infection and immunity revision part 1 Flashcards
(38 cards)
A student is returning home and is approached in the street by someone who is asking for directions to the underground station. As he tries to help he is stabbed by a needle. He is concerned the needle may be contaminated with HIV. QUESTION: which subtypes of immune cells does the HIV virus infect?
- The virus infects T lymphocytes
- The virus infects B lymphocytes
- The virus infects Th cells
- CD8 positive T cells are infected
- Cytotoxic T cells are infected
- The virus infects Th cells
HIV attacks a specific type of immune system cell in the body. It’s known as the CD4 helper cell or T cell. When HIV destroys this cell, it becomes harder for the body to fight off other infections.
T cytotoxic cells have a major role in killing infected cells but Th cells are the main infected lymphocytes.
There are studies that show HIV can affect B cell function – but the question is which cells does the virus infect
An HIV infected patient has developed Kaposi’s sarcoma. QUESTION: why are HIV infected individuals prone to developing Kaposi’s sarcoma?
- Reduced levels of antibody against the infectious organism
- Low levels of cytotoxic T lymphocytes
- Phagocytes infected with HIV and unable to present antigens
- CD4+ cells reduced in number affecting Th cell mediated immune function
- Decline in number of eosinophils
CD4+ cells reduced in number affecting Th cell mediated immune function
HIV attacks a specific type of immune system cell in the body. It’s known as the CD4 helper cell or T cell. When HIV destroys this cell, it becomes harder for the body to fight off other infections.
A 52 year old female patient has had urinary tract infection and has been taking antibiotics for a period of one week. She comes to see her GP because she is now concerned that she has thrush. The GP explains to her that the thrush may be a result of taking antibiotics. QUESTION: why would taking antibiotics result in thrush?
- Hypersensitivity reaction to antibiotics
- Removal of harmless residual bacteria allowing replication of candida
- Antibiotics down regulate the number of CD4+ T helper cells
- Antibiotic resistance results in T cell apoptosis allowing candida infection to progress.
Removal of harmless residual bacteria allowing replication of candida
Candidiasis is a fungal infection caused by a yeast (a type of fungus) called Candida.
A patient with phagocyte disorder is experiencing frequent infections. Phagocytes are essential components of the immune response. Which of the following statements explains the increased risk of infection in patients with phagocyte defects?
- Phagocytic cells generate antibodies that prevent infection- false they don’t generate antibodies
- Phagocytes identify pathogens through MHC presented antigens killing infected cells
- Phagocytes activate cells encouraging antibody production
- Phagocytes process and present antigens initiating T cell activation
Phagocytes process and present antigens initiating T cell activation
but could also be the one before
What statement best describes the role of Natural killer cells?
- Each NK cell has specific affinity for an antigen and can engage in killing infected cells- not specific
- NK cells have specific receptors that engage in release of complement – not specific
- Able to identify cells that have altered surface antigens and can engage in killing these cells
- NK cells have a surveillance role for bacterial pathogens
- Able to identify cells that have altered surface antigens and can engage in killing these cells
- Natural killer cells
- Surveillance role
- Any cell that has changed is a target for killing
What statement best describes the structure of antibodies?
- Tetrameric protein with two identical heavy chains and two identical light chains
- Each immunoglobulin molecule has a kappa and a lambda chain
- IgG antibodies have a constant region with no variable section
- IgM antibodies have two constant chains and no variable chains.
Tetrameric protein with two identical heavy chains and two identical light chains.
antibody: -Y-shaped Tetrameric protein - 2 identical heavy chains - 2 identical light chains
A patient who has recently developed symptoms of hepatitis is tested for hepatitis A antibodies. What is the best laboratory based diagnostic strategy for hepatitis A infection?
- Measure Hepatitis A virus specific circulating IgG levels.
- Measure Hepatitis A total immunoglobulin levels
- Assess levels of IgE immunoglobulin in peripheral blood
- Test for the presence of IgM antibodies to hepatitis A virus.
-Test for the presence of IgM antibodies to hepatitis A virus.
Immunoglobulin E(IgE) – usually an immediate response to a foreign substance that has entered the body normally found in small amountsin theblood.
IgGcan take time to form after an infection or immunisation
ImmunoglobulinM (IgM): Found mainly in blood and lymph fluid, thisisthe first antibody the body makes when it fights a new infection.
ImmunoglobulinA (IgA) – plays a rolein theimmune function of mucous membranes.
What do B lymphocytes do?
Make antibodies Immunoglobulins There are two types IgM – made first IgG – made later
How do T cells recognise antigens?
- T cells have T cell receptors which are able to attach to antigens and recognise them.
- T cells have MHC class I receptors which bind to antigenic sites on infected cells
- CD4+ T cells recognise antigens displayed on infected cells by MHC I
- CD8+ T cells have T cell receptors which recognise antigen displayed by MHC I molecules
- CD8+ T cells have T cell receptors which recognise antigen displayed by MHC I molecules
CD4+ helper T cells: antigens (peptides) displayed by MHC class II
CD8+ cytotoxic T cells: antigens (peptides) displayed by MHC class I
how do natural killer cells use perforin and granzymes work to destroy defective cells? also what is the one other thing that they produce apoptosis
perforin- creates pores in the target cell
granzymes- release cytotoxic enzymes which cause apoptosis. (granzyme B can trigger mitochondrial apoptotic pathway)
- interferon y (gamma)
how are natural killer cells inhibited or activated.
Inhibitiory receptors recognise self MHC class 1 and then send a blockadge of signals from the activated recptors.
