Fiche de révision : Innate Immunity and Viral Recognition

📋 Course Outline

1. Innate Immune Response
2. Pattern Recognition Receptors
3. Toll-like Receptors
4. RIG-I Receptor
5. Cytokines and Chemokines
6. Immune Cell Roles
7. Macrophages and Neutrophils
8. Natural Killer Cells
9. Viral Evasion Strategies
10. Interferon Signaling

📖 1. Innate Immune Response

🔑 Key Concepts & Definitions

• Immediate innate immune response: The rapid activation of immune defenses upon pathogen detection, occurring within minutes to hours, before the adaptive immune system is engaged (source). It involves pre-existing cells and mechanisms that respond instantly to infection.

• Recognition of PAMPs by innate immune cells: The process by which innate immune cells detect pathogen-associated molecular patterns (PAMPs), which are conserved molecular motifs unique to microbes, via pattern recognition receptors (PRRs) (source). This recognition triggers immune activation and inflammation.

• Lack of memory in innate immunity: Innate immune responses do not generate immunological memory; they respond similarly upon each encounter with the same pathogen, without enhanced or faster responses upon re-exposure (source).

• Interdependence of innate and adaptive immunity: Innate immunity initiates and shapes adaptive responses; it recognizes pathogens quickly and produces signals such as cytokines and inflammation that are essential for activating adaptive immune cells (source).

• Role of inflammation in innate immunity: Inflammation is a key response triggered by innate immune recognition of PAMPs, leading to increased blood flow, recruitment of immune cells, and production of cytokines, which collectively help contain infection and activate adaptive defenses (source).

• Differences between innate and adaptive immune responses: Innate immunity is immediate, non-specific, and lacks memory, involving cells like macrophages and NK cells; adaptive immunity is delayed (around 6 days), highly specific, and capable of memory, mediated mainly by lymphocytes (T and B cells) (source).

📝 Essential Points

• The innate immune response acts immediately after pathogen invasion, primarily through cells already present in tissues such as macrophages, neutrophils, and NK cells (source).
• Recognition of PAMPs by PRRs (e.g., TLRs, RIG-I) is crucial for pathogen detection, leading to activation of signaling pathways that induce cytokine production and inflammation (source).
• Unlike adaptive immunity, innate responses do not improve with repeated exposure; they respond with the same intensity each time (source).
• Inflammation induced by innate recognition not only helps contain infection but also facilitates the activation of adaptive immunity by recruiting lymphocytes and antigen-presenting cells (source).
• The interdependence of innate and adaptive responses ensures a coordinated defense: innate responses provide the initial rapid defense and set the stage for a more specific, long-lasting adaptive response (source).

💡 Key Takeaway

The innate immune response provides an immediate, non-specific defense that detects pathogens through conserved molecular patterns, initiating inflammation and bridging to adaptive immunity, which offers a delayed but highly specific and memory-capable response.

📖 2. Pattern Recognition Receptors

🔑 Key Concepts & Definitions

• Pattern Recognition Receptors (PRRs): Receptors of innate immunity that detect pathogen-associated molecular patterns (PAMPs). AUTHOR (date): "They recognize motifs microbiens" and activate immune responses.
• Recognition of PAMPs by PRRs: The process where PRRs identify conserved microbial motifs (PAMPs) on pathogens, triggering immune activation. AUTHOR (date): "Dès que les PAMPs sont reconnus par les cellules de l’immunité innée via le PRR, celles-ci s’activent."
• Types of PRRs: Include surface, secreted, and intracellular receptors. Surface PRRs (e.g., TLRs) detect extracellular pathogens; secreted PRRs (e.g., collectins) circulate or are present in serum; intracellular PRRs (e.g., RIG-I) detect pathogens inside cells. AUTHOR (date): "Ils peuvent être de différents types : Molécules de surface, molécules sécrétées, molécules intracellulaires."
• Conservation and invariance of PRRs: PRRs are highly conserved and invariant across individuals, ensuring a rapid and universal recognition of pathogens. AUTHOR (date): "Ils sont conservés et invariants."
• PRRs involved in influenza detection: Include Toll-like receptors (TLR-3, TLR-7, TLR-8), RIG-I, and collectins like surfactant D, which recognize viral RNA or surface proteins to initiate immune responses. AUTHOR (date): "Les PRR qui reconnaissent les IAV sont : TLR-3, TLR-7, TLR-8, RIG-I, collectines."

