fourteen- cell biology
The Role of the Complement System
In the immune system, effector cells maintain a specific function, and an essential effector of the humoral response (in which there is B cell-antigen interaction, with the B cells differentiating into plasma cells possessing the ability to secrete antibody), is the complement system. Composed of three pathway, the classical pathway, the lectin pathway, and the alternative pathway, complement is composed of (mainly) liver hepatocyte-synthesized soluble proteins and glycoproteins. They are also made form tissue macrophages, blood monophages, and gastrointestinal and genitourinary epithelial cells.
The fundamental responsibilities of the complement system include lysis of cells, bacteria, and viruses; binding to specific complement receptors on cells of the immune system to trigger particular cell functions, inflammation, and to secrete immunoregulatory molecules; and optimization, the induction of phagocytosis of specific antigens. The three pathways conclude with formation of C5b, and the steps that result in the creation of the membrane-attack complex are identical for all three.
Activated by IgG or IgM molecules, and the formation of soluble antigen-antibody complexes, the classical pathway is notably antibody dependant, in contrast to the antigen dependent alternative pathway, which is part of the innate immune system. Following initiation (antigen binding to the C1 component), the classical pathway centers around the formation of the C3 and C5 convertases, regulated enzymes involved in the membrane-attack complex.
The alternative pathway also operates as a humoral component of the body’s defence against infections and it, too, results in the creation of the C3/C5 convertase. The lectin pathway works in a similar manner- it does not require activation via antigen. This pathway is activated, as the name suggests, by mannose binding lectin, which binds to glycoproteins or carbohydrates on the surface of, for instance, bacteria; however, it performs similarly to the classical pathway.
The three pathways conclude in cleavage of the C5 convertase and along with C5b, C6, C7, C8, and C9, the macromolecular membrane attack complex is made. The complex allows for the free diffusion of small molecules and ions, the cell fails to maintain the required osmotic stability, and is killed by the loss of electrolytes and the gaining of water.
Additionally, both passive and active mechanisms regulate the pathways, due the ability of the complement system to attack foreign cells and microorganisms along with host cells. These mechanisms ensure only the right targets feel the effect of the complement system.
Works Cited
Alberts, et al. The Cell. New York: Garland Science, 2002.
Kindt, Goldsby, and Osborne. Kuby Immunology. New York: W.H Freeman and Co.,
2007.
Merralls, Stephanie. "The Role Of Complement InThe Elimination
Of Microorganisms." Immunology. 30 Apr. 2007
~dmsander/WWW/Merralls/Merralls.html>.
and
How do Tumors Acquire Enhanced Production of Angiogenic Factors?
One of the key characteristics of cancerous cells is the ability to recruit adequate blood supply, as part of its way to survive and proliferate, metastasize. Angiogenesis is the formation of new blood vessels, which is essential for growth of primary tumors. The procurement of the blood supply provides the growing tumor with oxygen and necessary nutrients. It is also thought that they may play a role in allowing escape routs for metastatic cells and take up residence in other organs.
The important new vessels grow via a cascading series of events, beginning with special proteins, angiogenic growth factors, which bind to receptors located on endothelial cells, and through intracellular signaling, new molecules are produced from the endothelial cell, i.e. enzymes. This is followed by the proliferation of endothelial cells and the directional migration towards the diseased tumor. Integrins aid in the formation of the vessel itself. The tube forms as endothelial cells roll up; loops are created from the tubes connecting to each other. Eventually, structural support is provided by smooth muscle cells, after which blood may begin to flow.
In tumors, the BCL2 oncogene has been discovered to increase stimulators of angiogenesis, like the fibroblast growth factor (FGF) and the vascular endothelial growth factor (VEGF), after which the tumor cell’s oncogenes begin the production of angiogenic factors. Interestingly, the tumor’s progeny will also display these factors, resulting in the correlation that as a tumor increases, so does the number of angiogenic cells. Consequently, estimates show that a tumor 1cm in diameter can release about 2 million cells in roughly 24 hours thanks to the newly formed blood vessels.
Works Cited
Alberts, et al. The Cell. New York: Garland Science, 2002.
"Cell Biology and Cancer." Rediscovering Biology. 30 Apr. 2007
cancer_6.html>.
"About Angiogenisis." Angiogenisis Foundation. 1 May 2007
.
"Tumor Metastasis." Zetter Research Laboratory. 1 May 2007
mainpageS229P5.html>.
