Repetition Flashcards
Where are PRRs located, and give an example of its function in that location.
PRRs can be transmembrane proteins and located on the surface of many types of host cells where they recognise extracellular pathogens. For example, on macrophages and neutrophils they can mediate the uptake of pathogens into phagosomes to destroy the pathogens. PRRs can also be located intracellularly, where they can detect intracellular pathogens such as viruses. These PRRs are either free in the cytosol or associated with the membranes of the endolysosomal system.
How do bacteria defend themselves against viruses?
Bacteria defend themselves from viruses using intracellular proteins called restriction factors, which block viral propagation.
What is the function of natural killer (NK) cells?
NK cells, which can be enhanced by type 1 interferons (interferon-a and interferon-b) are recruited to the site of inflammation and destroy virus-infected cells by inducing apoptosis.
What happens if a pathogen is too large to be phagocytosed by phagocytic cells?
Instead of phagocytosing the pathogen, phagocytic cells like macrophages, neutrophils, and eosinophils will gather around the invader. They secrete defensins and other damaging agents and release the toxic products of the respiratory burst. This barrage is often sufficient to destroy the pathogen.
What is xenophagy? How does it function?
Xenophagy is the autophagy of microbial invaders. Xenophagy functions in the direct elimination of invaders, activation of immune responses, inflammasome control, and antigen presentation.
Give the pathway of xenophagy. How does this compare to viral phagocytosis?
In xenophagy, phagocytic cells engulf a pathogen, and the pathogen is sequestered in a double membrane vesicle named the autophagosome. Subsequently, the autophagosome is fused with a lysosome containing antimicrobial toxins, and the pathogen is degraded in this autolysosome. In xenophagy with viral pathogens, a virus is engulfed by a phagocytic cell and viral nucleic acids are then sequestered in an autophagosome. The autophagosome containing viral nucleic acid is then turned into an endosome and the viral nucleic acid can be recognised to induce expression of type 1 interferons (interferon-a and interferon-B).
How do selective autophagy receptors (SLRs) function in xenophagy.
Salmonella can escape phagocytosis and end up in the cytosol, after which it is recognised by the ubiquitin machinery, after which the bacterium can be sequestered in an autophagosome and lysed. SLRs, like Atg8, recognise ubiquitin and/or galectins on bacteria or damaged phagosomes and target them to LC3-II. SLRs also deliver neo-antimicrobial peptides derived from ubiquitinated proteins. These ubiquitinated proteins are often useful precursors for new antimicrobial peptides. These neo-antimicrobial peptides and the ubiquitinated pathogen end up in the same autophagosome, where the antimicrobial peptides can degrade the pathogen.
What is Persephone and how is it activated?
Persephone is a serine protease that belongs to a danger pathway activated by abnormal proteolytic activities, and results in the activation of the Toll pathway. The Persephone pathway can be activated by the exogenous proteases of a range of different microorganisms, including Gram-negative bacteria. Persephone itself is an immune receptor able to sense a broad range of microbes through virulence factor activities rather than molecular patterns.
Explain the Ca2+-dependent CAX1/3 activation pathway.
The Ca2+ sensor CBL couples with CBL-interacting protein kinases (CIPKs) and form a complex. CBL-CIPK modules can then activate CAX1/3 by phosphorylating the conserved S-cluster in the auto-inhibitory domain. CAX1/3 may also serve as a convergent point of other Ca2+ signalling events in response to abiotic stress factors.
Explain the Ca2+-independent CAX1/3 activation pathway.
Ca2+-independent activation of CAX1/3 occurs through pattern-triggered immunity (PTI). In response to MAMPs, the immune receptor complex of flagellin sensitive 2 (FLS2) and brassinosteroid insensitive 1-associated kinase 1 (BAK1) is assembled. Downstream cytoplasmic kinases BIK1 and PBL1 can then phosphorylate the conserved S-cluster in the auto-inhibitory domain of CAX1/3.
When is a plant protected against a pathogen.
If an avirulent (Avr) allele in a pathogen responds to an R allele in the host plant, the host plant will have resistance, making the pathogen avirulent.
Name some examples of PAMPs/MAMPs.
Flagellin in bacterial flagella, peptidoglycan in bacterial cell walls, EF-Tu (bacterial elongation factor for protein translation), chitin in fungal cells walls, and oligosaccharides in fungal and plant cell walls.
What is the signalling cascade of flagellin recognition in plant immunity.