📝 Essential Points

• PRRs are essential sensors of innate immunity, responsible for early detection of pathogens by recognizing PAMPs, which are molecular motifs unique to microbes.
• Recognition of PAMPs by PRRs activates signaling pathways that lead to the production of cytokines, chemokines, and interferons, initiating inflammation and antiviral states.
• Different PRRs are localized in specific cellular compartments: TLRs are mainly in endosomes, RIG-I is cytosolic, and collectins are secreted into serum or extracellular fluids.
• The recognition process involves ligand binding, receptor dimerization (e.g., TLRs), and activation of transcription factors NFkB and IRF, which induce immune response genes.
• PRRs involved in influenza detection include TLR-3, TLR-7, TLR-8 (endosomal), RIG-I (cytoplasmic), and collectins like surfactant D, which neutralize the virus.
• PRRs are highly conserved and invariant, allowing for a rapid, broad, and effective innate immune response across different individuals and species.

💡 Key Takeaway

Pattern Recognition Receptors are conserved innate immune sensors that detect microbial PAMPs through surface, secreted, or intracellular mechanisms, triggering early immune responses critical for controlling influenza virus infection.

📖 3. Toll-like Receptors

🔑 Key Concepts & Definitions

• Toll-like receptors (TLRs) (see pattern recognition receptor): A class of membrane-bound pattern recognition receptors (PRRs) that detect microbial components, particularly within endosomes, and initiate innate immune responses.

• TLR-3, TLR-7, TLR-8: Specific TLRs involved in influenza detection; TLR-3 recognizes double-stranded RNA (dsRNA), while TLR-7 and TLR-8 recognize single-stranded RNA (ssRNA) of viral origin (see section on TLRs involved in influenza detection).

• Localization of TLRs in endosomes: TLRs such as TLR-3, TLR-7, and TLR-8 are situated within endosomal compartments, allowing them to detect viral RNA during endocytosis of viruses like influenza (see recognition of viral RNA).

• Ligand recognition by TLRs (viral RNA): TLR-3 binds dsRNA, whereas TLR-7 and TLR-8 recognize ssRNA, enabling detection of viral genomes within endosomes and triggering immune signaling cascades (see ligand recognition).

• TLR dimerization and signaling cascade: Upon ligand binding, TLRs undergo dimerization, which activates downstream signaling pathways involving adaptor proteins, leading to the activation of transcription factors NFkB and IRF (see TLR signaling cascade).

• Activation of transcription factors NFkB and IRF by TLRs: Dimerized TLRs initiate signaling that activates NFkB, promoting cytokine production, and IRF, inducing interferon genes, essential for antiviral responses (see activation of NFkB and IRF).

📝 Essential Points

• TLRs are crucial PRRs located in endosomes, specifically TLR-3, TLR-7, and TLR-8, which detect viral RNA from influenza virus during endocytosis (see localization of TLRs in endosomes).

• Recognition of viral RNA by TLR-3, TLR-7, and TLR-8 triggers receptor dimerization, initiating a signaling cascade that activates transcription factors NFkB and IRF (see TLR dimerization and signaling cascade).

• NFkB activation leads to transcription of cytokines and chemokines, mediating inflammation, while IRF activation induces interferon genes, establishing an antiviral state (see activation of transcription factors NFkB and IRF).

• These pathways are vital for initiating innate immune responses and subsequently shaping adaptive immunity against influenza infection.

💡 Key Takeaway

Toll-like receptors, particularly TLR-3, TLR-7, and TLR-8 located in endosomes, detect viral RNA from influenza, triggering signaling pathways that activate NFkB and IRF, which orchestrate inflammatory and antiviral responses essential for innate immunity.

📖 4. RIG-I Receptor

🔑 Key Concepts & Definitions

• RIG-I (Retinoic acid-inducible gene I): A cytosolic pattern recognition receptor (PRR) that detects viral RNA within the cytoplasm, particularly recognizing viral RNA lacking a 5' cap, and initiates antiviral immune responses (source content).

• Recognition of viral RNA lacking 5' cap by RIG-I: RIG-I specifically identifies viral RNAs that do not possess a 5' coiffe, distinguishing them from host mRNAs, which typically have a 5' cap, thus enabling detection of certain viral genomes such as influenza (source content).

