What is the primary function of eosinophils in attacking large parasites like helminths?

Correct answer: To release the contents of their granules by exocytosis onto the parasite's surface.

Explanation

This question describes the effector mechanism used by eosinophils to attack large extracellular parasites that cannot be phagocytosed, a process known as exocytosis or degranulation.

Other questions

Question 1

Which of the following is NOT one of the three main ways that antibodies contribute to immunity, as introduced in Section 1-20 and described in Chapter 10?

Question 2

What is the term for antigens that can induce antibody production in the absence of helper T cells and are typically highly repetitive molecules like bacterial polysaccharides?

Question 3

In the process of linked recognition, how much more efficient is a B cell at presenting peptide fragments of a specific antigen it binds compared to a B cell that processes the antigen through macropinocytosis alone?

Question 4

Which chemokine receptor is expressed by circulating naive B cells, directing them to enter primary lymphoid follicles where the chemokine CXCL13 is abundant?

Question 5

What is the primary function of the SLAM-associated protein (SAP) in the interaction between TFH cells and B cells?

Question 6

What is the fate of an antigen-stimulated B cell that fails to interact with a T cell recognizing the same antigen within the peripheral lymphoid organ?

Question 7

Which of the following is a characteristic of plasma cells that distinguishes them from plasmablasts, according to Figure 10.9?

Question 8

What is the primary function of the dark zone of a germinal center?

Question 9

What is the approximate rate of somatic hypermutation in immunoglobulin V-region genes during a germinal center reaction?

Question 10

What is the name of the enzyme responsible for initiating somatic hypermutation and class switch recombination by deaminating cytidine residues in DNA?

Question 11

What is the clinical syndrome characterized by a lack of both somatic hypermutation and class switching, leading to the production of predominantly IgM antibodies, due to mutations in the AID gene?

Question 12

The process of class switch recombination is guided by stretches of repetitive DNA that lie upstream of each heavy-chain constant region gene. What are these regions called?

Question 13

Which cytokine, when acting on an activated B cell, preferentially induces class switching to IgE?

Question 14

Genetic deficiency of CD40 ligand on T cells prevents effective class switching and results in what clinical condition?

Question 15

Which transcription factor is considered a transcriptional repressor that switches off genes for B-cell proliferation and is induced by IRF4 to drive differentiation into plasma cells?

Question 16

Thymus-independent (TI-1) antigens are often called B-cell mitogens because at high concentrations they can cause the proliferation of most B cells regardless of their antigen specificity. This is known as:

Question 17

What is the principal class of antibody found in blood and extracellular fluid, which efficiently opsonizes pathogens for engulfment by phagocytes?

Question 18

The transport of dimeric IgA across mucosal epithelia is mediated by a specific receptor. What is this receptor called?

Question 19

The neonatal Fc receptor (FcRn) is responsible for the selective transport of which antibody class from mother to fetus across the placenta?

Question 20

What is the conformation of a pentameric IgM molecule in plasma before it binds to an antigen on a pathogen surface?

Question 21

In patients with deficiencies in the early components of complement (C1, C2, C4), immune complexes are not cleared effectively and tend to deposit in the basement membranes of small blood vessels, particularly in which organ?

Question 22

What is the name of the novel cytosolic IgG receptor that has E3 ligase activity and is involved in clearing antibody-coated viruses from the cytoplasm?

Question 23

The process by which NK cells recognize and destroy antibody-coated target cells is known as:

Question 24

Which Fc receptor binds monomeric IgE with very high affinity (approximately 10 to the power of 10 M-1), even in the absence of antigen?

Question 25

According to Section 10-15, which immunoglobulin subclass has the unusual ability to form hybrid antibodies by exchanging one heavy-light chain pair with another?

Question 26

What is the primary cytokine produced by TFH cells that activates the transcription factor STAT3 in B cells to support their proliferation and differentiation?

Question 27

What is the effect of the B-cell co-receptor complex, including CD21, binding to C3d deposited on a microbial surface?

Question 28

After their initial encounter at the follicle border, some activated B cells migrate to form a primary focus. Where in the lymph nodes is this primary focus located?

Question 29

What are the densely packed, rapidly proliferating B cells in the dark zone of a germinal center called?

Question 30

The enzyme AID acts on cytidine residues to initiate somatic hypermutation. What type of DNA structure is required for AID to access the cytidine?

Question 31

After AID creates a U:G mismatch, which DNA repair pathway, when combined with an error-prone polymerase, tends to introduce mutations at nearby A:T base pairs?

Question 32

What is the consequence for B cells if the BAFF-R signaling pathway, which activates the non-canonical NF-kappa-B pathway, is defective?

Question 33

What is the ratio of IgA1 to IgA2 in human blood, according to Section 10-15?

Question 34

Secretory component, which remains attached to dimeric IgA after transcytosis, is the cleaved extracellular domain of which receptor?

Question 35

For the classical complement pathway to be activated by IgG, what is the minimum requirement for C1q binding?

Question 36

Which Fc receptor is NOT expressed by macrophages, according to the table in Figure 10.38?

Question 37

What is the principal mechanism by which Fc receptors on phagocytes distinguish between antibody molecules bound to a pathogen and free, unbound antibody molecules?

Question 38

Activation of mast cells occurs when multivalent antigens cross-link which type of antibody bound to their surface receptors?

Question 39

The Hapten-Carrier Effect explains how a small, non-immunogenic molecule (hapten) can elicit an antibody response. What is the role of the carrier protein in this process?

Question 40

Which property of TI-2 antigens, such as bacterial capsular polysaccharides, allows them to activate mature B cells, likely by cross-linking a critical number of B-cell receptors?

Question 41

What is the typical cell division time for B cells in a germinal center?

Question 42

What happens to centrocytes that fail to acquire sufficient antigen from FDCs to engage TFH cells in the germinal center?

Question 43

Which of the following properties is a shared characteristic of both Thymus-Dependent (TD) and Thymus-Independent type 2 (TI-2) antigens, according to Figure 10.26?

Question 44

How do neutralizing antibodies primarily block the infectivity of animal viruses?

Question 45

How many molecules of FcRn are thought to bind to a single molecule of IgG to transport it across the placenta?

Question 46

What is the role of erythrocyte complement receptor 1 (CR1) in the clearance of immune complexes?

Question 47

Which of the following is an INHIBITORY Fc receptor that contains an ITIM and negatively regulates the activity of B cells and mast cells?

Question 48

According to Figure 10.2, what is the second signal delivered to a B cell for activation by a thymus-dependent antigen?

Question 50

During the first few days of a secondary antibody response, which cells are primarily responsible for producing antibodies?