Microbiology project 2 Biological & Biomedical Sciences Research Paper

Microbiology
Student Name
Institution Affiliation
Microbiology
Question 1: Secondary Immune Responses to Antigen
Memory B cells especially lymphocytes are used for secondary response against antigens. During their first exposure to antigens they produce antibodies, but the amount increases after the second exposure. The cells are formed in two ways; first, when the T cells differentiate in short lived plasma cells and second, when T cells differentiate in lymphoid organs. Their abilities to fight antigens very fast is based on the fact that they can quickly differentiate in the plasma cells and specifically in the IgG+ Bm cells which are of huge significance in tackling infections (Ratajczak et al., 2018).
Having many memory B cells has the advantage of responding rapidly to antigens. However, the ability of the cells is ineffective, and that is the reason why scientists have resorted to vaccination. The T cells and memory B do not fight infections. Effector cells and antibodies, thus putting the efficacy of memory B cells into question, fight the infections. The cells only guarantee a quick response, but they don’t offer protection against diseases (Campos & Godson, 2003). Therefore, a combination of vaccination and memory B cells offers protection against diseases. The only concern is about the longevity of resistance because sometimes it doesn’t last for the projected time frames and makes it difficult to maintain the same level of immunity. In some occasions, this is attributed to the low rate of cloning of the memory cells.
Protection against some parasite infections has indicated that secondary cells cannot differentiate in time to control diseases. This affects credibility of effector cells to offer the required resistance against diseases. Another instance is malaria, where it has proven to be hard for memory B cells to guarantee protection. In this scenario, secondary response immune system is takes longer time to get strong (Campos & Godson, 2003). Naturally acquired resistance of individuals against malaria develops slowly over long periods, which can prevent deaths.
Even though cloning of memory B cells is significant for the quick response of antigens, they do not guarantee 100 percent protection. They cannot be relied upon to fight infections, and thus have to be blended with artificial measures like immunizations and vaccinations.
Question 2: Causes and treatment of skin grafting rejection
Jack's graft was successful because the skins were identical (syngeneic graft) hence they had the same DNA, making grafting easy. The immune responses in Jill originated from angiogenic mediators, macrophages, cytokines, polymorphonuclear cells, and dendritic cell (DCs) which was in turn accompanied by activation of the T cells (CD4+ and CD8+). The skin rejection was furthered by the accumulation of effector T cells and inflammatory cytokines. The stimulus that triggered the rejection of his graft was caused by the mismatch in Jack’s major histocompatibility complex (MHC) and his T cell receptors (TCRs). The MHC is very critical that a single genetic difference can lead to skin graft rejection. The DCs in Jill's body might have migrated into the lymphoid organs, which are influenced by the Langerhans cells (LCs), thereby initiating the process of rejection (Dixit et al., 2017).
The situation could have also been solved by the use of innate immunity, which is composed of natural killer (NK) cells, macrophages, monocytes, and neutrophils. The NK cells kill the stressed and infected cells by the use of CD4+ T cells, though research has labeled it not being very efficient. The macrophages exist in large numbers and are induced by IL-4 to respond to injuries. They act in defense against the pro-inflammatory cytokine secretion and necrosis. The neutrophils work in skin grafting by the secretion of chemokines causing activation of T cells and proliferative approaches.
Another possible way of treatment is to conduct therapy on Jack, addressing his DCs by inducing skin graft tolerance. The above strategy aims at inhibition of the antigens involved by targeting the donor’s LCs and DCs. The LCs and DCs subpopulations express the MHC, which is significant in the skin graft rejection. Strategies involving use of chemicals such as gliotoxin and epipolythio have proved to be instrumental in survival of grafted skin.
Jill could have also explored the use of immunosuppressive drugs. The common type of immunosuppressive drug used in the treatment of skin graft rejection is cyclosporine. The drugs work through preventing the T cell phosphatase. The T cell phosphatase is needed in the activation of transcription factor nuclear of the activated T cells, which have an effect of stopping cytokine in the T cells (Abbas et al., 2019). However, this method can expose Jill to the risk of contracting other infections.Question 3: Summary of James P. Allison and Tasuku Honjo scientist’s major cancer discovery.
Cancer consists of the uncontrolled proliferation of abnormal cells which can spread to normal tissues and healthy organs. The immune system of the body can identify and attack foreign bodies, thereby protecting the body from its harmful effects. T-cells have been identified to have receptors that can bind to non-self-structures which in turn triggers and activates immune systems. There are some proteins in the body that can can act as a brake to avoid excessive activation leading to the autoimmune destruction of healthy cells and tissues.<...