In the immune system, effector cells maintain a specific function, and an essential effector of the humoral response (in which there is B cell-antigen interaction, with the B cells differentiating into plasma cells possessing the ability to secrete antibody), is the complement system. Composed of three pathway, the classical pathway, the lectin pathway, and the alternative pathway, complement is composed of (mainly) liver hepatocyte-synthesized soluble proteins and glycoproteins. They are also made form tissue macrophages, blood monophages, and gastrointestinal and genitourinary epithelial cells.
The fundamental responsibilities of the complement system include lysis of cells, bacteria, and viruses; binding to specific complement receptors on cells of the immune system to trigger particular cell functions, inflammation, and to secrete immunoregulatory molecules; and optimization, the induction of phagocytosis of specific antigens. The three pathways conclude with formation of C5b, and the steps that result in the creation of the membrane-attack complex are identical for all three.
Activated by IgG or IgM molecules, and the formation of soluble antigen-antibody complexes, the classical pathway is notably antibody dependant, in contrast to the antigen dependent alternative pathway, which is part of the innate immune system. Following initiation (antigen binding to the C1 component), the classical pathway centers around the formation of the C3 and C5 convertases, regulated enzymes involved in the membrane-attack complex.
The alternative pathway also operates as a humoral component of the body’s defence against infections and it, too, results in the creation of the C3/C5 convertase. The lectin pathway works in a similar manner- it does not require activation via antigen. This pathway is activated, as the name suggests, by mannose binding lectin, which binds to glycoproteins or carbohydrates on the surface of, for instance, bacteria; however, it performs similarly to the classical pathway.
The three pathways conclude in cleavage of the C5 convertase and along with C5b, C6, C7, C8, and C9, the macromolecular membrane attack complex is made. The complex allows for the free diffusion of small molecules and ions, the cell fails to maintain the required osmotic stability, and is killed by the loss of electrolytes and the gaining of water.
Additionally, both passive and active mechanisms regulate the pathways, due the ability of the complement system to attack foreign cells and microorganisms along with host cells. These mechanisms ensure only the right targets feel the effect of the complement system.
Works Cited
Alberts, et al. The Cell. New York: Garland Science, 2002.
Kindt, Goldsby, and Osborne. Kuby Immunology. New York: W.H Freeman and Co.,
2007.
Merralls, Stephanie. "The Role Of Complement InThe Elimination
Of Microorganisms." Immunology. 30 Apr. 2007
~dmsander/WWW/Merralls/Merralls.html>.
and
How do Tumors Acquire Enhanced Production of Angiogenic Factors?
One of the key characteristics of cancerous cells is the ability to recruit adequate blood supply, as part of its way to survive and proliferate, metastasize. Angiogenesis is the formation of new blood vessels, which is essential for growth of primary tumors. The procurement of the blood supply provides the growing tumor with oxygen and necessary nutrients. It is also thought that they may play a role in allowing escape routs for metastatic cells and take up residence in other organs.
The important new vessels grow via a cascading series of events, beginning with special proteins, angiogenic growth factors, which bind to receptors located on endothelial cells, and through intracellular signaling, new molecules are produced from the endothelial cell, i.e. enzymes. This is followed by the proliferation of endothelial cells and the directional migration towards the diseased tumor. Integrins aid in the formation of the vessel itself. The tube forms as endothelial cells roll up; loops are created from the tubes connecting to each other. Eventually, structural support is provided by smooth muscle cells, after which blood may begin to flow.
In tumors, the BCL2 oncogene has been discovered to increase stimulators of angiogenesis, like the fibroblast growth factor (FGF) and the vascular endothelial growth factor (VEGF), after which the tumor cell’s oncogenes begin the production of angiogenic factors. Interestingly, the tumor’s progeny will also display these factors, resulting in the correlation that as a tumor increases, so does the number of angiogenic cells. Consequently, estimates show that a tumor 1cm in diameter can release about 2 million cells in roughly 24 hours thanks to the newly formed blood vessels.
Works Cited
Alberts, et al. The Cell. New York: Garland Science, 2002.
"Cell Biology and Cancer." Rediscovering Biology. 30 Apr. 2007
cancer_6.html>.
"About Angiogenisis." Angiogenisis Foundation. 1 May 2007
.
"Tumor Metastasis." Zetter Research Laboratory. 1 May 2007
mainpageS229P5.html>.