• Intracellular localization of RIG-I in cytoplasm: RIG-I is situated within the cytoplasm of host cells, allowing it to survey intracellular space for viral RNA, especially during viral replication cycles that occur in the cytosol (source content).

• Role of RIG-I in detecting influenza virus RNA: RIG-I recognizes the single-stranded viral RNA (ssRNA) of influenza virus that lacks a 5' coiffe, triggering signaling pathways that lead to the production of interferons and other antiviral genes (source content).

📖 5. Cytokines and Chemokines

🔑 Key Concepts & Definitions

• Cytokines: Small signaling proteins produced by immune cells after stimulation, mediating immune responses through autocrine, paracrine, or endocrine actions (Author: source content). They are crucial for inflammation and antiviral defense, including families like interleukins (IL), interferons (IFN), and TNF.

• Chemokines: A subset of cytokines primarily responsible for chemoattractant functions, guiding immune cells to infection sites (Author: source content). An example is CCL3, which recruits leukocytes during inflammation.

• Cytokines as mediators of inflammation: Cytokines such as IL-1, IL-6, and TNF-α promote inflammation by inducing vascular changes and recruiting immune cells (Author: source content). They coordinate the immune response to pathogens like influenza virus.

• Induction of cytokine and chemokine genes by NFkB: NFkB is a transcription factor activated upon PRR recognition of pathogens, leading to the expression of pro-inflammatory cytokines and chemokines (Author: source content). This process amplifies inflammation and immune cell recruitment.

• Role of interferons as antiviral cytokines: Interferons (IFN), especially type I (IFN-α, β), are cytokines induced by IRF that establish an antiviral state in cells by stimulating ISG expression, inhibiting viral replication (Author: source content).

📝 Essential Points

• Cytokines are pivotal in orchestrating immune responses, with their actions classified as autocrine, paracrine, or endocrine, depending on the target cells (Author: source content). They include mediators like IL-1, IL-6, TNF-α, and antiviral IFNs.

• Chemokines, such as CCL3, specifically attract immune cells like leukocytes to infection sites, facilitating inflammation and pathogen clearance (Author: source content). They are cytokines with a primary chemoattractant function.

• The recognition of viral PAMPs by PRRs (e.g., TLR-3, TLR-7, RIG-I) activates signaling pathways that induce NFkB and IRF transcription factors, leading to cytokine and chemokine gene expression (Author: source content). This cascade is crucial for initiating innate immunity.

• Interferons, particularly type I, are induced by IRF and trigger the expression of ISGs, which inhibit various stages of viral replication, establishing an antiviral state (Author: source content). They also modulate immune responses and activate other immune cells.

• The inflammatory response involves cytokines like IL-1, IL-6, and TNF-α, which increase vascular permeability and recruit immune cells, essential for controlling viral infections such as influenza (Author: source content).

💡 Key Takeaway

Cytokines and chemokines are essential mediators that coordinate inflammation and antiviral defenses by recruiting immune cells and inducing an antiviral state, primarily through NFkB and IRF pathways activated by PRRs during infection.

📖 6. Immune Cell Roles

🔑 Key Concepts & Definitions

• Leukocytes (white blood cells): Cells involved in immune defense, including various immune cell types such as macrophages, neutrophils, lymphocytes, NK cells, and monocytes, which coordinate responses to pathogens (see Roles of leukocytes in immune defense).

• Innate immune cells: Cells that provide immediate, non-specific defense against pathogens, including macrophages, neutrophils, NK cells, and certain dendritic cells, which recognize PAMPs via PRRs (see Overview of immune cell types in innate immunity).

• Adaptive immune cells: Cells that develop a specific response and memory to pathogens, primarily lymphocytes such as T cells and B cells, which are distinguished from innate cells by their ability to remember previous encounters (see Distinction between innate and adaptive immune cells).

• Importance of knowing immune cell names and functions: Understanding the specific roles and recognition mechanisms of immune cells is crucial for comprehending immune responses, disease mechanisms, and designing targeted therapies (see Importance of knowing immune cell names and functions).

📝 Essential Points

• Leukocytes encompass a variety of immune cells that act in innate immunity, including macrophages, neutrophils, NK cells, monocytes, and collectins, each with specialized functions such as phagocytosis, cytokine production, and pathogen recognition (see Roles of leukocytes in immune defense).

• Innate immune cells are characterized by their ability to recognize PAMPs through conserved receptors like PRRs, enabling rapid response without prior exposure, but they lack memory capabilities (see Overview of immune cell types in innate immunity).

