cytokine secretion during the development of innate and adaptive immune responses. Cytokine Growth Factor Rev. 2007, 18, 85-96. 

Cytokines form a family of proteins including interleukins and lymphokines that are released by cells in the immune system and act as intercellular mediators in immune response. Cytokines are produced by various cell populations, although they are predominantly produced by helper T cells and macrophages. Cytokines that are secreted from lymphocytes are referred to as lymphokines, whereas those secreted by monocytes or macrophages are referred to as monokines. Many lymphokines are also referred to as interleukins (ILs), because they are also capable of affecting leukocyte cellular responses. 

Cellular cytokines (interferons, G-CSF) and immune response modifiers originally produced from human cells, most often leukocytes, have now been replaced with recombinant products with well-defined structure/function. Futuristic advances in experimental hematology portend development of human blood cells produced from the hemopoetic stem cells. Yet for the foreseeable future, homologous blood donated by healthy, altruistic voluntary blood donors remains the principal source of safe and adequate supply of blood and blood products for transfusion therapy. 

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... 

Several cytokines are in clinical use that support immune responses, such as IL-2, DFNs, or colony-stimulating factors. IL-2 supports the proliferation and effector ftmction of T-lymphocytes in immune compromised patients such as after prolonged dialysis or HIV infection. IFNs support antiviral responses or antitumoral activities of phagocytes, NK cells, and cytotoxic T-lymphocytes. Colony-stimulatory factors enforce the formation of mature blood cells from progenitor cells, e.g., after chemo- or radiotherapy (G-CSF to generate neutrophils, TPO to generate platelets, EPO to generate erythrocytes). 

Two main strategies are presently used to suppress immune responses (summarized in Fig. 3). The first focuses on cytokines, the central mediators of the immune system. Efficient inhibition of cytokine production can be achieved by glucocorticoids. Specific anticytokine strategies include the use of monoclonal antibodies, soluble receptors, or receptor constructs. 

Lymphocytes are specialized white blood cells that play a crucial role in an immune response.They can be T lymphocytes, which can directly target and destroy defective cells, or B lymphocytes, which produce antibodies directed against specific antigens. Both T and B lymphocytes produce a variety of cytokines to augment and amplify the immune response. 

The key end result of TLR signalling is the induction of cytokines. Cytokines are proteins produced during an immune response that allow the maturation, activation and differentiation of effector cells in the immune system. The activation of NFkB and AP-1 by the MyD88 and the TREF dependent pathways leads to the production of proinflammatory cytokines such as IL-6, TNF-a and various chemokines. This pathway can also activate IRF-7 via TLR-7and TLR-9 allowing Type-I interferons to be produced. 

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. 

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.)... 

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