Example Of T-Helper Cells And Immune System Research Paper
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T-Helper cells play a fundamental role in adaptive immune response i.e. the type of response exhibited by lymphocytes later in infection. T-Helper cells are essentially inactive, but are activated by the antigen displayed on the surface of mature Antigen Presenting Cells (APC’s) activated by infection. T-Helper cells provide signals to B cells to mature into Plasma cells, which secrete antibody specific to the same type of antigen that is displayed on the surface of APC’s (such as dendritic cells). Antibodies primarily function to neutralize and eliminate microbes present in the extracellular environment of the cell. Similarly, activated T-Helper cells release cytokines (mediators of immune response) that convert the pre-CD8 T cell to Cytotoxic T Lympocytes(CTL’s). CTL’s directly kill transformed and infected cells and thus eliminate microbes residing in intracellular vesicles. Macrophages also require help from T-Helper cells to destroy the microbes ingested by them in the phagosomes (Wilson and Hunt 2002).
Understanding the structure and function of cell is critical to the understanding of the retroviruses including HIV. In particular, it allows the investigators to understand virus-host cell interactions. The approach involves elucidating the events in the viral replication cycle, with emphasis on virion attachment, entry and transmission. A detailed mechanism behind the viral infection, nuclear import and integration is useful for regulating gene expression in the infected host cells. Moreover, the synthesis of new viruses by the infected cells is under study. More research needs to be done to characterize the location of the assembly of the virus particles. (Freed and Mouland)
The numbers of thymocytes or T cells inside the human body remain constant due to the homeostasis process. A decline in T helper cells and systemic immune activation are characteristics of HIV pathology. In the acute infection phase, dramatic loss of T-Helper Cells in the mucosa occurs. The chronic phase is characterized by the overproduction of pro-inflammatory cytokines responsible for clonal deletion (through apoptosis) and resultant decline of peripheral CD4+ T Cells. (Freed and Mouland)
Loss of CD4+ T cells after HIV infection is also a result of several mechanisms such as impairment of de novo production of T lymphocytes by the thymus, induction of syncytium formation, alteration of Understanding the HIV cycle is essential for knowing its replication mechanism. HIV attacks the cell especially through the Gastro-Intestinal Tract. The virus enters the host cell and replicates using the viral accessory genes. During primary HIV-1 infection, HIV infects the CD4+ T Cells or the Helper Cells, leading to their depletion and subsequent massive viremia before the onset of antiviral immune response. HIV-1 infects primarily those helper cells that are specific for HIV-1, instead of targeting CD4+ T cells specific for unrelated antigens. The host cell’s adaptive immune responses are activated; HIV-specific Cytotoxic T Lymphocytes lowers viral replication to a lower viral set point. Partial control of viral replication is achieved, but the virus is not completely eliminated from the body. So, the infection becomes chronic in most people, with slow net decrease in T helper Cells over time. The reduction in the number of T Helper cells in the body results in an increased susceptibility to bacterial and viral infections which the body can otherwise normally fight. (Février, Dorgham and Rebollo 2011)
In the final phase of HIV infection, the immune system becomes compromised and severe symptoms start appearing. T-Helper cells level decreases, and consequently viral load increases. In the case of United States, when blood CD4+ T Cell count is lowered below 200 per millimeter cube, and a person is diagnosed positive for a stage 4 HIV-related condition (such as cancer, TB), then HIV progression to AIDS is established. There is a high probability of deaths in AIDS patients. With advancements in modern medicine, the remaining life of the AIDS patients has been prolonged and it is hoped that in the coming years, we will have even better results (Février, Dorgham and Rebollo 2011).
HIV enters host cell by binding viral envelope glycoprotein Env to the CD4 molecule on target cells along with a chemokine co-receptor, such as CCR5 or CXCR4 which determines the specificity of the virus for particular cell types. It is found that the majority of newly transmitted HIV strains use CCR5 as a coreceptor. T Helper cells, macrophages, monocytes and microglial cells are attacked and subsequently destroyed by the virus, but activated CD4+ T cells are the optimal viral targets for HIV. Afterwards, viral RNA is converted into double stranded DNA by the enzyme reverse transcriptase. The provirus combines with the cellular genetic material with the help of integrase enzyme. Viral genes are translated into proteins by using the host’s cellular machinery. Protease enzyme catalyzes the breakdown of proteins into small fragments, which are assembled. Budding takes place on these viral protein fragments, which are released later on to start the HIV cycle again (Holland).
Thus we come to know that T helper cells are an important part of the adaptive immune system. Their control and influence over other cells’ functions through the production of cytokines is a unique feature of the complex immune system. If we can control the production of cytokines, the immune responses of the body can in turn also be manipulated artificially. AIDS is a disease that deteriorates the body’s immune system over long periods of time. The T helper cells are greatly reduced in number at the end of an HIV infection and it may even lead to complete dysfunction of these cells. Once the immune system is completely compromised, there is no chance left for the patients to live a normal life and their life spans are cut drastically. In order to find a sustainable cure for the HIV infected patients, T helper cells hold the key for further advancements. Not even HIV, other immune affecting diseases can also be treated better if we know more about T cells.
HIV infection is linked with the depletion of T Helper Cells in the blood and the resultant suppression of the infected person’s immune system. A severe loss of CD4+ T cells occurs in the gastro-intestinal tract instead of blood. Initially, the virus decreases levels of CD4+ T cells in the mucosal tissue of the gut as they are the prime targets of the virus (activated CD4+ T cells, near the residence of the virus). In this process, the virus also destroys the gut mucosa‘s structural cells, allowing harmful bacteria species and other opportunist organisms to enter the body; these permanently damage the immune system. The theory and research regarding the T helper cells is linked to a possible solution for AIDS one of the deadly diseases rampant around the world. More work needs to be done on these cells to find a possible cure.
Février, Michèle, Karim Dorgham, and Angelita Rebollo. 'CD4+ T Cell Depletion In Human Immunodeficiency Virus (HIV) Infection: Role Of Apoptosis'. Viruses 3.12 (2011): 586-612. Web. 25 Feb. 2015.
Freed, Eric O, and Andrew J Mouland. Retrovirology 3.1 (2006): 77. Web. 25 Feb. 2015.
Holland, Kimberly. 'How HIV Affects The Body'. Healthline. N.p., 2013. Web. 25 Feb. 2015.
Wilson, John H, and Tim Hunt. Molecular Biology Of The Cell, 4Th Edition. New York: Garland Science, 2002. Print.
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