Ch. 19 Book Questions Hypersensitivity Flashcards
Which of the following conditions is NOT associated with immune complex deposition?
a. Arthus reaction
b. Autoimmune hemolytic anemia
c. Serum sickness
d. Systemic lupus erythematosus
e. Chronic Hepatitis B virus infection
b. Autoimmune hemolytic anemia
Autoimmune hemolytic anemia is a type II hypersensitivity disease caused by autoantibodies against erythrocyte membrane proteins, such as Rh blood group antigens. Antibody-mediated opsonization and phagocytosis of erythrocytes leads to hemolysis and subsequent anemia. Hepatitis B virus infection is sometimes associated with a systemic vasculitis caused by complexes of viral antigen and antibody. In systemic lupus erythematosus, autoantibody-self antigen complexes cause vasculitis in many different organs. Serum sickness is a disease caused by injection of foreign proteins into the circulation, leading to antibody responses to the proteins and deposition of immune complexes in blood vessel walls. The Arthus reaction is an experimental model of serum sickness.
Which one of the following statements concerning autoimmune disease is true?
a. Autoimmunity manifests as organ-specific, not systemic, disease
b. Infectious microorganisms are frequently present in autoimmune lesions
c. Effector mechanisms in autoimmunity include circulating autoantibodies, immune complexes, and autoreactive T lymphocytes
d. Among the genes associated with autoimmunity, associations are particularly prevalent with class I MHC genes
e. Many autoimmune diseases show higher incidence in males than in females
c. Effector mechanisms in autoimmunity include circulating autoantibodies, immune complexes, and autoreactive T lymphocytes
Various effector mechanisms are responsible for tissue injury in different autoimmune diseases. These include circulating autoantibodies, immune complexes, and autoreactive T lymphocytes. Autoimmune diseases may be either systemic (e.g., systemic lupus erythematosus) or organ specific (e.g., type 1 diabetes mellitus, multiple sclerosis). Among the genes associated with autoimmunity, the strongest associations are with MHC genes and usually with class II MHC genes (ankylosing spondylitis is an exception). In most cases of autoimmunity, infectious microorganisms are neither present in lesions nor detectable in patients when autoimmunity develops; this suggests that lesions in autoimmunity result not from the infectious agent directly but from host immune responses that may be triggered by microbes. Finally, many autoimmune diseases show higher incidence in females than in males, although the reasons for this are not well understood.
A college student develops a blistering rash on his legs a day after returning from a camping trip. He visits the student health clinic and a nurse makes the diagnosis of a poison ivy reaction, a form of contact hypersensitivity to organic chemicals called urushiols produced by the poison ivy plant. Which of the following statements about this student is correct?
a. His rash is caused by mediators released by mast cells after the crosslinking of anti-urushiol antibodies bound to mast cell IgE Fc receptors
b. His rash is caused by activation of memory CD4+ and CD8+ T cells specific for peptides of urushiol-modified self proteins, and secretion of inflammatory cytokines by the T cells
c. Because the rash took more than 24 hours to develop since exposure to the poison ivy, the student most likely had never been exposed to poison ivy before
d. His rash is caused by anti-urushiol antibodies that bind to the urushiols in the skin and activate complement
e. The best treatment for this students condition is epinephrine
b. His rash is caused by activation of memory CD4+ and CD8+ T cells specific for peptides of urushiol-modified self proteins, and secretion of inflammatory cytokines by the T cells
Contact hypersensitivity to urushiols is mediated by memory T cells that emerge after at least one previous encounter with these compounds. The urushiols covalently modify self proteins in the skin, including MHC molecules, which are processed and presented to and activate CD4+ and CD8+ T cells. The rash will usually take at least 24 hours to fully develop because it requires the recruitment of the T cells to the skin, local activation of these cells by antigen, and secondary recruitment of inflammatory cells. Epinephrine is not used to treat contact hypersensitivity, but rather to treat severe immediate hypersensitivity reactions with life threatening cardiovascular and respiratory complications.
A patient presents to an emergency room complaining of chronic cough, night sweats and fevers. A chest X-ray shows multiple nodules in the hilar regions of both lungs. A sputum sample stains positive for mycobacteria, and a rapid molecular test for Mycobacterium tuberculosis is positive. What type of immune response is taking place in the lung nodules?
a. An antibody mediated autoimmune response
b. An innate immune response with abscess formation
c. An immune complex vasculitis
d. A superantigen induced polyclonal T cell response
e. A chronic delayed type hypersensitivity reaction with granuloma formation
e. A chronic delayed type hypersensitivity reaction with granuloma formation
Mycobacterium tuberculosis infection often results in a chronic TH1 response and formation of granulomas due to persistence of bacterial antigen in macrophages.
Which of the following would NOT be a likely therapy for treating autoimmune diseases?
a. Corticosteroids
b. Small molecule inhibitor of VLA-4
c. Anti-TNF antibody
d. CTLA-4 antagonist (e.g., anti-CTLA-4 antibody)
e. Plasmapheresis
d. CTLA-4 antagonist (e.g., anti-CTLA-4 antibody)
The mainstay therapy for hypersensitivity diseases is anti-inflammatory drugs, particularly corticosteroids and, more recently, cytokine antagonists. In contrast, blocking CTLA-4, a negative regulator of T cell responses, is likely to enhance immune responses and exacerbate hypersensitivity reactions. An inhibitor of VLA-4 would be effective in blocking leukocyte transmigration into tissues, thus exerting an anti-inflammatory effect. TNF is an important inflammatory mediator in rheumatoid arthritis and other autoimmune diseases. Plasmapheresis has been used during exacerbations of antibody-mediated diseases to reduce circulating levels of antibodies or immune complexes.
Experimental autoimmune encephalomyelitis (EAE) is a mouse model of a human organ-specific autoimmune disease mediated by T lymphocytes. In EAE, rodents are immunized with proteins found in the myelin sheath of central nervous system neurons. EAE is a model for which of the following human diseases?
a. Rheumatoid arthritis
b. Autoimmune myocarditis
c. Systemic lupus erythematosus
d. Diabetes mellitus type 1 (insulin-dependent)
e. Multiple sclerosis
e. Multiple sclerosis
Experimental autoimmune encephalomyelitis (EAE) is an animal model for multiple sclerosis, a central nervous system (CNS) demyelinating disease with an autoimmune etiology. EAE is induced by immunizing mice with antigens normally present in CNS myelin, in conjunction with adjuvant, which is necessary to stimulate the innate immune system. One to 2 weeks after immunization, animals develop an encephalomyelitis, characterized by perivascular infiltrates composed of lymphocytes and macrophages in the CNS white matter, followed by demyelination. Both TH1 and TH17 cells contribute to the disease. Neurologic lesions can be mild and self-limited or chronic and relapsing, depending on the animal species and strain and antigen-adjuvant preparation used.
