Adaptive and Innate Immunity
Introduction
Our bodies are incessantly required to defend themselves from a barrage of potentially noxious invasions such as bacteria, viruses, and other microbes. The body’s defense system is put up by the immune system. The immune system of the body is split further into innate and adaptive immunity. The immune system is also made up of specific effector cell whose job is to sense and respond to antigens of foreign origin unfamiliar to the human tissues(Hall & Yates, 2012). Furthermore, immune responses in the body are usually aided and amplified by tissue macrophages. The tissue macrophages are originally derived from the monocytes. The macrophages acting with other cells give the body dominant defenses against viral infections and other types of infection. This paper will discuss the immune reactions in the body of Melissa who has suffered a viral infection.
To begin with, the immune system of Melissa will typically trigger an inflammatory process due to the viral infection she has had. The inflammatory process is the manner in which her body defends itself against damage by the viral infection. Among the major sub-classifications of the cells of the immune system are the macrophages and the T lymphocytes. The T cells are made to recognize the molecular markers of specific proteins like those from bacteria or viruses; the T cells subsequently activate an immune response by the body(Hall & Yates, 2012). Macrophages, on the other hand, engulf the other cells and are further able to pull apart their proteins to present them to the T cells.
The macrophages frequently interact with the T cells. The interaction is necessary to bring about the activation of the T cells in the target organs. The interaction is mutual and goes on since the T cells produce inflammatory messenger molecules known as the cytokines that activate the macrophages. The macrophages then produce chemicals that are toxic such as nitric oxide. The nitric oxide can kill the cells that are surrounding including the viruses in Melissa’s body. Studies have previously revealed that macrophages that have been stimulated by T cells need to produce a second inflammatory cytokine(Hall & Yates, 2012). The second inflammatory cytokine is necessary as a signal to alert the macrophages to produce nitric oxide.
Moreover, there many other signals that could be either chemical that is secreted or interactions on the surface of the cell. The interactions control the outcome of the interaction between the T cells and the macrophages. In summary the T lymphocytes cells that are designed and programmed to remember, recognize and to respond to antigens. Therefore, the T lymphocytes in Melissa’s body will remember, understand and respond to the viral antigens. The T cells will then direct and regulate the immune response(Lydyard, Whelan, Fanger, &Lydyard, 2011). When the T cells have been stimulated by the antigens that have been presented to them by the macrophages, the T cell will make lymphokines that will be used to signal other cells in the immune system.
Similarly, macrophages are the first line of defense against the viral infection for Melissa. Their major role in the interaction with T is to break the virus into smaller proteins after engulfing them. The macrophages will then present the viral proteins to the T calls for recognition, remembrance and response(Lydyard, Whelan, Fanger, &Lydyard, 2011).
Interferons play a vital role in the body’s first line of defense against viral infections. The interferons form part is a non-specific immune system. The interferons are induced at an early stage during the viral infection; this is usually before the particular immune systems have ample time to stage a response. The interferons are made by cells that are responding to a stimulus that is appropriate; they are then released into the surrounding medium. The interferons will subsequently bind to target cells. What follows is the induction of transcription of approximately 20-30 genes within the target cells(Fensterl&Sen, 2009). The process will then result in an antiviral state within the target cells.
Type I interferons otherwise known as interferon alpha or leukocyte interferons are produced by virus-infected leukocytes. The interferon-a usually comprises of a family of about 20 related proteins(Platanias, 2005). Type I interferon is not often produced in cells that are normal. It is, however, important to note that a viral infection of a cell causes the interferon alpha to be made and subsequently released from the cells. The cells that have released them will typically die because of the viral infection. The interferons produced by the cells will then bind onto target cells and induce an antiviral state(Fensterl&Sen, 2009). The induction of the antiviral state is how the interferons will enable Melissa’s body to fight the viral infection.
A key fact to observe is that both RNA and DNA viruses will induce interferon making by the cells. So regardless of the type of virus that Melissa has, her cells will produce interferons. However, it is worth noting that the RNA viruses usually induce higher levels of than the DNA viruses. The double-stranded RNA may, therefore, be a vital induction agent. There also other factors that will similarly cause the making of interferons by the cells(Fensterl&Sen, 2009); exogenous double stranded DNA, lipopolysaccharides and other viral and bacterial components.
Studies conducted on the interferons type I have revealed that these interferons induce about 20-30 proteins. Most of the functions of the proteins are not clearly understood, but there are three proteins that have been noted to play a clearer role in the creation of the antiviral state in the cell. The expression of one of these proteins known as 2’5’ oligo-A synthase ends in the activation of the second of these proteins that are called a ribonuclease. This can break down mRNA, and further causes the expression of the third protein, which is a protein kinase(Platanias, 2005). The third protein inhibits the initiation of protein synthesis. The high flow chain targets the synthesis of viral proteins, and therefore they affect their antiviral effect on the viruses(Fensterl&Sen, 2009). The proteins are responsible for pathways that are potentially harmful to the viruses in the body of Melissa; they help eliminate the viral infection. Type I interferon is thus used in the treatment of viral infections.
