Test 4 Study Guide Part 7 Flashcards
Coreceptors:
- Helper T-cells have which coreceptor?
- How does this effect them?
- Cytotoxic T-cells have which coreceptor?
- How does this effect them?
- Helper T-cells have which coreceptor?
CD4 - How does this effect them?
can only be activated by MHC-2 presenting cells - Cytotoxic T-cells have which coreceptor?
CD8 - How does this effect them?
Can only kill MHC-1 antigen presenting cells
What happens after T Helper cell activation by binding with a MH2?
- What molecule effects cytotoxic t-cells?
Turn into effective Th1, Th2 or other specialties.
B-cell differentiation into plasma cell
cytotoxic T-cell proliferation
- What molecule effects cytotoxic t-cells?
(interleukin-2)
FAS:
- Stands for?
- FASL and FAS?
- Where will FASL be found?
- Stands for?
First Apoptosis Signal - FASL and FAS?
FAS receptor on T-cells, FAS ligand activates FAS and causes apoptosis - Where will FASL be found?
In a few days into infection T - cells make FASL to kill themselves
Immune privileged sites (Eye, testes)
Mechanisms to defend the testes:
Sertoli cells have tight gap junctions.
Sertoli cells produce FASL
Mechanisms to defend the anterior chamber of the eye:
Coating of interior of the eye with FasL
Secretion of different cytokines which inhibit inflammation
How do tumor cells use FasL?
Not all but some produce it to protect them from the immune cells by triggering apoptosis of lymphocytes
Severe Combined Immunodeficiency Disease:
- other name?
- Cause of disorder:
- Define:
- other name?
Bubble boy disease - Cause of disorder:
inherited, WBC stem cells lack adenosine deaminase - Define:
Lack antibody-mediated and cell-mediated immunity
Adenosine deamanise is involved in what condition?
A lack of this causes Severe Combined Immunodeficiency Disease
Treatment for Severe Combined Immunodeficiency Disease:
Gene therapy with retrovirus.
- many developed leukemia
Infection with one disease protects from another closely related one
Cross reactive immunity:
Edward Jenner and cow pox (vaccinia) vaccine:
Milk maid exposed to cowpox -> immunity to small pox
Edward Jenner and cow pox (vaccinia) vaccine:
Milk maid exposed to cowpox -> immunity to small pox
Innoculate orphan with vaccinia (cow pox) -> infect small pox -> protected orphan
Louis Pasteur anthrax vaccine:
Heated anthrax -> lost virulence (attenuated), antigenicity maintained -> inoculated sheep -> they survived
Four types of adaptive immunity:
Naturally acquired active immunity
Naturally acquired passive immunity
Artificially acquired active immunity
Artificially acquired passive immunity
Naturally acquired active immunity:
Get infected and recover
Naturally acquired passive immunity:
Placenta: IgG transfer into plasma
Breast Feeding: IgA and some IgG into gastrointestinal tract (does not enter circulation from GI tract!)
Artificially acquired active immunity:
Vaccination
Artificially acquired passive immunity:
Gamma globulin shots (IgG injection)
Intravenous immunoglobulin
Antiserum/antitoxin (target and neutralize a toxin)
Antivenom shots (antitoxin)
RhoGam (Rh system, antibodies against big D antigen)
Response time:
- Primary response:
- Secondary response:
- Primary response:
5 - 10 days - Secondary response:
~ 2 hours
Secondary response is dependent on what?
Memory B cells
Memory T cells (lesser extent?)
NOT CAUSED BY RESIDUAL ANTIBODIES, exists without them
- B- cells inherent there specificity in a massive library
- Each B cell produces one of these antigen options
- When the B-cell finds the antigen it is specific for, it multiplies
- These progeny/clones become plasma cells and memory cells, which respond to infection
Clonal Selection Theory:
What are the most abundant lymphocytes in adult?
When do these lymphocytes reduce in levels?
Long-lived T cells of different subtypes, specific for the antigen that caused their generation
About age 70
Germinal centers:
- Formation:
- Formation:
B-cell is activated, becomes the center of a massive dividing group of clones, both b memory cells and plasma cells
Advantages of germinal centers:
Somatic hypermutation occurs here
Plasma cells are longer lived
Plasma cells have faster replication
Plasma cells have better antibody production
Somatic hypermutation:
Occurs in germinal centers. An activated B cell has a higher mutation rate as it continues to divide.
This results in plasma cells which make antibodies which are either slightly more or less effective against the invader
Vacca:
Latin for cow.
Start of vaccination because of cow pox
Salk vaccine:
1st polio vaccine
inactivated virus
- Only inactivated salk type vaccines are used in the US
Sabin vaccine:
Oral live attenuated polio vaccine. Caused about 100 polio cases a year in the US, but is no longer used
Three ways to make a vaccine:
- Live viruses (attenuated virulence):
- Killed virulent viruses:
- Recombinant viral proteins
Adjuvants:
- How do they work?
