AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
Macrophages and Natural Killer Cells
http://doctor-jones.co.uk/Immunology/Tutorial/NK%20Cells.htm
Many viruses inhibit the production or expression of the MHC-I
molecule. This is entirely logical as the killing of the virus by cytotoxic Tcells depends upon the MHC-I molecule presenting viral antigen. One
example of this is the adenovirus E3 that produces a glycoprotein that
sequesters MHC-I molecules in the endoplasmic reticulum and thus
prevents their expression on the cell surface. This is where NK cells
function. In the absence of the MHC molecule, there is no signal to
override that of the NKR-P1 molecule and hence the killing action of the
NK cell is activated and the cell not expressing MHC-I will be killed. It is
possible that NK cells act against tumour cells in the same way, by
inducing killing in response to the down-regulation of MHC molecules.
Natural killer cells (or NK cells) are a type of cytotoxic lymphocyte
critical to the innate immune system. The role NK cells play is
analogous to that of cytotoxic T cells in the vertebrate adaptive immune
response. NK cells provide rapid responses to virally infected cells and
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AP Biology: Chapter 43: Immune System
Margaret Bahe
http://www.youtube.com/watch?v=0zosnn-QUvI
Natural killer cell
Natural killer cells (also known as NK cells, K cells, and killer cells) are
a type of lymphocyte (a white blood cell) and a component of innate
immune system.
NK cells play a major role in the host-rejection of both tumours and
virally infected cells.
NK cells are cytotoxic; small granules in their cytoplasm contain special
proteins such as perforin and proteases known as granzymes.
Upon release in close proximity to a cell slated for killing, perforin forms
pores in the cell membrane of the target cell through which the
granzymes and associated molecules can enter, inducing apoptosis.
The distinction between apoptosis and cell lysis is important in
immunology - lysing a virus-infected cell would only release the virions,
whereas apoptosis leads to destruction of the virus inside.
NK cells are activated in response to interferons or macrophagederived cytokines.
They serve to contain viral infections while the adaptive immune
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
1.  Mast cells release histamines
2.  Macrophages release cytokines
3.  Capillaries dilate
4.  Fluicd with antimicrobial peptides enter tissue
5.  Signals attract neutrophils
6.  Neutrophils digest pathogens
7.  Tissue heals
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AP Biology: Chapter 43: Immune System
Margaret Bahe
http://www.youtube.com/watch?v=Un9-vubdtmY
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
Inhibits protein synthesis activates protein kinases which lead to the
formation of proteins that inhibit protein syn
and promotes breakdown of mRNA with RNase
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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Margaret Bahe
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Margaret Bahe
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Margaret Bahe
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Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
Granzymes destroy proteins - enter the infected cell via endocytosis
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
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AP Biology: Chapter 43: Immune System
Margaret Bahe
Draw:
What is happening inside a well during an ELISA test which tests for the
presence of an antigen.
Feedback loop for dehyrdration & ADH
Sequence for blood clotting
Diagram of the heart’s electrical system
Fish in salt and fresh water – homeostasis for salt and water balance
Draw a nephron and label what is happening in each section
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AP Biology: Chapter 43: Immune System
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AP Biology: Chapter 43: Immune System
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AP Biology: Chapter 43: Immune System
Margaret Bahe
David Vetter, the original "bubble boy", had bone marros translant of the
first transplantations, but eventually died because of an unscreened
virus, Epstein-Barr (tests were not available at the time), in his newly
transplanted bone marrow from his sister, an unmatched bone marrow
donor.
Today, transplants done in the first three months of life have a high
success rate. Physicians have also had some success with in utero
transplants done before the child is born and also by using
cordAshanthi DeSilva blood which is rich in stem cells. In utero
transplants allow for the fetus to develop a functional immune system in
the sterile environment of the uterus
In 1990, four-year-old became the first patient to undergo successful
gene therapy. Researchers collected samples of Ashanthi's blood,
isolated some of her white blood cells, and used a virus to insert a
healthy adenosine deaminase (ADA) gene into them. These cells were
then injected back into her body, and began to express a normal
enzyme. This, augmented by weekly injections of ADA, corrected her
deficiency. However, the concurrent treatment of ADA injections may
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http://www.nytimes.com/2005/07/03/books/chapters/0703-1stnaam.html?pagewanted=all&_r=0
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AP Biology: Chapter 43: Immune System
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B-cells make antibodies against antigens on pollen grains
These antibodies bind to receptors on Mast cells (mucus membranes)
2nd exposure à antibodies interact with antigen (pollen grain) à
release histamines and inflammatory chemicals
Causes sneezing, teary eyes, contraction of smooth muscle in lungs
(hard to breath)
Currently, the only effective treatment for anaphylaxis is an
intramuscular injection of epinephrine, a hormone the body produces
naturally in the adrenal glands. Epinephrine counteracts the symptoms
of anaphylaxis by constricting the blood vessels and opening the
airways. The down side is that its effects last only 10 to 20 minutes per
injection, it has some potentially serious side effects, and it must be
administered correctly at or before the onset of symptoms to be
effective.
