Question

1.

The prevention of inflammatory immune responses to inhaled antigens in healthy individuals has mechanisms in common with those that prevent inflammatory immune responses to commensal microbes in the gut. One important component of immune regulation shared by these two situations is:

a. The induction of increased numbers of IFN-g-producing T cells and ILCs in the airway and gastrointestinal epithelium

b. The presence of tissue-resident mast cells that bind IgE through the high affinity IgE receptor

c. The high levels of constitutive IL-10 present in the mucosal surfaces of both the airway and the gastrointestinal tract

d. The important role for CD4 regulatory T cells in suppressing inflammatory immune responses in these tissues

e. The presence of tissue-resident dendritic cells that produce IL-23 when activated

2.

Individuals with peanut allergies can exhibit a variety of symptoms following exposure to the peanut allergen. These symptoms can include a runny nose, skin reactions such as hives, itching in the mouth and throat, digestive problems such as cramps, diarrhea or vomiting, and shortness of breath or wheezing. This variety of symptoms is a result of:

a. Systemic production of inflammatory mediators causing responses in many tissues

b. The simultaneous exposure of skin, oral mucosa, throat, and gastrointestinal tract to an ingested allergen

c. The presence of high concentrations of monomeric IgE in the circulation

d. The high concentrations of histamine present in pre-stored mast cell granules

e. The presence of mast cells with pre-bound IgE in all mucosal tissues

3.

Some early studies aimed at deciphering the mechanisms involved in immunological tolerance, and its breakdown in cases of autoimmune disease, were based on generating transgenic mice that constitutively expressed a viral protein in the b-islet cells of the pancreas. These mice were crossed to transgenic mice expressing a T-cell receptor specific for MHC class I bound to a peptide of this viral protein. The double transgenic mice generated large numbers of CD8 T cells capable of recognizing this viral antigen on b-islet cells, yet the mice never spontaneously developed type I diabetes, a disease in which b-islet cells are destroyed by T cells. This lack of response most likely reflects:

a. The absence of infection or tissue damage needed to trigger the priming of effector T cell responses

b. The fact that b-islet cells in the pancreas are few in number, and therefore unable to generate enough antigen to prime T cell responses

c. The deletion of all the antigen-specific T cells by central tolerance mechanisms in the thymus

d. The fact that the pancreas is an immune privileged site

e. The absence of CD4 T cells that recognize the same viral antigen

Answer 1

1.d.The important role for CD4 regulatory T cells in suppressing inflammatory immune responses in these tissue.

2.b.The simultaneous exposure of skin, oral mucosa, throat, and gastrointestinal tract to a ingested allergen.

3.e.The absence of CD4 T cells that recognize the same viral antigen.