However virus infected and malignant cells downregulate the expression of MHC 1 so there would be low levles of it on the cell. hence the inhibitory receptors are not ligated my MHC 1 as low levels. so signals from activating receototrs are not blocked. NK cells are activated and attack.
what are the receptors involved in NK cells activation and inhibition.
ITIM (for inhibition) and ITAM (for activation) have tyrosine motifs that can become phosphorylated in order to propagate the cell signalling to lead to either inhibition or activation depending on the receptor.
CD4+ and CD8+ are types of t cells what are they exactly?
CD4+ are helper t cells (cannot kill but oder other cells to do so) looks for MCH2 from APCs
CD8+ are cytotoxic cells (can kill cancer/virus infected cells) looks for MCH1
which is not an a ‘lymphoctye with limited capacity’
- dendritic cell
- γδ (gamma/delta) T cells
- NK-T cells
- Mucosa-Associated Invariant T (MAIT) cells
- B-1 B cells
- Marginal zone B cells
dendritic cell
which immune cells are from myeloid lineage and which are from lymphoid lineage?
myeloid: phagocytes, basophils, eosionphils, mast cells
lymphoid cells:T lymphocytes, B lymphocytes, NK cells, innate lymphoid cells, lymphocytes with limited diversity
how do macrophages and nk cells work together to create and immune response.
when macrophages engage in phagocytosis they produce cytokine IL-12 which is good at activating NK cells. The NK cells then become activated and produce interferon y (gamma) which also enhances macrophages ability to kill.
innate lymphoid cells (ILCs) and lymphocytes with limited diversity are the innate immune system what are their roles.
ILCs similar to T lymphoctes but do not express T cell receptors hence no colonal expansion (proliferation). main mechanism is to produce cytokines
Lymphocytes with limited diversity combine feautres of T/B cells and innate cells
what is the role of histamine and where is it released from?
histamine stimulates inflammation and is released from mast cells
- causes vasodilation (causes redness)
- makes blood vessels more permeable
- pain at site of injury and attracts immune cells.
what is the general mechanism of B lymphocytes?
B cells have receptors that bind to a specific antigen when it meets the right one it digests it and projects MHC 2 cells for helper t cells to bind to it.
It also releases lymphokines which cause the B cells to make plasma cells and the plasma cells make antibodies. Some memory cells are also made.
for the helper t cells that bind they also proliferate and make cytotoxic t cells and memory t cells do the immune response will be faster next time
what is the difference between humoral and cell mediated immunity?
humoral immunity (makes antibodies)
- targets exogenous antigens (outside cells)
-macrophages/ APCs englulf exogenous antigens and break them into fragments which are projected into MHC class 2 receptors. this signals the material as being foreign
-
cell mediates immunity
-targets endgroenous antigens (cancer cells or virus infected cells.
what is the difference between humoral and cell mediated immunity?
humoral immunity (makes antibodies)
- targets exogenous antigens (outside cells)
- macrophages/ APCs engulf exogenous antigens and break them into fragments which are projected into MHC class 2 receptors. this signals the material as being foreign
- helper t cells bind to this and releases cytokines to activate B cells
- the specific b cell will form antibodies by producing plasma cells.
cell mediates immunity
- targets endgroenous antigens (cancer cells or virus infected cells.
- all nucleated cells present MCH 1s if this is abnormal then this time a different type of t cells (cytotoxic t cells) will respond by killing the cell. can also be done by NK cells.
what are some defects that can happen in the innate immune system?
Chediak-hiagashi syndrome
deficiencies in complement proteins
chronic granulomatous disease
leukocyte adhesion disease
Chediak-hiagashi syndrome- decreased number of neutrophils do recurrent infections. As giant granules in cytosol of neutrophil and defects in lysosome fusion. remember lysosomes found in cells and contain digestive enzymes.
deficiencies in complement proteins-
complement proteins aid pathogens destruction by piercing membrane (cellysis) or by making them more attractive to phagocyte cells (osponisation)
chronic granulomatous disease-
- mutation in NADPH component- defects in oxidative burst.
- phagocytosed microbes can’t be killed –> recurrent infections
leukocyte adhesion disease-
impairment of molecules that transport phagocytes out of the blood to the site of infection at the tissue.
List the organisms that commonly cause:
community acquired pneumonia, croup, epiglottis, tonsillitis, pharyngitis (sore throat)
CAP- The most common cause of bacterial pneumonia in the is Streptococcus pneumoniae.
Legionella and Staph aureus - significant in very severe CAP
Croup- virsuses e.g Parainfluenza virus.
epigolttitis- • Usually caused by Haemophiluis influenzae (Capsulate type b) = ‘Hib’
• Ages it effects 6-12 years
pharyngitis (sore throat)- bacteria Streptococcus pyogenes)
common cold- rhinovirus
tonsilitis- Usually caused by group A streptococcus bacteria.
Explain how COPD may be exacerbated (made worse) by respiratory infections and the treatment for it.
- The current evidence indicates that bacterial infection causes approximately 40–50% of acute exacerbations of COPD.
- Viral Infection – RSV, Flu, Paraflu
- Non-infective causes – Cold, Allergens, etc
COPD patients have:
Chronic sputum production
Chronic colonisation with
bacteria:
Pneumococcus
Haemophilus influenzae
Moraxella catarrhalis
But: these may also be the causes of exacerbations
COPD Exacerbation – Treatment
• Maintain oxygenation • Treat (possible) underlying cause • Amoxicillin 500mg tds/doxycycline • Treat airways obstruction o bronchodilators o corticosteroids • Hydration/nutrition