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http://www.pennmedicine.org/health_info/allergy/000001.html
Bee venum, penicillin, peanuts, shelfish
Epinepherin is a bronciole dilator and a vasoconstrictor of peripheral
vessels and increases blood pressure
Increases heart rate which prevents cardiovascular collapse and
prevents further release of histamines (?)
Epipens are a temporay solution - seek med attention
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Interferons
http://pathmicro.med.sc.edu/mayer/vir-host2000.htm
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b) Inducers of Interferons - Normal cells do not contain preformed IFN
nor do they secret interferon constitutively. This is because the
interferon genes are not transcribed in normal cells. Transcription of the
IFN genes occurs only after exposure of cells to an appropriate inducer.
Inducers of IFN-alpha and IFN-beta include virus infection, double
stranded RNA (e.g. poly inosinic:poly cytidylic acid; [poly I:C]), LPS, and
components from some bacteria. Among the viruses, the RNA viruses
are the best inducers while DNA viruses are poor IFN inducers, with the
exception of poxviruses. Inducers of IFN-gamma include mitogens and
antigen (i.e. things that activate lymphocytes).
Fig. 3. Mode of action of interferon c) Cellular Events in the Induction
of Interferons
The IFN genes are not expressed in normal cells because the cells
produce a labile repressor protein that binds to the promoter region
upstream of the gene and inhibits transcription. In addition, transcription
of the genes require activator proteins to bind to the promoter region
and turn on transcription. Inducers of IFN act by either preventing
synthesis of the repressor protein or increasing the levels of the
activator proteins, thereby turning the IFN gene on. After the inducer is
gone, the IFN gene is again turned off by the repressor protein and/or
the lack of activator proteins. Once the gene is turned on, it is
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Regulation of RA FLS activation by Ras family GTPases. In RA FLS,
the H-Ras –specific GEF RasGRF1 is over-expressed. Furthermore,
unidentified cellular proteases cleave RasGRF1, resulting in its
constitutive activation. This leads to H-Ras activation, promoting high
basal transcription of IL-6 and MMP-3. Exposure of RA FLS to
inflammatory cytokines leads to further activation of H-Ras, as well as
inducing activation of K-Ras and N-Ras. Through their combined and
redundant activation of MAP kinase and PI3-kinase signaling pathways,
H-, K-, and N-Ras each contribute to RA FLS chemokine, cytokine, and
MMP production that perpetuates inflammation and promotes disease
progression.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3460313/
Contributions of Ras and Rap signaling to RA synovial T cell activation.
Exposure of T cells to IL-1β and TNFα, among other inflammatory
cytokines, leads to activation of unidentified T cell Ras GEFs and Ras
proteins. ROS-dependent and –independent pathways downstream of
Ras can stimulate T cell inflammatory gene transcription. Rasdependent signaling in T cells is usually buffered, directly or indirectly,
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http://hopestemcell.com/cancer-immunology
In spite of this fact, however, many kinds of tumor cells display unusual
antigens that are either inappropriate for the cell type and/or its
environment, or are only normally present during the organisms'
development (e.g. fetal antigens). Examples of such antigens include
the glycosphingolipid GD2, a disialoganglioside that is normally only
expressed at a significant level on the outer surface membranes of
neuronal cells, where its exposure to the immune system is limited by
the blood–brain barrier. GD2 is expressed on the surfaces of a wide
range of tumor cells including neuroblastoma, medulloblastomas,
astrocytomas, melanomas, small-cell lung cancer, osteosarcomas and
other soft tissue sarcomas. GD2 is thus a convenient tumor-specific
target for immunotherapies.
Other kinds of tumor cells display cell surface receptors that are rare or
absent on the surfaces of healthy cells, and which are responsible for
activating cellular signal transduction pathways that cause the
unregulated growth and division of the tumor cell. Examples include
ErbB2, a constitutively active cell surface receptor that is produced at
abnormally high levels on the surface of breast cancer tumor cells.
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