The PAMP flagellin can be recognised by the FLS2 PRR, after which it dimerises with BAK1, which is a co-receptor of several PRRs. Subsequently, BIK1, a receptor-like cytoplasmic kinase (RLCK) is recruited and mitogen-activated protein kinases (MAPKs) and calcium-dependent protein kinases (CDPKs) are activated.
How do specialised pathogens, like certain bacteria or fungi, affect PTI in plants?
With specialised pathogens, like certain bacteria or fungi, the fungi grows inside the plant cell and secretes effector proteins, or the bacterium secretes effector proteins inside the plant cell using a pilus. These effector proteins inhibit the PTI response and can be recognised by an R-proteins’ nucleotide-binding leucine-rich repeats (NB-LRR), resulting in an ETI response. These effector proteins have an effect on a lot of different parts of the PTI. For example, the effector proteins can inhibit PRRs and BAK1, MAPK, and GRP7, which are important in mRNA translation.
On which responses is plant immunity based?
Plant immunity is based on a hypersensitive response (cell death), and the production of pathogen-related proteins (toxic proteins and enzymes that degrade bacterial/fungal cell walls).
Plant responses can be divided into two categories. Give these two categories and explain what they entail.
Plant responses can be divided into a local defence and a systemic defence. The local defence, which happens at the site of inflammation, consists of a hypersensitive response (HR) and the secretion of antimicrobial secondary metabolites (e.g. alkaloids in some plant species, glucosinolates in Arabidopsis), antimicrobial proteins (e.g. defensins, pathogenesis-related (PR) proteins), and antimicrobial cell wall-degrading enzymes (e.g. chitinases and B-glucanases). The systemic defence consists of systemic acquired resistance (SAR; depends on salicylic acid and ethylene) and induced systemic resistance (ISR; depends on jasmonic acid and ethylene).
What are the 5 key requirements of the immune system?
- Rapidly and efficiently eliminate dangers
- Be able to recognise a diverse range of molecules
- Be tightly controlled (up- and downregulated)
- Be tolerant to own cells and tissues, and commensals
- Memorise and transfer protection to progeny
Name all types of phagocytic cells and their function.
Neutrophils, macrophages, and dendritic cells are all phagocytic cells. Of those, macrophages and dendritic cells function also as antigen presenting cells (APCs). Proteins that are eaten by APCs are broken down to small pieces (peptides), which are loaded on special receptors (MHCs) and transported to the cell surface. A peptide-MHC complex can be recognised by a T cell and that interaction can lead to an adaptive immune response.
What does activation of a Toll-like receptor do?
TLR signalling activates the inflammatory response. A signalling cascade leads to NFkB inducing the expression of cytokines (TNF, IL-1, and IL-6), chemokines (CCL2, CXCL8, and others), endothelial adhesion molecules (E-selectin), and costimulatory molecules (CD80 and CD86).
Macrophages can polarise into two states. Explain these states.
Macrophages can differentiate into different phenotypes, of which the main extremes are M1 and M2, due to activation by certain compounds. The M1-macrophage phenotype has a pro-inflammatory, bactericidal, and phagocytic function. The M2-macrophage phenotype has an anti-inflammatory, matrix producing, pro-angiogenesis, and pro-wound healing function. Macrophage polarisation goes along with metabolic change. In the inflammatory M1-macrophage phenotype, due to two breaks in the TCA cycle, the production of antimicrobial nitric oxide is activated due to an excess of citrate, and due to an excess of succinate, IL-1B and IL-5 are produced. In the anti-inflammatory M2-macrophage phenotype, the TCA cycle is not broken at two points, resulting in an absence of nitric oxide, and IL-1B and IL-5 production.
With insect immunity, the innate immune system is split into two parts. What are these parts and what function do they have?
The innate immune system of insects is split into the systemic/humoral part and the local part. With the systemic/humoral part, the fat body secretes antimicrobial peptides (AMPs) upon infection into the haemolymph that circulates through the whole insect, and reactive oxygen species (ROS) are produced. The local system consists of a cellular response with haemocytes.
What is the function of plasmatocytes in insect immunity, and which proteins play an important role in this function?
Plasmatocytes can conduct phagocytosis. In this phagocytosis, scavenger receptors, eater proteins, and DSCAM play a very important role.
What is the function of crystal cells in insect immunity, and which protein plays an important role in this function?
Crystal cells can conduct melanisation, where prophenoloxidases play a very important part.
What is the function of lamellocytes in insect immunity?
Lamellocytes can conduct encapsulation. Lamellocytes differentiate and migrate to the infection.