In humoral or B-cell immunity, the body develops circulating antibodies. These antibodies are globulins that are found in the plasma, and they possess a capability of attacking the agent that is invading the body; in Melissa’s case the virus. In this type of immunity (which is a sub-type of the acquired or adaptive immunity)(Wilson, Di Camillo, Doughty, &Dax, 2006), the antibodies are produced by the B-lymphocytes. The virus-infected cells or the virus itself can stimulate the B-lymphocytes to produce antibodies. These antibodies are specific for the viral antigens. The neutralization of the antibodies is most active during the time the virus is present in large spaces of fluid like in serum. The large fluid spaces could also be in the respiratory or the gastrointestinal tracts(Dörner&Radbruch, 2007). IgM, IgG, and IgA have all been shown to cause antiviral activity.
The antibody can neutralize the antibody by blocking all the interactions between the virus and the host cells. The antibodies can also recognize viral antigens that are found in the virus-infected cells of the body. That will lead to antibody dependent cytotoxic cells or a complement-mediated lysis. IgG antibodies are known to be responsible for the majority of the antiviral actions in the serum(Wilson, Di Camillo, Doughty, &Dax, 2006). IgA, on the other hand, comes into play most importantly when viruses attack the mucosal surfaces.
Plasma cells that have been differentiated are important players in the humoral immunity response. They secrete antibodies that are essential especially against toxins and pathogens that exist extracellularly(Wilson, Di Camillo, Doughty, &Dax, 2006). The antibodies coat the extracellular virus and neutralize them. The antibodies do this by causing key sites on the virus that enhance its infectivity; these are sites such as the receptors that the viruses use to interact with the host cells. Neutralization by the antibody can prevent the pathogen from entering into the host cell. The host cells are thereby protected from infection by the pathogens(Dörner&Radbruch, 2007). The pathogens that have been coated with the antibodies are then filtered by the spleen and excreted out in the feces or urine.
The antibodies also key another pivotal role since they mark the pathogens. By marking them, they make them easy to be recognized by the phagocytic cells in the immune system like the macrophages. The process by which the antibodies mark the pathogen making it easy for engulfing by phagocytes is called opsonization. To add to the above processes, there is complement fixation. Here, IgG and IgM within the serum bind themselves to the viral antigen(Wilson, Di Camillo, Doughty, &Dax, 2006). In doing that, they provide attachment sites onto which the complement proteins will then bind. The combination of the complement and antibodies boosts opsonization, even more, triggering clearance of pathogens.
Conclusion
In conclusion, this paper has looked at the manner in which the body defends itself. The paper has done this through discussion of a case study old a 15-year-old girl; Melissa who has a viral infection, mononucleosis. The body has an immune system that is further divided into two. The adaptive or acquired immunity, which Melissa would develop after her body, interacts with pathogens and learns to recognize them upon later infection. The other type of protection is the innate immunity which Melissa or any other person is born with. The paper has focused on the adaptive type of immunity. The interaction between the T cells and the macrophages is useful to Melissa. The T cells and the macrophages mutually supplement each other. The T cells recognize, respond to and remember small proteins from the pathogenic antigens. The recognition by the T cell is only made possible by the macrophages that engulf the viral particles and break them to smaller proteins.
Finally, there is type I interferons that are produced by the cells before the specific immunity of the body reacts to the viral infestation. The interferons cause the cells to assume an antiviral state thus therapeutic during viral infections. Humoral immunity through antibody action is useful in viral infection. The antibodies cause pathogen neutralization and enhance phagocytic response against the pathogens such as viruses.
References
Dörner, T. &Radbruch, A. (2007). Antibodies and B Cell Memory in Viral Immunity. Immunity, 27(3), 384-392. http://dx.doi.org/10.1016/j.immuni.2007.09.002
Fensterl, V. &Sen, G. (2009).Interferons and viral infections. Biofactors, 35(1), 14-20. http://dx.doi.org/10.1002/biof.6
Hall, A. & Yates, C. (2012). Immunology (1st ed.).
Lydyard, P., Whelan, A., Fanger, M., &Lydyard, P. (2011). Immunology (1st ed.). New York: Garland Science.
Platanias, L. (2005). Mechanisms of type-I- and type-II-interferon-mediated signalling. Nature Reviews Immunology, 5(5), 375-386. http://dx.doi.org/10.1038/nri1604
Wilson, K., Di Camillo, C., Doughty, L., &Dax, E. (2006).Humoral Immune Response to Primary Rubella Virus Infection. Clinical And Vaccine Immunology, 13(3), 380-386. http://dx.doi.org/10.1128/cvi.13.3.380-386.2006
