Overview of the Immune System
What are the two main types of immunity in the body?
→ Innate immunity and adaptive immunity
What does the term “phagocytosis” mean?
→ “Cell eating” – the process by which cells engulf and digest particles or pathogens
Which specialized immune cells are important for attacking parasitic worms?
→ Eosinophils
What are cytokines?
→ Small proteins released by immune cells that regulate immune responses
What are the four cardinal signs of inflammation?
→ Redness, heat, swelling, and pain
Which type of immunity is present at birth and responds quickly to pathogens?
→ Innate immunity
Name one main type of phagocyte in the immune system.
→ Examples: Neutrophils, macrophages, dendritic cells
Which cells release histamine and other chemicals during allergic reactions?
→ Basophils and mast cells
What type of antimicrobial protein helps protect cells against viral infections?
→ Interferons
Which immune cells release histamine to trigger inflammation?
→ Basophils and mast cells
Which type of immunity develops with exposure to pathogens and builds memory?
→ Adaptive immunity
What is the primary role of phagocytosis in immunity?
→ To engulf and destroy pathogens and debris
Which immune cells are known as “large granular lymphocytes” that can destroy virus-infected or tumor cells?
→ Natural Killer (NK) cells
Which antimicrobial system involves a group of plasma proteins that enhance immune responses?
→ Complement system
What causes the redness and heat seen in inflamed tissue?
→ Increased blood flow (vasodilation)
What is the “first line of defense” in innate immunity?
→ Physical and chemical barriers, such as skin and mucous membranes
What is the first step of phagocytosis?
→ Recognition and adherence to the pathogen
How do eosinophils kill large parasites that cannot be phagocytosed?
→ They release toxic granules and enzymes onto the parasite’s surface
How do interferons protect nearby cells from viral infection?
→ They signal neighboring cells to produce antiviral proteins that block viral replication
What causes swelling during inflammation?
→ Increased capillary permeability leading to fluid leakage into tissues
What is the “second line of defense” in innate immunity?
→ Internal defenses such as phagocytes, NK cells, inflammation, fever, and antimicrobial proteins
What is the phagosome?
→ A vesicle that contains the engulfed pathogen inside the phagocyte
What unique feature allows NK cells to kill target cells without needing prior activation by antigens?
→ They recognize abnormal or missing self-markers (such as altered MHC) and induce apoptosis
Name one effect of cytokines in immune system regulation.
→ Stimulate inflammation, recruit immune cells, or promote adaptive immunity
What is the main benefit of fever during infection?
→ Inhibits microbial growth and enhances immune responses
What is the “third line of defense,” and which immune cells are central to it?
→ Adaptive immunity involving lymphocytes (B cells and T cells)
Which organelle fuses with the phagosome to digest the pathogen?
→ Lysosome, forming a phagolysosome
What do mast cells and basophils release that increases blood vessel permeability during inflammation?
→ Histamine, Heparin and Eicosanoids
What are the three major outcomes of complement activation?
→ Opsonization, inflammation, and cytolysis
Which chemical “resets” the hypothalamus to produce fever?
→ Pyrogens (e.g., interleukin-1, bacterial toxins)
Compare how the innate and adaptive immune systems differ in specificity.
→ Innate immunity responds to general features common to pathogens, while adaptive immunity is highly specific, targeting unique antigens
Compare neutrophils and macrophages in their roles as phagocytes.
→ Neutrophils are short-lived, rapid responders; macrophages are long-lived and can activate adaptive immunity
Compare the roles of basophils and mast cells in immune responses.
→ Basophils circulate in blood; mast cells are resident in tissues; both release histamine to enhance inflammation
How does the complement system enhance phagocytosis?
→ Through opsonization: complement proteins coat pathogens, making them easier for phagocytes to bind and ingest
Compare the short-term benefits of inflammation vs. fever.
→ Inflammation recruits immune cells locally; fever provides a systemic defense by slowing pathogen growth and boosting immune activity
How do the innate and adaptive immune systems interact to protect the body?
→ Innate defenses slow or contain pathogens early, while adaptive immunity activates later for targeted elimination and memory formation
Why are macrophages considered “antigen-presenting cells”?
