Immune response and Principles of Infection Flashcards
Innate system description
Barriers to infection?
Cells involved and function
- Low specificity, no memory
- Physical barriers e.g. mucosa, skin, hair, tears, flora, gastric acid
- Phagocytes: acute response by killing any microbe found through ingestion/chemical secretion. Complements: proteins that help phagocyte attach to microbe.
Interferons: interfere with virus-infected cells.
Natural killer cells: kill any cell that has an abnormal structure
Inflammatory cytokines
Adaptive system description
What are its 2 types? What lymphocyte type do they use?
Difference between T and B lymphocytes?
- High specificity, memory
- Humoral (B lymphocytes) and Cell-mediated (T lymphocytes)
- T cells mature in Thymus and B cells mature in Bone marrow
Function of T cells
T-helper: release cytokines, and bind to APCs. Cytokines stimulate B cell activity.
T-cytotoxic (CTL): kill the microbes. “Foreign proteins” attach to the MHC on the cell surface.
T-regulatory: reduce immune response after microbe killed.
Function of B cells
Bind to complementary antigen and release the correct antibodies (immunoglobulin). Antibodies carry out neutralisation (coats the virus and stops it entering cells) and opsonisation (coat the microbe). *IgM made first, IgG made later.
Define:
- Saprophyte
- Commensals
- Pathogen
- Opportunistic infection
- Microbe/plant/fungus living off dead/decaying matter
- Natural flora
- Disease-causing microbe
- An infection can easily occur when immunosuppressed
Stages of infection and modes of infection
- Surviving in the environment and can form spores
- Entering body:
- Droplets e.g. TB
- GIT e.g. salmonella
- Skin e.g. malaria
- Fomites e.g. clothes
- Epithelial contact e.g. STD - Multiplication - can be local/systemic spread
- Avoid host’s defence system
- Damage to host by toxin release and the host’s own immune response
- Microbe leaves to find a new host - leaves similar to how it gets in
Define:
Acute infection
Chronic infection
Asymptomatic infection
- < 6 months
- > 6 months
- infection present without any symptoms
Modes of viral transmission?
How to diagnose viral infections?
- Epithelial contact, animal/insect bites
- Clinical: look at the type/duration of symptoms, lifestyle, location.
Lab: look for antibodies for the virus - IgM = recent infection, IgG = past infection. Look for virus itself.
Define phagocytosis
Characteristics of the main phagocytes?
- Ingestion of cells, and is the mechanism of the innate immune system
- Neutrophils have a short lifespan. Monocytes become macrophages in tissue, which secrete inflammatory factors. Dendritic cells present Ag’s to T cells, which links the innate and adaptive immune systems.
What is chemotaxis?
How are pathogens recognised?
- Phagocytes drawn to area of inflammation along the chemoattractant gradient.
- Pathogens have PAMPs on their surface, allowing it to survive. Phagocytes have PRPs (receptor) to recognise the PAMPs - detect foreign cells.
What are the next stages of phagocytosis, and how do they work?
Opsonisation: Opsonins are proteins that coat microbes - can make phagocytosis easier, and neutralise the pathogen.
Engulfment: Microbe are surrounded by pseudopods, bringing it into the phagocyte. Vesicle with pathogen = Phagosome. The phagosome then fuses with lysosomes = Phagolysosome. Lysosomes release digestive enzymes to break down microbe.
What are some of the pathogen killing mechanisms?
Importance of phagocytosis in removing dead cells?
- Oxygen independant: Lysozyme, Proteolytic/Hydrolytic enzyme
Oxygen dependant: Generation of reactive oxygen species, like Hydrogen peroxide - Apoptotic cells have signals to attract phagocytes while healthy cells release signals to repel phagocytes. Phagocytes that have engulfed apoptotic cells release cytokines = ↓inflammation, and ↑healing.
Describe the structure of an antibody/Ig
- 4 polypeptide chains held by non-covalent bonds and disulphide bonds. 2 light and 2 heavy chains, with 2 identical antigen-binding sites. A hinge region for flexibility. Fab fragments bind to antigen and Fc fragments bind to phagocyte receptors. Sequence of Fc determines which antibody class is made.
What are the different Ig classes and what are their functions?
Function of Ig class switching?
IgA - Found in breast milk, sweat, tears, saliva etc. Are in first line of defence, and initiate inflammatory reactions.
IgD - rare and unknown role.
IgE - rare and respond to parasitic worms.
- IgG - most common, only ones that can CROSS PLACENTA to protect foetus. Can act as opsonins to aid phagocytosis. They stay in the body for a long time, therefore its presence in serum shows past infection.
- IgM - can have an extra heavy chain membrane bound to B cell, or come with J chain to attach to many other IgM. Work to induce phagocytosis. Made first, so indicate recent/current infection.
- Some cytokines signal for Ig’s to switch class.
How are B cells activated?
APC’s engulf the pathogen, break up the antigens and present it on its surface bound to a MHC. In the exogenous antigen pathway, they bind to MHC Class II, which only a CD4 (T-helper) can bind to activate = cytokine release to attract B cells.
In the endogenous antigen pathway, MHC Class I is used, which only CD8 (T-helper) can bind to activate = cytokine release.
B cell activation depends on T cells being activated. B cell binds to APC and then attracts T-helper cells. But, for antibodies to be produced, it has to be stimulated by Th cells that have already been bound to APC. Once B cell is activated, it becomes a plasma cell.
