Pattern Recognition Receptors

The body’s protection against viruses, bacteria and other types of invasions is our immune system (Tortora, 2014).

The innate and adaptive immune response start with exposure to an antigen in the epithelium of

Signaling proteins that alert the immune system an infection is present and that sometimes directly fight pathogens are the:

Innate Immune System – Nonspecific and abrupt first response; comprised of epithelial surfaces (physical barriers), neutrophils, and macrophages.

2. NOD proteins (p.456): Another set of receptors for PAMPs that are located inside a cell rather as part of a cell’s cytoplasmic membrane.

The human immune system creates a series of responses in the body to defend the body. If a foreign organism, such as a virus or a cold invades your body, it recognizes these foreign organisms, and, in turn, attacks them to get rid of them. One can think of the immune system as an army of many cells which have set up their own bastion in the human body. They have only one job: To defend. The immune system’s cells are various kinds of white blood cells. The human body typically creates about 1000 million white blood cells on a daily basis. A group of these cells, macrophages, establish a patrol of sorts throughout the body killing germs as soon as they enter the body. However, sometimes an infection can cause the macrophages to succumb to it. The body begins to fight back with stronger T- and B-cells.

Despite the wide-range of microbes affected by the innate immune system, the activity of peptides associated with the immune response seem to be highly sequence specific. The peptides specifically target areas of the membrane with high curvature. (Mark, 601)

The mechanisms whereby a lack of microbial stimuli results in dysregulation of the immune system are poorly defined but are often attributed to a dysregulation of Th1 and Th2 responses. Douwes et al. explains that microbes are often recognized by innate immune cells through the binding of pathogen recognition receptors (PRR). This recognition results in the induction of Th1 responses which in turn down regulate the Th2 responses that are commonly associated with chronic inflammatory disorders (Barnes). While this is a candidate mechanism it is vastly incomplete; downstream affects of PRR induction are highly dependent on the stimulus and may result in proinflammatory induction rather than an anti-inflammatory Th1 response (Kielian). While this lack of a defined mechanism has lead some to reject the hygiene hypothesis, others have looked to animal models can case studies to support

Cellular Basis Of Disease: Why has the discovery of Toll-like receptors revolutionised our understanding of how the innate immune system works, and what is the therapeutic potential?

After some careful reading, it appears feature detectors are simply the individual neurons or groups of neurons in the human brain which code for perceptually significant stimuli. Feature detectors are located in the visual cortex, although Barlow’s idea is that the retina could allow act as a feature detector. The visual cortex is located in the most posterior part of the brain occipital lobe, which is one of the four major lobes of the cerebral cortex and can’t be seen outside of the brain or at the back of the head.

If a pathogen breaches barriers: innate immune response result into an immediate effect of non- specific response. All Innate immune systems derived from plants and animals, when a pathogen evades the innate response, a third layer of protection is possessed by vertebrates in which activation of adaptive immune system takes place. The immune system response adopts itself within an infection and pathogen recognition is improved. As a result of the improved response, its then retains itself when the pathogen is eliminated in form of an immunological memory and allows the adaptive immune system to mount faster and stronger when pathogen is encountered each time.

NFkB is a protein complex involved in cellular stimulate responses to environmental stress such as UV, free radicals, bacterial or viral infection.it also plays a key role in regulating the immune response to infection (κ light chains are critical components of immunoglobulins). Incorrect regulation of NF-κB has been linked to cancer, inflammatory, and autoimmune diseases, septic shock, viral infection, and improper immune development

RIG-I recognizes bacterial ligands in glial cells. RIG-I is traditionally viewed as a viral pattern recognition receptor, however, more recently the pathogen ligands for RIG-I have been expanded to include bacteria nucleic acids. In non-CNS cell types RIG-I has been documented to identify bacteria RNA directly or DNA indirectly via an RNA polymerase III dependent mechanisms. RIG-I dependent recognition of bacterial nucleic acids was demonstrated to be pathogen and cell type specific. In glial cells the role and mechanism of RIG-I in pathogen detection has not fully been explored. We have previously demonstrated expression of RIG-I and the contribution of RIG-I to recognition of RNA and DNA viruses. However, the requirement of RIG-I for

Our immune system is the second most complex system in our body. It is made up of organs, cells and proteins that work together to protect our bodies from harmful bacteria, viruses or other microorganisms that can cause diseases. Usually we don’t notice our immune system defending us against pathogens, but if the pathogen (harmful microorganism) is aggressive or if our body hasn’t ever come into contact with it, we can get sick. The jobs of our immune system are to recognise pathogens, as well as neutralise and remove them from our body. Our immune system also has to fight our own cells if they have changed due to an illness, for example, cancer. (1)