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The Innate Immune System Vs. Adaptive System

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The Innate Immune System Vs. Adaptive System
The human body has developed a great variety of mechanisms to protect itself from invasion by pathogenic microorganisms. These host defences include prevention of entry and dealing with the pathogens once they have breached the outer defences of the body.
Once a pathogen is inside the body, the immune system must recognize the pathogen as foreign and dispose of it.
The overall immune system is divided into two separate systems that do work together to protect the body. The Innate system, is the initial immune response from childhood which functions in the same way whether or not the individual has already encountered the same pathogen. Whereas, the Adaptive system matures with a person as it adapts to the first encounter with the pathogen
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The main differences between the two systems are the speed and intricate specificity of the pathogen recognition systems and the memory capacity of the adaptive system.

The Innate immune system mediates the initial protection against infections; it has no memory but can recognise and respond to microbes (seen in Figure 1).
The innate immune response is triggered by damaged hosts and has the exact same response to recurrent infections by a microbe, although it doesn’t react with the non-self-host cells.
The receptors of the innate immune system are fixed on to the germline and are not subjected to recombination as they are identical on all cells of the same lineage.
There is constant communication with the adaptive immune system as it often uses mechanisms of the innate immune system to eradicate infections.

Figure 1: shows an overview of the innate immune response and its quick protection over a 12 hour period.

The components of the innate immune system identify specific components that are common in various classes of microbes, that are not present on host
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They produce different patterns of cytokines in response to host cell defence mechanisms, however, they both express CD4+ molecules that interact with the MHC/HLA class II molecules that have not bound with the microbial peptides. Th1 cells are activated by peptides associated with macrophages and dendritic cells.
The production of IL-2 by Th1 cells stimulates T cell proliferation while IFN-Y induces the dendritic cells. This allows for the presentation of the microbial peptides with MHC/HLA class I molecules to cytotoxic CD8+ T cell precursors.
Additional molecules on the surface of the Th1 cells interact with ligands on the surface of the dendritic cells to enhance this process. Different ligands of dendritic cells can also suppress the adaptive immune response.
Mature cytotoxic cells derived from cytotoxic CD8+ T cell precursors interact with virus-infected cells that are presenting viral peptides through their MHC/HLA class I molecules. Killing of infected cells occurs via two mechanisms, both designed to cause apoptosis:
1. Perforin-mediated cell death: mature cytotoxic T cells have cytoplasmic granules containing Perforin and granzymes that induce apoptosis.
2. Fas-mediated

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