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Ch. 16 - Innate Immunity: Nonspecific Defenses of the Host
Tortora - Microbiology: An Introduction 14th Edition
Tortora14th EditionMicrobiology: An IntroductionISBN: 9780138200398Not the one you use?Change textbook
Chapter 16, Problem 1

Legionella uses C3b receptors to enter monocytes. This
a. prevents phagocytosis.
b. degrades complement.
c. inactivates complement.
d. prevents inflammation.
e. prevents cytolysis.

Verified step by step guidance
1
Step 1: Understand the role of C3b in the immune system. C3b is a component of the complement system that tags pathogens for destruction by phagocytes, a process called opsonization.
Step 2: Recognize that Legionella uses C3b receptors to enter monocytes, which are immune cells responsible for engulfing and destroying pathogens.
Step 3: Analyze what happens when Legionella binds to C3b receptors on monocytes. Instead of being destroyed, Legionella exploits this mechanism to gain entry into the monocytes.
Step 4: Consider the consequences of this entry method. By using C3b receptors, Legionella avoids triggering the usual immune responses such as phagocytosis that would normally kill the bacteria.
Step 5: Conclude that the correct effect of Legionella using C3b receptors is that it prevents phagocytosis, allowing the bacteria to survive inside the monocytes.

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Key Concepts

Here are the essential concepts you must grasp in order to answer the question correctly.

Complement System and C3b

The complement system is a part of innate immunity that tags pathogens for destruction. C3b is a key complement protein that opsonizes microbes, marking them for phagocytosis by immune cells like monocytes and macrophages.
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Phagocytosis and Pathogen Entry

Phagocytosis is the process by which immune cells engulf and destroy pathogens. Some bacteria, like Legionella, exploit receptors such as C3b receptors to enter monocytes, using the host's own mechanisms to avoid destruction.
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Intracellular Survival Mechanisms of Legionella

Legionella can survive inside monocytes by preventing the normal phagosome-lysosome fusion, allowing it to replicate within the host cell. Using C3b receptors facilitates entry but also helps the bacteria evade immune responses like cytolysis and inflammation.
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