• Adaptive immune cells, mainly lymphocytes (T and B cells), are highly specific, capable of forming memory, and are responsible for long-term immunity, with their activation often dependent on signals from innate immune cells (see Distinction between innate and adaptive immune cells).

• Recognizing the names and functions of immune cells allows for better understanding of immune mechanisms, disease progression, and the development of immunomodulatory treatments (see Importance of knowing immune cell names and functions).

💡 Key Takeaway

Understanding the diversity and specific roles of innate and adaptive immune cells is fundamental to grasping how the immune system defends against pathogens and how immune responses can be modulated for therapeutic purposes.

📖 7. Macrophages and Neutrophils

🔑 Key Concepts & Definitions

• Functions of macrophages in innate immunity: Macrophages are phagocytic cells that detect, engulf, and destroy pathogens such as viruses and infected cells. They also secrete cytokines and chemokines to orchestrate inflammation and recruit other immune cells (see section 10). They play a crucial role in maintaining tissue homeostasis and initiating immune responses.

• Phagocytosis and antigen presentation by macrophages: Macrophages recognize pathogens via PRRs like the mannose receptor (MR), internalize them into phagosomes, which fuse with lysosomes to degrade the pathogen. Processed pathogen fragments are then presented on macrophage surface MHC molecules to activate adaptive immunity (see section 10).

• Roles of neutrophils in inflammation and pathogen clearance: Neutrophils are rapid responders that migrate to infection sites, where they perform phagocytosis of pathogens and release enzymes and reactive oxygen species to kill microbes. They are essential for early pathogen clearance and amplifying inflammation.

• Differences between macrophages and neutrophils: Macrophages are longer-lived, tissue-resident cells capable of antigen presentation and cytokine secretion, while neutrophils are short-lived, highly motile cells specialized in immediate pathogen destruction through phagocytosis and degranulation.

• Monocytes as precursors to macrophages: Monocytes are circulating precursors in blood that migrate into tissues during infection or inflammation, where they differentiate into macrophages, acquiring specialized functions depending on tissue environment.

📝 Essential Points

• Macrophages are key players in innate immunity, performing phagocytosis and secreting cytokines like IFN, TNFα, IL-1, and IL-6, which promote inflammation and activate other immune cells (see section 10). They recognize pathogens through PRRs such as the mannose receptor (MR) and TLRs, enabling detection of viruses like influenza A (see section 10).

• During phagocytosis, macrophages form phagosomes that fuse with lysosomes containing digestive enzymes, leading to pathogen degradation. They also process and present antigens on MHC molecules, linking innate and adaptive immunity.

• Neutrophils are recruited rapidly to infection sites via chemokines like CCL3, where they perform phagocytosis and release antimicrobial substances. Their primary role is early pathogen clearance and amplifying inflammatory responses.

• Macrophages are tissue-resident, longer-lived cells capable of antigen presentation, whereas neutrophils are short-lived, highly motile cells focused on immediate microbial killing.

• Monocytes circulate in blood and, upon tissue entry, differentiate into macrophages that adapt to local signals, becoming specialized for tissue-specific immune functions.

💡 Key Takeaway

Macrophages and neutrophils are essential innate immune cells with distinct roles: macrophages provide sustained defense, antigen presentation, and immune regulation, while neutrophils act as rapid first responders for immediate pathogen clearance and inflammation amplification. Monocytes serve as precursors that replenish macrophage populations in tissues.

📖 8. Natural Killer Cells

🔑 Key Concepts & Definitions

• Natural Killer (NK) cells: Innate immune effectors that can recognize and destroy infected or abnormal cells without prior sensitization, playing a crucial role in early viral defense (source).
• Recognition of infected cells by NK cells: NK cells identify infected cells primarily through a balance of activating and inhibitory signals received via specific receptors, allowing them to distinguish between healthy and compromised cells (source).
• Killing of infected cells by NK cells: NK cells induce apoptosis in target cells through the release of cytotoxic granules containing perforin and granzymes, leading to cell death and limiting viral spread (source).
• Role of NK cells in early viral defense: NK cells are among the first responders during viral infections, providing rapid containment before the adaptive immune response is fully activated (source).
• Localization and activation of NK cells: NK cells are predominantly found in the blood, spleen, and tissues such as the liver and lungs; their activation is triggered by cytokines like interferons and interleukins produced during infection (source).

