inflammation and immunity

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Antigen-presenting cells function to a. display foreign antigen on their cell surfaces bound to MHC. b. stimulate cytokine production by macrophages. c. phagocytose and degrade foreign antigens. d. initiate the complement cascade by way of the alternative pathway.

ANS: A Antigen-presenting cells function to display foreign antigen on their cell surfaces bound to MHC for T cell recognition. Antigen-presenting cells do not stimulate cytokine production or initiate the complement cascade. They also do not phagocytose and degrade foreign antigens, but instead present these to T cells for these functions.

Functions of B cells include a. synthesizing antibodies. b. secreting cytokines. c. killing antigen-presenting cells. d. stimulating B cells. e. killing virally infected cells.

ANS: A B lymphocytes mature into plasma cells and synthesize antibodies. B cells do not secrete cytokines, kill antigen-presenting cells, or kill virally infected cells; T cells do these.

Which clinical finding is most indicative of an acute bacterial infection? a. Increased (band) neutrophils. b. Elevated temperature. c. Elevated erythrocyte sedimentation rate. d. Elevated WBC count.

ANS: A Neutrophils are early responders and most active in bacterial infections, and the number of neutrophil bands indicates the severity of the infection. Elevated temperature can occur in infection caused by any organism. The erythrocyte sedimentation rate is non-specific for the type of organism causing an infection. The total WBC count can increase in any infection. The specific type of WBC that is elevated indicates the type of organism involved.

The primary function of eosinophils is to a. kill parasitic helminths (worms). b. kill bacteria. c. stop viral replication. d. phagocytize fungi.

ANS: A The primary function of eosinophils is to kill parasitic helminths (worms); this is evident by the elevation in eosinophil level in parasitic infections. Neutrophils, not eosinophils, function to kill bacteria. Eosinophils have no role in stopping viral replication. The primary role of eosinophils does not involve phagocytizing fungi.

Leukocytosis with a "shift to the left" refers to a. elevated segmented neutrophils. b. elevated immature neutrophils. c. decreased monocytes. d. decreased immature neutrophils.

ANS: B During acute inflammation, the bone marrow releases stored neutrophils. As they are consumed, the demand exceeds the production resulting in an immature (band) neutrophil. Segmented neutrophils are mature neutrophils. Monocytes are immature macrophages and are only 5% of the total WBC. Leukocytosis with a "shift to the left" refers to increased immature leukocytes.

Immunity to a specific organism can be determined by a. active phase protein count. b. antibody titer. c. erythrocyte sedimentation rate. d. WBC count.

ANS: B Specific serum antibody concentration for a particular organism can be measured by a blood antibody titer. Active phase protein count indicates level of inflammation. Erythrocyte sedimentation rate indicates degree of inflammation. WBC count helps determine if infection with any organism is present.

Proteins that are increased in the bloodstream during acute inflammation are called a. membrane attack complexes. b. selectin receptors. c. acute phase proteins. d. major histocompatibility complexes.

ANS: C Acute phase proteins are produced in the liver during acute inflammation and circulate in the bloodstream. Two of the most important acute phase proteins are C-reactive protein (CRP) and serum amyloid A. Membrane attack complexes are porelike structures that function within the complement system. Selectin receptors are receptors on neutrophils that help neutrophils stick to capillary endothelium. Major histocompatibility complexes are a cluster of genes on chromosome 6 involved in antigen presentation.

The primary function of kinins is a. phagocytosis of antigens. b. production of antibodies. c. to limit immune reactions. d. vasodilation to enhance inflammation.

ANS: D Kinins are especially active in inflammation via powerful vasodilation to bring immune cells to the site of infection. Kinins are not phagocytic, but bring phagocytes to an area of infection via vasodilation. B cells produce antibodies. Kinins do not limit immune reactions.

Interleukin-1, interleukin-6, and tumor necrosis factor-α are inflammatory cytokines secreted by a. plasma cells. b. neutrophils. c. lymphocytes. d. macrophages.

ANS: D Macrophages secrete cytokines, including IL-1, IL-6, IL-12, and tumor necrosis factor-α that promote inflammation. Plasma cells, neutrophils, and lymphocytes do not secrete inflammatory cytokines.

The "classical pathway" for activation of the complement cascade is triggered by a. activation of C3. b. inflammation. c. first recognition of an antigen. d. antigen-antibody complexes.

ANS: D The classical pathway for activation of the complement cascade is triggered by the presence of IgG or IgM antigen-antibody complexes. Activation of C3 initiates the alternative pathway. Inflammation does not initiate the classical pathway, but instead inflammation is enhanced by the complement cascade. First recognition of an antigen initiates the lectin pathway or the alternative pathway.

The spleen is an important defense against infection, because it a. activates the complement cascade. b. initiates inflammation. c. controls phagocytosis. d. filters the blood.

ANS: D The spleen filters the blood; macrophages in the spleen filter out foreign substances. Lymphocytes activated in the spleen can be transported to other lymphoid tissue to fight infection. The spleen does not activate the complement cascade, initiate inflammation, or have a role in controlling phagocytosis.

The membrane attack complex formed by complement is similar in function to a. CD4+. b. granzymes. c. gp120. d. perforin.

ANS: D The membrane attack complex functions in a similar manner to perforin. CD4+ do not function similar to the membrane attack complex. Granzymes do not function similar to the membrane attack complex. gp120 does not function similar to the membrane attack complex.


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