Act as PAMPs or DAMP to bind to pathogen recognition receptors of dendrites.
Enhances adaptive immune response.
Therefore enhances vaccine ‘strength’
Fetal self recognition:
Fetus originally capable of targeting self antigens.
Continuous exposure early in fetal and postnatal life results in toleration of an antigen
Antibodies targeting the body are called?
T-cells targeting the body are called?
Autoantibodies
Autoreactive T cells
Mechanisms of self-antigen removal:
- Clonal Deletion:
lymphocytes recognizing self-antigens are destroyed - Clonal Anergy:
lymphocytes recognizing self-antigens are prevented from becoming inactive (regulatory t cells)
Thyroid gland:
- Imune privilege status?
- Protein that is hidden self antigen:
- Imune privilege status?
Immune privileged - Protein that is hidden self antigen:
Thyroglobulin
Central Tolerance:
- Define:
- Controlled by:
- Define:
Regulation of potential self targeting lymphocytes in thymus or bone marrow. - Controlled by:
Apoptosis, clonal deletion, or anergy
Peripheral Tolerance:
- Define:
- Controlled by:
- Define:
Regulation of potential self targeting lymphocytes outside thymus or bone marrow. - Controlled by:
Anergy (provided partly by regulatory T lymphocytes)
Forbidden clones:
Auto-reactive T Cells, which are kept in check by regulatory T cells.
Person’s ability to develop active immunity is called:
Immunological competence
Immunological competence:
- When does it occur?
- What helps in the meantime?
- What might happen if immune competence occurred in utero?
- When does it occur?
~1 month post-parturition - What helps in the meantime?
Passive immunity from IgG that crosses the placental - What might happen if immune competence occurred in utero?
Fetus could target mom
The fetus is immune to the same antigens as the ____:
How long is breast feeding recommended?
Mother
Exclusively breast milk for 6 months at least (then it can continue)
Intravenous immunoglobulin:
- Source:
- Example of:
- Treats:
- Source:
Pooled plasma from thousands of people. - Example of:
Artificial passive immunity - Treats:
First used: combat microbial infections in immunodeficient individuals
Now used: Treat autoimmune conditions, immuno-comprimised cancer patients
Polyclonal antibody:
- What is it?
- Why/how is it made?
- What is it?
Antibodies in a variety of specificities, some of which have optimal specificity, others of which have poorer specificity - Why/how is it made?
Due to somatic hypermutation activated B cells undergoing clonal expansion will produce slightly modified forms. Some with higher affinity and some with low. Polyclonal antibodies include all of these.
Monoclonal antibodies:
- What is it?
- Three letter designation:
- Why/how is it made?
- What is it?
Pure antibody with optimal antigenic specificity - Three letter designation:
MAB - Why/how is it made?
Myeloma and plasma cell -> fused -> form hybridoma -> immortalized cell line producing monoclonal antibody
Hybridoma:
Immortalized plasma b cell for antibody production.
Made by:
- myeloma (cancerous cell) fused with plasma B cell
- Define: monoclonal antibody against HER2 receptors of invasive breast cancers - Treats: invasive breast cancers - Is a type of: Artificially acquired passive immunity
Herceptin:
- Define:
- Treats:
- Is a type of:
Avastin:
- Define:
- Treats:
- Is a type of:
- Define: monoclonal antibody which block VEGF (vascular endothelial growth factor) from binding to its receptors - Treats: Cancer. Colorectal, lung, kidney, brain. - Is a type of: Artificially acquired passive immunity
Natural Killer Cells:
- Target:
- Mechanism of action:
- Inhibitory receptors:
- Target:
Cancer/virus ( - Mechanism of action:
(receptor recognition mechanism unexplained, but does not use MHC)
Cell-mediated (perforins and granzymes)
Destroy on sight, no delay for verification - Inhibitory receptors:
MHC inhibits them, stopping them from killing normal host cells.
How do NKCs get reinforcements?
Cytokine release to bring in acquired immune cells
Three categories of disease of the immune system:
Autoimmune diseases
Immune complex disease
Allergy (hypersensitivity)
Who gets autoimmune diseases more often?
- Why?
Women
2x as likely as in men
- Why?
Andy thinks its from escaped fetal cells
Six reasons for the failure of self tolerance:
1: Immune system exposed to antigen not normally in circulation
2: Self-antigen combines with foreign antigen (or hapten) altering it
3: Antibodies against other antibodies
4: Antibodies produced against foreign antigens may cross-react with self-antigens.
5: Self antigens may be presented with MHC-2 complexes to helper T lymphocytes
6: Inadequate activity of regulatory (suppressor) T lymphocytes