📝 Essential Points

• NK cells are innate immune effectors capable of immediate response to virally infected cells, crucial for early containment of infections (source).
• They recognize infected cells through a combination of activating receptors (e.g., NKG2D) that detect stress-induced ligands and inhibitory receptors (e.g., KIRs) that recognize self-MHC class I molecules; a decrease in MHC I expression on infected cells often triggers NK cell activation (source).
• Once activated, NK cells release cytotoxic granules (perforin and granzymes) and produce cytokines such as IFN-γ, which enhance the antiviral immune response (source).
• NK cells are activated by cytokines like type I interferons (IFN-α/β) and IL-12, produced early during viral infection, which amplify their cytotoxic activity (source).
• Their strategic localization in tissues such as the lungs allows NK cells to respond rapidly at sites of viral entry and replication (source).

💡 Key Takeaway

Natural Killer cells are vital innate immune effectors that provide immediate defense against viral infections by recognizing and killing infected cells early, primarily through receptor-mediated mechanisms and cytokine activation.

📖 9. Viral Evasion Strategies

🔑 Key Concepts & Definitions

• Mechanisms of viral evasion of innate immunity: Strategies employed by viruses to avoid detection and destruction by the host’s innate immune system, such as altering PAMPs or inhibiting PRR signaling pathways (source content).
• Strategies influenza virus uses to avoid detection: The influenza virus develops methods like modifying its RNA (e.g., adding a coiffe) to escape recognition by PRRs like RIG-I and TLRs, thereby reducing immune activation (source content).
• Impact of viral evasion on immune response effectiveness: Viral evasion diminishes the ability of innate immunity to recognize and respond promptly, leading to delayed or weakened immune responses, which can facilitate viral replication and disease progression (source content).
• Balance between viral attack and host defense: The dynamic equilibrium where host immune mechanisms attempt to detect and eliminate the virus, while the virus evolves evasion tactics to persist and propagate within the host (source content).

📝 Essential Points

• Viruses, including influenza A, employ various mechanisms to evade innate immunity, such as modifying PAMPs like viral RNA to prevent recognition by PRRs such as RIG-I and TLRs (source content).
• Influenza virus can alter its RNA, for instance by adding a coiffe, to mimic host mRNA, thus avoiding detection by cytosolic sensors like RIG-I (source content).
• The virus can also inhibit signaling pathways downstream of PRRs, such as blocking the activation of transcription factors NFkB and IRF, which are crucial for cytokine and interferon production (source content).
• These evasion strategies impair the induction of cytokines, chemokines, and interferons, weakening the inflammatory response and antiviral state, ultimately affecting the overall immune response effectiveness (source content).
• The balance between viral attack and host defense is a continuous evolutionary arms race, where successful evasion allows the virus to replicate more efficiently, challenging the immune system's capacity to contain infection (source content).

💡 Key Takeaway

Viruses like influenza A have evolved sophisticated mechanisms to evade innate immune detection, which can compromise the host’s early antiviral response and tip the balance in favor of viral persistence and disease progression.

📖 10. Interferon Signaling

🔑 Key Concepts & Definitions

• Interferon signaling pathway: A cascade initiated when interferons bind to their specific receptors on cells, leading to activation of transcription factors like IRF and NFkB, which induce antiviral gene expression (see "LIESENTRE PRR E T C Y TO K I N E S" for cascade details).

• Role of IRF transcription factors in interferon gene induction: IRF (Interferon Regulatory Factors) are critical transcription factors that, upon activation by PRRs (such as TLRs and RIG-I), stimulate the transcription of interferon genes, especially Type I interferons (see "CO N T R O L E R - A T T A Q U E" and "LIESENTRE PRR E T C Y TO K I N E S").

• Type I interferons as antiviral cytokines: A class of cytokines, including IFN-α and IFN-β, produced mainly by infected cells, which induce an antiviral state in both infected and neighboring cells by stimulating the expression of ISGs (Interferon Stimulated Genes) (see "CYTO K I N E S E T C H I M I O K I N E S" and "LIESENTRE PRR E T C Y TO K I N E S").

• Effects of interferon signaling on infected and neighboring cells: Interferons act autocrinely on infected cells and paracrinely on neighboring cells, inducing ISGs that inhibit viral replication, enhance antiviral defenses, and prepare cells for potential infection (see "LIESENTRE PRR E T C Y TO K I N E S" and "CE L L U L E S D E L’ I M M U N I T E I N N E E E T IAV").

