Please answer and explain your reasoning with detail. This is for immunology spe
ID: 69707 • Letter: P
Question
Please answer and explain your reasoning with detail. This is for immunology specifically. Thank you
Type I diabetes is a type I hypersensitivity mediated by CTL. There is a mouse model for the disease that can be used for research. The mice are inbred and all have the same MHC. It is hypothesized that a virus causes the activation of the CTL that destroy the beta cells in the islets. Design a study (set of procedures) that could be used to identify the virus. Combining other fields of study, such as genetics, along with immunological techniques is appropriate.Explanation / Answer
We suppose to study the polymorphisms in MHC since, that is linked with disease susceptibility in nonobese diabetic (NOD) mouse. The linkage to the class II MHC allele (H2-Ag7, is a non-asp 57-containing allele ) in NOD is the most significant susceptibility loci and the only allele that expressed on the surface of cells from NOD mice. Type 1 diabetes (TD1) also caused by the viral infection that makes CD8+ autoreactive against pancreatic beta-cells. CVB4 an enteroviral strain is responsible for TD1, in which, viral infection has the tendency to “unmask” -cells for recognizing by CD8+ T-cells (promoting interferon production and upregulation of MHC class I molecules on -cells). These events combined may be sufficient to condition the pancreatic islets for autoimmune attack. In this manner, the NOD mice constituted as a critical tool to address viral exposure during the pre-diabetic phase leads to subsequent disease development. It is a process called molecular mimicry in which, the T-cell receptors expressed by particular autoreactive T-cells enable to recognize viral antigens, both autoreactive and antiviral T-cells will be activated as a consequence of presentation of viral antigens by antigen-presenting cells (APCs). Activation of autoreactive T-cells upon CVB4 infection was proposed to occur by molecular mimicry.
Developing antigen-specific antibodies could help in identifying autoreactive T-cells. By following the genetic approaches like sequence analysis, we can determine antigenic variation in cells followed by infection compared noninfected cells. Immunoprecipitation offers an idea of interaction between viral antigens and T-cells. Identifying the polymorphism in MHC or molecular changes in its gene structure could determine the possibility of TD1 in NOD mice. DNA sequencing preferably identifies the viral genome insertion into the host cells resulting alterations. Study of the expression of surface markers on autoreactive and effector antiviral T-cells can discriminate the TD1 occurence.