→ They display digested pathogen fragments (antigens) on their surface to activate adaptive immunity
How do NK cells differ from cytotoxic T cells in their mechanism of killing?
→ NK cells act without prior antigen exposure, release granzymes that cause apoptosis; cytotoxic T cells require antigen presentation
Compare the roles of interferons and complement in fighting infection.
→ Interferons defend against viruses by warning nearby cells; complement defends against bacteria by opsonizing, lysing, and enhancing inflammation
How do mast cells amplify inflammation once activated?
→ They release histamine, heparin, and other chemicals that attract phagocytes and increase vascular permeability
Case: A patient is exposed to a novel virus. Which immune system will respond first, and how will the other system contribute later?
→ Innate immunity (barriers, phagocytes, NK cells) acts first; adaptive immunity develops targeted antibodies and T-cell responses later
Case: A person with defective lysosomes can engulf bacteria but still develops chronic infections. Why?
→ They cannot digest pathogens inside the phagosome without lysosomal enzymes
Case: A patient has chronic parasitic infections but normal bacterial/viral immunity. Which specialized immune cell is likely deficient?
→ Eosinophils
Case: A patient with a genetic defect in interferon production struggles with viral infections but not bacterial ones. Why?
→ Without interferons, their cells cannot mount an early antiviral defense; bacteria are still targeted by other immune mechanisms
Case: A patient takes strong anti-histamine medication. Which part of the inflammatory response will be most affected?
→ Reduced vasodilation and vascular permeability, limiting redness and swelling
Why is it advantageous that the adaptive immune system has “memory,” and how does this affect future infections?
→ Memory allows a faster, stronger response upon re-exposure, often preventing illness
How do opsonins (like antibodies or complement proteins) enhance phagocytosis?
→ They coat pathogens, making them easier for phagocytes to recognize and bind
How might overactivation of mast cells contribute to disease?
→ Excessive histamine release can cause allergies, asthma, or anaphylaxis
Why is uncontrolled cytokine release (“cytokine storm”) dangerous?
→ It causes excessive inflammation, damaging host tissues and leading to severe illness
Why might an excessively high fever be dangerous for the body?
→ It can denature proteins, disrupt cellular functions, and cause organ damage
Case: A patient lacking functional T cells can still fight off many infections. Which defense system compensates, and what limitations remain?
→ Innate immunity compensates with barriers, phagocytes, NK cells, etc., but the patient cannot form adaptive, antigen-specific memory
Case: In a patient lacking neutrophils, which other phagocytic cells can partly compensate, and what is the trade-off?
→ Macrophages; they are slower responders but provide sustained defense and antigen presentation
Case: A tumor manages to evade detection by NK cells. What might be the mechanism?
→ The tumor may express normal self-MHC or secrete inhibitory signals to avoid NK cell recognition
Case: A patient has recurrent bacterial infections due to a deficiency in complement proteins. Which part of their immune defense is impaired?
→ The complement cascade, leading to reduced opsonization, cytolysis, and inflammation
Case: A patient has normal immune cells but cannot produce pyrogens. What immune defense is weakened?
→ Fever response, reducing systemic pathogen control
How could a defect in the “first line of defense” increase the burden on both innate and adaptive systems?
→ If barriers like skin/mucosa fail, pathogens gain entry more easily, overwhelming innate defenses and forcing adaptive immunity into frequent activation
How does defective phagocytosis impair both innate and adaptive immunity?
→ Innate defenses fail to clear pathogens effectively, and antigen presentation to adaptive immune cells is disrupted
Explain how specialized cells like eosinophils, NK cells, and basophils/mast cells form a bridge between innate and adaptive immunity.
→ They provide rapid responses (innate), but their actions (antigen presentation, inflammation, histamine release) help activate and regulate adaptive immunity
How do cytokines, interferons, and complement work together to integrate innate and adaptive immunity?
→ Cytokines coordinate responses, interferons inhibit viral spread, and complement enhances pathogen clearance — all helping activate and regulate adaptive immunity
How do basophils, mast cells, inflammation, and fever together illustrate the integration of local and systemic defenses?
→ Basophils/mast cells trigger local inflammation, while fever spreads systemic defense; both coordinate to slow pathogens and activate broader immune responses