Notetaker 14&15&16&17 essayAdaptive immunity has several features that distinguish it from innate immunity. Specificity in that each adaptive immune response is induced by a particular antigen, or surface feature that generates an antibody. An innate immune response might be stimulated by a PAMP, while an adaptive immune response is stimulated by a single feature of a bacteria. In addition, cells of adaptive immunity, B and T cells, are allowed to proliferate under certain conditions to mount a defense, this feature is clonality The adaptive immune system is tuned to be unresponsive to self antigens, usually although autoimmune diseases which are many times more common in women, may result from blurred distinctions between self and nonself. In addition, because some differentiated B and T cells are allowed to survive kiss of death that follows cell proliferation after an initial contact with an antigen. These are memory cells that may multiply rapidly on second contact with an antigen with the benefit of differentiation.
1. Describe a B cell and a T cell based on its distinctive cell surface markers or receptors. p476-479
Antibodies are free immunoglobulins not attached to membranes. Ab are peptides with two heavy chains and two light chains joined by disulfide bridges. The Ab stem is the lower portion of the two heavy chains, this is also called the constant fragment (Fc). The arms of the Ab contain the antigen binding site, or Fab. The primary function of an Ab is to bind to an antigen. Once an Ab-Ab complex is formed there are five possible outcomes that help with immune responses.
1. Activation of complement and inflammation. For example IgE might bind to an Ag with its antigen binding sites and use the stem to bind to a mast cell stimulating the release of inflammatory factors.
2. Neutralization, for example Ab can bind to a virus and prevents its attachment to a cell.
3. Agglutination is the aggregation of multiple Ab-Ag complexes with Ab bound to two different Ag, since each Ab has two antigen binding sites.
4. Antibodyd dependent cell mediated cytotoxicity in which the stem of Ab bound to antigen on a microbes surface bind to natural killer cells which then utilize the perforin-granzyme pathway to induce apoptosis in the microbe.
5. Opsonization when Ab act as opsonins to enhance phagocytosis. 2. Would an Ab be effective at interrupting viral synthesis once the virus has entered a cell? Why or why not?
The five classes on antibodies are IgM, IgG, IgA, IgE and IgD. The following describes what to learn first about each class of antibody so that you might be able to understand the distinctions and the similiarities.
IgM is the first class of antibodies synthesized by B cells after the first encounter with an given Ag. IgM is a pentamer, and has 10 antigen binding sites. As a pentamer, IgM can activate complement, cause aggultination and neutralization. IgM is 5-10% of serum antibodies, and may be used to identify a current infection.
IgG is a monomer that has two Ag binding sites and is 80% of serum antibodies. IgG functions to activate complement, neutralization, opsonization, production of hydrogen peroxide, agglutination, ADCC, and crosses the placenta to protect the fetus.
IgA is a monomer in serum and a dimer on mucous membranes. IgA protects the body from infections in the RT, UT, and reproductive tracts.
IgE is a monomer that is in low concentration in the serum. IgE is a signal molecule that triggers mast cells and basophils to release inflammatory chemicals. IgE is associated with allergic reactions and parasitic worm infections.
IgD function is uncertain.
3. Why does the body make five classes on antibodies?
4. Distinguish between a B cell receptor and IgG.
Cytokines are regulatory proteins that act as signals between cells, creating a network for cell to cell signalling. Cytokines of the immune system are:
Interleukins which signal among leukocytes. At least 37 human IL have been identified.
Interferons (IFN) gamma IFN activated phagocytes and is secreted by T helper cells. Review the fucntion of IFN type I in chapter 15.
Growth factors stimulate leukocyte stem cells to divide and help with proliferation of certain cells of the immune system.
Tumor necrosis factor is secreted by macrophages and T cells to kill tumor cells.
Chemokines are chemotactic cytokines.
Be able to diagram an overivew of the immune system, include macrophages, eosinophils, basophils, neutrophils, natural killer cells, T helper cells, T cytotoxic cells and B cells. For each cell type include relevant information about receptors or markers on that cell's membrane.
B cells are lymphocytes that may differentiate into Plasma cells and memory cells. B cells have B cell receptors that bind to one Ag and each B cell has hundreds of BCR on its membrane surface. B cells also have a MHC I protein to present self Ag and a MCH II protein to present forgein Ag, or Ag that was able to bind that cell's BCR. Plasma cells have a great deal of RER and express antibodies. Memory cells are specialized to release IgG and are allowed to live a long cell life. The memory cells respond to a second contact with a given Ab by secreting large quantities of IgG within a few days of contact with the Ag.
T helper cells have a T cell receptor and a CD4 protien that work together to evaluate foreign Ag presented in MHC II proteins by antigen presenting cells. B cells and macrophages are examples of Ag presenting cells. T helper cells may release cytokines to stimulate B cells to proliferate and differentiate into memory cells and plasma cells. T helper cells would also have MHC I to present self Ag.
T cytotoxic cells also have a T cell receptor and CD8 protein to evaluate Ag presented in MHC I proteins. T cytotoxic cells identify tumor cells or virally infected cells by recognizing altered self Ag presented in a given cell's MHC I protein. T cytotoxic cells also have two modes of killing a target cell, the perforin-granzyme pathway and the CD95 pathway. p.487
5. Name one other cell of the immune system that utilizes perforin -granzyme pathway and explain how that cell's use differs from a T cytotoxic .
6. Does a T helper cell directly kill a foreign cell or a virally infected cell? What is the role of a T helper cell in the immune system?
7. HIV lowers a person's T helper cell count. What effect would a very low T helper cell count have the immune system function?
T regulatory cells moderate T cytotoxic cell activity. Cell mediated responses must be regulated to reduce the possibility of autoimmune responses.
8. Describe how graft rejection involves T cytotoxic cells. p532
The primary immune response to an antigen is slow, the antibodies are synthesized by plasma cells which take days of cell division to develop. The IgM antibodies may be in the serum in 7-10 days from the initial contact.
9. If the bacteria is releasing a toxin that within hours, will the body be able to make antibodies to neutralize the toxin within hours? How long might it take? How can that person acquire immunity quickly?
When an Ag is encountered for the second time, the activation of memory cells ensures the production of Ab for that Ag is fast and at high concentration is the serum.
10. The flu virus mutates its Ag quickly, does having the flu one season confer immunity through memory cells for the next season? If so why, if not why not?
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