Question 40 of 50

Which of the following is an antimicrobial enzyme secreted in tears and saliva that attacks the peptidoglycan component of bacterial cell walls?

The complement system is a collection of soluble proteins that provides protection early in an infection. What is the process of coating a pathogen with complement proteins to make it more readily destroyed by phagocytes called?

Which of the three pathways of complement activation is initiated when mannose-binding lectin (MBL) or ficolins bind to carbohydrates on pathogen surfaces?

Defensins are an evolutionarily conserved class of antimicrobial peptides that are short and cationic. What is the approximate length of these peptides in amino acids?

Which of the following is NOT a recognized function of mucus secreted by internal epithelia?

Which of the following best describes the initiation of the classical pathway of complement in an innate immune response, before adaptive immunity has developed?

What is the primary role of the protein properdin (factor P) in the complement system?

The membrane-attack complex (MAC) forms a pore in the pathogen membrane. This pore is primarily assembled from the polymerization of which terminal complement component?

Which two small complement fragments are potent anaphylatoxins that can induce local inflammatory responses?

Hereditary angioedema (HAE) is a disease characterized by excessive swelling due to chronic spontaneous complement activation. This disease is caused by a deficiency in which regulatory protein?

What is the most abundant complement protein in plasma, with a concentration of about 1.2 mg/ml?

Which component is formed when C3b binds to the classical or lectin pathway C3 convertase (C4b2a)?

What is the key feature of the C3 protein that allows its fragment, C3b, to form a covalent bond with microbial surfaces upon cleavage?

Deficiencies in the terminal complement components, C5 through C9, are primarily associated with an increased susceptibility to infection by which genus of bacteria?

Which human protein, also known as protectin, is a host-cell membrane protein that protects against the membrane-attack complex by inhibiting the binding of C9?

Which pathogen-secreted protein from Staphylococcus aureus directly binds to the Fc regions of immunoglobulins, thereby interfering with C1 activation and complement-mediated clearance?

The alternative pathway C3 convertase is designated as C3bBb. Which plasma protease is responsible for cleaving factor B to generate the active Bb fragment?

What is the composition of the C5 convertase of the alternative pathway?

Factor H is a plasma regulatory protein that helps protect host cells from complement attack. It achieves this in part by having a higher affinity for C3b bound to host cells due to its ability to recognize which specific molecule on their surface?

The inactive derivative of C3b, known as iC3b, cannot form a convertase but can still act as an opsonin. Which complement receptors are capable of binding iC3b?

Which of the following is NOT one of the five major classes of pathogenic agents discussed in the chapter?

What is the term for nonsecreted constituents of bacterial structure, such as lipopolysaccharide (LPS), that trigger phagocytes to release cytokines?

Human RegIII alpha (HIP/PAP) is a bactericidal protein that kills Gram-positive bacteria by forming what structure in the bacterial membrane?

The assembly of the C1 complex in the classical pathway involves the pathogen sensor C1q and two serine proteases. What are these two proteases?

Which of the following describes the mechanism by which lysozyme is more effective against Gram-positive bacteria compared to Gram-negative bacteria?

What is the common name for the inherited disease caused by defects in the CFTR gene, leading to abnormally thick and dehydrated mucus and frequent lung infections?

The cleavage of C3 into C3a and C3b is the critical step in complement activation. What is the general term for the enzyme complexes that perform this cleavage?

Paroxysmal nocturnal hemoglobinuria is a disease where red blood cells are lysed by complement. This is caused by a failure to express GPI-anchored proteins. Which two complement regulatory proteins are missing from the cell surface in this disease?

Ficolins initiate the lectin pathway of complement activation. Unlike mannose-binding lectin (MBL), which has a C-type lectin domain, what type of domain do ficolins use to bind to oligosaccharides containing acetylated sugars?

When the anaphylatoxin C5a binds to its receptor on macrophages, it can activate them to ingest bacteria that are bound to which other complement receptor?

What is the designation for the C3 convertase of the lectin pathway?

Natural antibodies, which are present without prior infection, are an effective means of activating complement against some bacteria. What immunoglobulin class are most natural antibodies?

The C-reactive protein (CRP) is an acute-phase protein that can activate the classical complement pathway. What molecular structure on bacterial and fungal surfaces does CRP bind to?

Following cleavage of C3b by factor I, the inactive fragment iC3b can be further cleaved by factor I and CR1 to release a fragment called C3c. What is the name of the final C3 fragment that remains bound to the pathogen and is recognized by complement receptor CR2?

Which of the following antimicrobial peptides are primarily produced in the oral cavity and are particularly active against pathogenic fungi like Candida albicans?

What is the primary function of Paneth cells, which are specialized cells deep in the epithelial crypts of the intestine?

The complement cascade is under tight regulation. What is the name of the plasma serine protease inhibitor, or serpin, that controls the activation of C1 by causing C1r and C1s to dissociate from C1q?

How many molecules of C3b can be deposited in the vicinity of a single active C3 convertase, leading to significant amplification of the complement signal?

The alternative pathway can be initiated by the 'tickover' of C3. What is the name of the short-lived, fluid-phase C3 convertase formed during this process?

Besides MBL, what other family of pathogen-recognition molecules, which have a fibrinogen-like domain, can initiate the lectin pathway of complement?

Surfactant proteins A and D (SP-A and SP-D) are members of the collectin family found in the lung. What is their primary immunoregulatory function?

What is the outcome for the C3b fragment if its reactive thioester bond does not form a covalent bond with a nearby surface shortly after cleavage?

Individuals with a deficiency in MBL-associated serine protease 2 (MASP-2) experience substantially more respiratory infections during early childhood. What does this susceptibility primarily illustrate?

Which component of the C1 complex is responsible for the pathogen-sensing function of the complex?

The Normally nonpathogenic commensal bacteria of the microbiota can help protect against pathogens by what mechanism?

How many C3b molecules are present in the C5 convertase of the alternative pathway (C3b2Bb)?

Innate immune mechanisms, if they fail, are followed by the early induced innate response (4–96 hours) and then the adaptive immune response (later than 96 hours). Which of the following belongs to the IMMEDIATE innate response that acts as soon as a pathogen breaches an anatomic barrier?

Individuals with a genetic deficiency in Factor I suffer from recurrent bacterial infections. What is the biochemical consequence of Factor I deficiency?

The assembly of the membrane-attack complex is initiated by C5b. What is the next component that binds to C5b to form the C5b6 complex?