29 Sep 2022

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The human immune system: adaptive and innate immunities

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Academic level: Master’s

Paper type: Research Paper

Words: 1177

Pages: 4

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The human body exists in a non-sterile environment. At all times, people are continually being bombarded by microorganisms, some harmless while others are carrying the potential to cause harm. As a design mechanism to help individuals cope with the same, the body has the immune system. The immune system is the defense mechanism that helps human beings fight off any microorganisms that are likely to cause disease. When the immune system is not functioning, one is at the risk of multiple infections, which lead to death (Chaplin, 2006) . The human immune system is made up of two distinct yet interrelated divisions. There is the first line of defense known as the innate immunity with the second line of defense known as the adaptive immune system. The second line of defense is responsible for handling any incidences of re-exposure (“Poster Session 1: Innate Immunity and Adaptive,” 2014) . Adaptive immunity is the immune system whose mechanism has been exploited in the design of vaccines, as will be discussed at a later stage in the paper.

The immune system generally has two components known as the cellular and humoral immunity. These two are present in the adaptive system as well as the innate. The innate system also has an anatomical component in it. While both systems work to offer a defense, they differ in a couple of ways (Rahman, 2014) . The innate immunity is always ready and simply needs the presence of a pathogen for it to be mobilized and begin attacking, the adaptive system, on the other end takes quite some time and is rather specific. By being specific, it means that the adaptive immune system only reacts to the antigen that provoked it; innate immunity does not choose in any way and attacks any pathogen present in the system. The adaptive immune system demonstrates memory in that it can recall a pathogen that it was previously exposed to. The ability to remember provokes a more rapid response to the pathogen, unlike during the initial encounter. Innate immunity does not have immunological memory. (Schmid & Münz, 2007) 

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The overall role of the immune system is anchored on its ability to distinguish between self and non-self-components. It is only after the body can tell that particular cells are not of its own that it is able to launch an immune attack. The cells of the body that are responsible for immunity originate from the bone marrow. These cells differentiate to take up distinct paths that are responsible for either of the earlier mentioned immune responses (Herwald & Egesten, 2017) . They include the myeloid cells that are basophils, neutrophils, dendritic cells, macrophages, and eosinophils. The other group is the lymphoid cells that comprise the B Lymphocytes, T lymphocytes, and Natural killer cells. The T cells migrate to the thymus, where there are differentiated further into CD4+ T helper cells and CD8+ pre cytotoxic cells. The T helper cells are of two groups; one is TH 1, which helps CD8+ while the second group is TH2 that helps the B cells convert into plasma cells that are responsible for the production of antibodies (Diefenbach, Colonna, & Koyasu, 2014) .

When a pathogen such as Clostridium Tetani, which is responsible for causing tetanus, an infection that is known to affect muscular function severely invades the body. It first meets the innate immunity anatomical barriers. The anatomical barriers are both chemical, biological, and mechanical. The mechanical factors are the skin and the epithelia. The skin forms a barrier that is impermeable to multiple organisms. The skin desquamates severally, ensuring that any organisms adhering are shed off with ease. When the pathogen falls on the epithelium of the gastrointestinal tract or air passages, the cilia are in constant motion that keeps the surfaces pathogen-free. These surfaces also have mucus which has a trapping effect, the mucus not only immobilizes the pathogen, it forms a barrier between it and the wall of the gut. (Sonnenberg & Artis, 2012) 

Chemical factors are the chemical components that can easily neuter the clostridium tetani even before it gets into the body. Fatty acids that are usually present in the human sweat are unfavorable to bacterial growth (Meyer, Stockfleth, & Christophers, 2007) . This means that the skin then forms a very unsuitable ground for growth. Lysozymes and phospholipases are found in tears, ensuring any pathogens coming through that route are attacked (Sonnenberg & Hepworth, 2019) . Saliva and nasal secretions have been known to break down the cell membranes of bacteria. Within the lungs, the surfactants are potent opsonins; these are chemicals that aid the phagocytic destruction of the microbes. Biological factors are the normal flora that exists on the body surfaces; they naturally compete for the spaces and fight off any new organisms within their territory. 

When the natural anatomical barriers are broken, and the organism gets into the body, a humoral component of the innate system is brought into place. Humoral factors result in inflammation, recruitment of phagocytic cells, and edema. There is usually activation of the complement system, which is a cascade that results in a complex that attacks the bacteria, eating them up and poring the membranes resulting in its death (Kobayashi & DeLeo, 2013) . The coagulation system is a chemotactic factor that facilitates the movement of phagocytes to the site of injury. Components of blood such as B lysin produced by broken down platelets also phagocytose some gram-positive bacteria. Other components of the innate humoral immunity are lactoferrins and transferrins that bind iron, denying the bacteria necessary nutrition (Černý & Stříž, 2019) .

