Pathology essay

Pathology essay

Question 1

Apoptosis uses a programmed mechanism to cause the death of cells following the response of multicellular organisms that can be either exogenous or endogenous. When these cells occur abnormally, it lends to disease. Apoptosis, therefore, eliminates pathogens when its host cells are induced as viruses preventing the multiplication and transmission of viruses that attach the cells. Autophagy, on the other hand, is a mechanism based on the catabolic survival of cells. During operation, there is a continuous and degrading process on the components of cytoplasm, ranging from intracellular pathogens to the destroyed organelles of the cytoplasm. Phagosome, which is also known as a membrane of isolation, takes part to isolate and expand the various components of cytoplasm, leading to the formation of a double layer. However, there are obligate and facilitative bacterial pathogens that can mutate to the killing mechanism by reproducing and increasing the host cell.

Question 2

1. Different genetic make up

Antigen presentation in class I MHC contain glycoproteins for encoding, which occur on the outer surface of almost every cell with a nucleus, while Class II MHC antigen presentation possesses glycoproteins used for encoding and genetically express themselves as APCs

2. The difference in MCH functionality

Class I MHC has a primary function of presenting the antigens of the peptide to the specific TH cell while class II MHC carries the already processed antigenic peptides and gives them to the appropriate TH cell.

3. Different structural appearance

The molecules of class I MHC contain a single membrane that spans a heavy chain and beta chain, while class II MHC is composed of a pair of membranes parts with strings of the same product.

4. Mode of expression

The class I MHC are just expressed in APCs with peptides of amino acid ranging between 8 and 10, while class II express themselves ubiquitously with peptides ranging between 14 and 18 amino acids.

5. Class I has its chains bound to invariant partners, while class II is known to be heterodimer in nature.

Question 3

The antigen-specific memory cells are functional when there is a need to mediate the response of the immune system against pathogens. They operate following an infection, where a considerable percentage of antigen cells are produced. The cells go through a clonal expansion process and later die while the few cells that survive become a long-term memory. These remaining cells become form a minority of the productive population. In contrast, during acute infections, there is proliferation and activation of the cells giving them the ability to respond to the attacking pathogen. After the activation process, the so-called naïve cells undergo a series of cell divisions, and their numbers are greatly multiplied, which eventually gets rid of the host cell with infection. Question 4

1. Pathogen-induced immune resistance.
2. This phenomenon refers to an immune regulation resistance used by chronic infections such as viruses and parasites to increase their rate of survival in the host. Some cases involve viral pathogens working through the effects of bacteria, therefore, posing a symbiotic result.
3. Developing an adaptive immune response

This is a persistent strategy where the pathogens systematically evolve to extreme levels of survival and go beyond detection by the immune system. The infector mainly targets the response of the host immunity.

4. Formation of antigen-antibody complex

This survival strategy enables some bacteria and viruses to continually cause infections through persistence and transmissibility by integrating with the cellular DNA of the host cell.

Question 5

The herpesviruses involve going through a continuous infection of the host cell or organism, followed by the spread and persistence of the disease. The operation of host factors is a possible mechanism of latent herpesvirus infections. The wild category of host proteins and negative mutants from the infectious genome causes the viral effect. The classical trigger mechanism involves several stimuli to the cytokines that are responsible for cellular divisions. The host cell may also be stressed by pathways of signal transduction, causing the effect. Besides, a novel trigger mechanism explains the occurrence of herpesviruses, which associates with the existence of unfavorable reactivation series. The theory shows the behaviors of the cells when attacked by human or murine viruses and the specific exposure-response by repositioning the molecular signature that occurs at the time of molecular infection

Question 6

Caspase-4 in humans is associated with inflammasome activations that occur in monocots. In humans, there is an unconventional behavior of monocots in a single step pathway while responding to lipopolysaccharide. There are high chances that the response mechanism, which is also restricted by the lineage, takes part in endotoxin shock pathology. This shock then conditions the pathway signals and monitor the simulation process. The stimulation process is an important aspect that reveals a common sign of activation. The specific stimuli then release a considerable amount of IL-1β. Besides, the inflammasome activation mechanism is crucial and shows how the monocytes differ from the macrophages. Hence, monocytes in human being show an alternative inflammasome behavior that is distinguished from DCs and macrophages