📝 Essential Points

• The interferon signaling pathway is activated when PRRs such as TLR-3, TLR-7, TLR-8, and RIG-I recognize viral PAMPs, leading to the activation of IRF and NFkB transcription factors (see "CO N T R O L E R - A T T A Q U E"). IRF activation is particularly crucial for the induction of Type I interferon genes (see "Role of IRF transcription factors").

• Once produced, Type I interferons (IFN-α and IFN-β) bind to the IFN receptor on the same or neighboring cells, triggering the JAK-STAT pathway, which results in the transcription of ISGs. These genes encode proteins that establish an antiviral state, such as MXA and GBP, which inhibit various stages of viral replication (see "CYTO K I N E S E T C H I M I O K I N E S" and "LIESENTRE PRR E T C Y TO K I N E S").

• The antiviral effects of interferons include the inhibition of viral genome replication, blocking of viral protein synthesis, and degradation of viral RNA, thereby limiting the spread of infection within tissues (see "LIESENTRE PRR E T C Y TO K I N E S" and "CE L L U L E S D E L’ I M M U N I T E I N N E E E T IAV").

• Interferon signaling not only affects infected cells but also primes neighboring cells, making them resistant to infection through the induction of ISGs, thus creating an antiviral environment that limits viral dissemination (see "LIESENTRE PRR E T C Y TO K I N E S" and "CE L L U L E S D E L’ I M M U N I T E I N N E E E T IAV").

💡 Key Takeaway

Interferon signaling is a crucial innate immune response that, through IRF activation and cytokine production, induces an antiviral state in both infected and neighboring cells, effectively limiting viral replication and spread.

📊 Synthesis Tables

⚠️ Common Pitfalls & Confusions

1. Confusing innate immunity with adaptive immunity; innate is immediate and non-specific, adaptive is delayed and specific.
2. Assuming PRRs are highly variable; they are conserved and invariant across individuals.
3. Misidentifying TLR localization; TLR-3, 7, 8 are in endosomes, not on the cell surface.
4. Overlooking that PRRs recognize conserved microbial motifs (PAMPs), not host molecules.
5. Mistaking cytokine production as solely adaptive; it is a hallmark of innate activation.
6. Confusing RIG-I with TLRs; RIG-I is cytosolic, TLRs are membrane-bound or endosomal.
7. Assuming all PRRs recognize the same PAMPs; different PRRs recognize different microbial motifs.

✅ Exam Checklist

• Know the definition and role of innate immunity in pathogen defense.
• Understand the recognition of PAMPs by innate immune cells and the importance of PRRs.
• Identify the different types of PRRs: surface, secreted, and intracellular.
• Recall that PRRs are highly conserved and invariant across individuals.
• Describe the key PRRs involved in influenza detection: TLR-3, TLR-7, TLR-8, RIG-I, collectins.
• Know the localization of TLRs, especially TLR-3, TLR-7, and TLR-8 in endosomes.
• Understand the ligand recognition mechanisms of TLR-3 (dsRNA), TLR-7/8 (ssRNA).
• Explain the process of TLR dimerization and subsequent activation of NFkB and IRF.
• Recognize that activation of NFkB leads to cytokine production, and IRF induces interferons.
• Know that innate responses are immediate, do not generate memory, and initiate inflammation.
• Understand how innate immunity bridges to adaptive immunity via cytokines and antigen presentation.
• Be familiar with the roles of macrophages, neutrophils, NK cells, and their activation pathways.
• Recognize viral evasion strategies, such as blocking PRR signaling or interferon responses.
• Master the key authors and references, e.g., "Author (date): 'PRRs recognize microbial motifs'" and "SMITH's definition of the TLRs."
• Know the signaling pathways activated by TLRs, including adaptor proteins and downstream transcription factors.
• Be able to differentiate between the recognition mechanisms of various PRRs and their cellular locations.
• Understand the role of cytokines and chemokines produced during innate activation.
• Know the function of RIG-I as a cytosolic sensor for viral RNA.
• Recall the importance of interferon signaling in establishing an antiviral state.
• Recognize common pitfalls in understanding innate immune mechanisms.
• Confirm mastery of vocabulary related to innate immunity, PRRs, TLRs, cytokines, and cell types.