The cellular innate immunity involves killing of the bacteria through different modes. Phagocytosis is where the foreign cells are swallowed up and digested by the immune cells. Other killing methods involve the production of oxygen radicals by the body, which attacks the bacteria and impairs their metabolic processes. Neutrophils, polymorph nuclear cells, natural killer cells, and macrophages are responsible for this innate cellular destruction (Sonnenberg & Hepworth, 2019) .

When the clostridium tetani get into the body, the B cells and T cells can recognize it as foreign through the immunogens on the bacterial surface. Ideally, a foreign cell has an antigen that has a portion known as an epitope that binds to the lymphocytes. The part on the B cell that binds the epitope is known as B cell receptor, which is an antibody molecule known as surface immunoglobulin. The body’s B and T cells have the ability to recognize millions of different epitopes. This means that the B and T cells are variant to the tune of millions. While this helps them recognize any new foreign agent, it is disadvantageous as only a few of the many available lymphocytes are able to bind the epitopes. These cells, once they bind, must then proliferate rapidly to be able to marshal enough numbers to stage a defense. During this proliferation that takes several days, the innate immunity is usually the only defense mechanism.

The adaptive immunity continually improves upon re-exposure. The cells can proliferate faster and are usually more aggressive. This is usually the principle behind the use of vaccines. The vaccines are the initial exposure; some vaccines are given severally to increase the responsiveness of the immune system to the particular pathogen. Once an actual pathogen attacks, there is a rapid and aggressive attack, which eventually results in the pathogen being eliminated. Without the vaccines, which are usually the antigen is smaller doses, the pathogen would take time to propagate as the adaptive lymphocytes proliferate, which would cause harm.

References 

Černý, J., & Stříž, I. (2019). Adaptive innate immunity or innate adaptive immunity? Clinical Science , 133 (14), 1549–1565. https://doi.org/10.1042/cs20180548 

CHAPLIN, D. (2006). 1. Overview of the human immune response. Journal of Allergy and Clinical Immunology , 117 (2), S430–S435. https://doi.org/10.1016/j.jaci.2005.09.034 

Diefenbach, A., Colonna, M., & Koyasu, S. (2014). Development, Differentiation, and Diversity of Innate Lymphoid Cells. Immunity , 41 (3), 354–365. https://doi.org/10.1016/j.immuni.2014.09.005 

Herwald, H., & Egesten, A. (2017). Cells of Innate and Adaptive Immunity: A Matter of Class? Journal of Innate Immunity , 9 (2), 109–110. https://doi.org/10.1159/000457176 

Kobayashi, S. D., & DeLeo, F. R. (2013). Systems Biology and Innate Immunity. Journal of Innate Immunity , 5 (2), 97–99. https://doi.org/10.1159/000347135 

Meyer, T., Stockfleth, E., & Christophers, E. (2007). Immune response profiles in human skin. British Journal of Dermatology , 157 , 1–7. https://doi.org/10.1111/j.1365-2133.2007.08264.x 

Poster Session 1: Innate Immunity and Adaptive. (2014). Hepatology , 60 , 501A-509A. https://doi.org/10.1002/hep.27506 

Rahman, M. M. (2014). Interactions of Host’s Innate and Adaptive Immune Components in the Pathogenesis of Viral Encephalitis: a Review. MOJ Proteomics & Bioinformatics , 1 (2). https://doi.org/10.15406/mojpb.2014.01.00007 

Schmid, D., & Münz, C. (2007). Innate and Adaptive Immunity through Autophagy. Immunity , 27 (1), 11–21. https://doi.org/10.1016/j.immuni.2007.07.004 

Sonnenberg, G. F., & Artis, D. (2012). Innate Lymphoid Cell Interactions with Microbiota: Implications for Intestinal Health and Disease. Immunity , 37 (4), 601–610. https://doi.org/10.1016/j.immuni.2012.10.003 

Sonnenberg, G. F., & Hepworth, M. R. (2019). Functional interactions between innate lymphoid cells and adaptive immunity. Nature Reviews Immunology . https://doi.org/10.1038/s41577-019-0194-8 

Wagner, J. A., & Fehniger, T. A. (2016). Human Adaptive Natural Killer Cells: Beyond NKG2C. Trends in Immunology , 37 (6), 351–353. https://doi.org/10.1016/j.it.2016.05.001 

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StudyBounty. (2023, September 15). The human immune system: adaptive and innate immunities.
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