Chapter 15 1. The antibodies might physically block the cell surface protein from interacting with something it would normally do in order for it to perform its function (for example, binding a hormone). If that cell surface protein interacts with signalling proteins, the binding of an antibody to that protein might activate the cell signalling pathways and the cell then responds. 2. Negative selection may have been imperfect and some cells simply escaped. This could happen if the MHC proteins were displaying a self-peptide, but it happened to be a different one that the T cell receptor displayed. If the AIRE transcription factor was not functional, then developing thymocytes would not be screened against non-thymic tissue specific antigens. B cells developing in the bone marrow would not see all of the proteins present in body - only those in the bone marrow. If a B cell is activated by the BCR binding to a pathogen protein that resembles a self-protein, then the self-protein may be attacked because the antibodies just happen to fit. Chapter 16 1. In MHC based graft rejection, T cells are activated when their TCRs interact with the MHC- self peptide on the grafted tissue. Even though the T cells are expected to have TCRs that are restricted to the MHC that they saw during positive/negative selection, the TCRs might "fit" well enough with the MHC-self peptide on the grafted tissue to become activated. T cells might also be activated by dendritic cells that take up the foreign MHC from the graft and process and present peptides (this is because there is always some tissue damage to the graft during the transplation). 2. Mature red blood cells no longer have a nucleus. Therefore, they no longer that the genetic information to keep expressing the MHC class I proteins. With time, the red blood cell does not have MHC class I.