An individual does not make an immune response to a self-protein because
A) self-proteins cannot be processed into peptides.
B) peptides from self-proteins cannot bind to MHC class I.
C) peptides from self-proteins cannot bind to MHC class II.
D) lymphocytes that express a receptor reactive to a self-protein are inactivated by deletion or
E) developing lymphocytes cannot rearrange V genes required to produce a receptor for self-
Which of the following statements is
A) Interaction of Fas and FasL can lead to apoptosis.
B) Both Fas and Fas L can be expressed on activated T cells.
C) Both Fas and Fas L can be expressed on B cells.
D) Cells in immunologically privileged sites can express FasL.
E) FasFasL-mediated apoptosis prevents uncontrolled T-cell clone growth.
Which of the following is
incorrect concerning immune tolerance?
A) Tolerance induction is antigen-specific.
B) Tolerance results from inactivation and/or elimination of B and/or T cells.
C) Tolerance can be induced in both young and old individuals.
D) Immature neutrophils are more susceptible to tolerance than mature neutrophils.
E) The breakdown of tolerance can result in autoimmunity.
Which of the following statements is
incorrect concerning the immune response to
A) Reactivity is influenced by extremes of age.
B) Greater immune responses are produced when antigen is given with adjuvant.
C) Impaired nutrition depresses immunity.
D) The presence of preexisting antibody does not affect the subsequent response to antigen.
E) Different protein antigens stimulate different levels of antibody production.
All of the following procedures would be likely to induce tolerance to a protein antigen except
A) intramuscular injection of the antigen in adjuvant.
B) intravenous injection of deaggregated protein.
C) injection of cyclosporine with the antigen.
D) injection of antigen at a stage in development before mature lymphocytes appear.
E) intravenous injection of small amounts of antigen.
When a tolerogenic injection of a protein antigen is given experimentally, it can be shown that
A) B-cell tolerance is more rapidly induced than T-cell tolerance.
B) B-cell tolerance is lost as new B cells come from the bone marrow.
C) B-cell tolerance can be induced only when low doses are used.
D) T-cell tolerance can be induced only when high doses are used.
E) T-cell tolerance is shorter lasting than B-cell tolerance.
Blocking any of the following processes can result in peripheral tolerance in mature T cells except
A) the interaction of costimulatory molecules on T cells with their ligands on APC.
B) intracellular signal transduction mechanisms.
C) negative selection of thymocytes.
D) activation of the IL-2 gene.
E) the binding of antigen with MHC molecules.
Online Only Review Questions
An individual with a defect in CTLA-4 (CD152) will be most likely to have which of the following?
A) Type I hypersensitivity
C) recurrent Neisseria infections
D) lymphoproliferative disease
Answers to Review Questions
1. D Negative selection generally ensures that a lymphocyte expressing a receptor reactive to a self-protein is inactivated by deletion or anergy.
2. C B cells express Fas but not FasL.
3. D Tolerance can be induced only in lymphocytes that express an antigen-specific receptor.
4. D Preexisting antibody may exert a negative feedback on the subsequent response to antigen.
5. A Injection into muscle and in the presence of adjuvant are likely ways to induce activate rather than tolerize the immune response. The remaining procedures generally induce tolerance. The use of cyclosporine in blocking transplantation rejection is discussed further in Chapter 19.
6. B T-cell tolerance is more rapidly achieved, occurs with lower doses, and lasts longer than B-cell tolerance. As new B cells are produced by the bone marrow, tolerance in this compartment wanes. T-cell tolerance, by contrast, persists because the thymus of an adult no longer actively produces new T cells.
7. C Interfering with negative selection of thymocytes disrupts central rather than peripheral T cell tolerance.
8. D CTLA-4, a T-cell surface molecule closely related to CD28, transmits a negative signal to activated T cells, shutting off IL-2 production. Defects in this signaling could lead to a general lymphoproliferative disorder.