Lymph / Immune - Lecture Flashcards

Question

**2nd line of defense**

Answer 1

Includes internal, nonspecific responses like phagocytosis, antimicrobial proteins, inflammation, and fever. **Neutrophils**: Rapid responders that phagocytize bacteria. Release lysosomal enzymes into tissue fluid (degranulation) and generate a respiratory burst (O₂⁻, H₂O₂, HOCl). Form NETs (neutrophil extracellular traps) by ejecting chromatin to trap and kill microbes extracellularly. **Eosinophils**: Target parasites and participate in allergic responses. Phagocytize antigen–antibody complexes and release enzymes and cytotoxins to damage large parasites. Accumulate at infection sites and contribute to inflammation. **Macrophages**: Long-lived phagocytes derived from monocytes. Can be fixed or free in tissues. Engulf debris, microbes, and apoptotic cells. Present antigens on MHC II to activate helper T cells and secrete cytokines to coordinate inflammation. **Dendritic cells**: Potent antigen-presenting cells found in tissues. Phagocytize pathogens and migrate to lymph nodes to present antigen on MHC II to naive T cells. Bridge innate and adaptive immunity. **Basophils**: Circulating granulocytes that release histamine, leukotrienes, and heparin during allergic and inflammatory responses. Promote vasodilation and leukocyte recruitment. **Mast cells**: Tissue-resident cells similar to basophils. Release histamine and other mediators upon activation (e.g., via IgE cross-linking). Key effector cells in allergic reactions and local inflammation. **Natural killer (NK) cells**: Lymphoid-derived cytotoxic cells that detect and kill virus-infected or tumor cells lacking MHC I. Release perforins to form membrane pores and granzymes to induce apoptosis. Operate without prior sens

Answer 2

Cytokines produced by virus-infected macrophages and dendritic cells that provide nonspecific antiviral defense by warning nearby cells and activating immune responses. 1. Induce neighboring cells to produce antiviral proteins that degrade viral RNA and inhibit protein synthesis. 2. Trigger apoptosis in infected cells to prevent viral replication and spread. 3. Activate NK cells and macrophages to destroy infected or cancerous cells.

Answer 3

A group of bloodborne antimicrobial proteins that enhance immune defense by promoting inflammation, opsonization, and lysis of pathogens. Complement activation begins when C3 is cleaved into C3a and C3b, triggering a cascade with signal amplification. 1. Classical pathway: Triggered by antibodies bound to antigens → part of specific (adaptive) immunity. 2. Alternate pathway: Spontaneous activation on microbial surfaces, stabilized in the absence of regulatory proteins like DAF → part of nonspecific (innate) immunity. 3. Lectin pathway: Initiated when mannose-binding lectin binds to pathogen surfaces → part of nonspecific (innate) immunity.

Answer 4

Once activated, complement proteins enhance immune defense through multiple coordinated functions. 1. Enhanced inflammation: Increases vascular permeability and recruits immune cells to the site of infection. 2. Phagocytosis: Promoted by opsonization, where complement proteins coat pathogens to mark them for engulfment by phagocytes. 3. Cytolysis: Complement proteins form the membrane attack complex (MAC), creating pores in the target cell membrane that lead to lysis. 4. Immune clearance: Red blood cells bind antigen–antibody complexes and transport them to macrophages in the liver and spleen for removal.

Answer 5

A nonspecific defense response to tissue injury that limits pathogen spread, removes debris, and initiates repair. Triggered by cytokines such as interleukins, interferons, tumor necrosis factor, and chemotactic factors. 1. Increases blood flow to the area. 2. Activates phagocytes to engulf pathogens and debris. 3. Increases capillary permeability for immune cell access. 4. Activates the complement system to enhance pathogen destruction. 5. Initiates clotting to wall off the infection site. 6. Raises local temperature to inhibit microbes and accelerate repair. 7. Stimulates activation of adaptive immune defenses.

Answer 6

1. **Mobilization** of body defenses: Chemicals like histamine and leukotrienes increase blood flow and capillary permeability to bring in immune cells and proteins. 2. **Containment and destruction of pathogens**: Clotting forms a barrier; chemotactic signals recruit neutrophils and macrophages to phagocytose pathogens. 3. **Tissue cleanup and repai**r: Macrophages clear debris while growth factors and cytokines promote healing and regeneration.

Answer 7

The first step of inflammation, initiated by cytokines and chemical mediators released from damaged cells, basophils, and mast cells. 1. **Kinins, histamine, and leukotrienes** promote vasodilation and increased capillary permeability, resulting in hyperemia, redness, heat, and delivery of immune cells and nutrients. 2. **Fluid and plasma proteins** enter tissue, enabling antibodies, complement proteins, and clotting factors to reach the site. Clotting walls off infection and supports repair. 3. Leukocyte deployment includes: - **Margination**: Selectins make leukocytes stick to endothelium. - **Diapedesis**: Leukocytes exit vessels by squeezing through endothelial gaps. - **Chemotaxis**: Leukocytes follow chemokines toward infection. **Defensins**: Small antimicrobial peptides secreted by neutrophils and epithelial cells that directly disrupt microbial membranes and contribute to pathogen elimination.

Answer 8

The second phase of inflammation, aimed at isolating the infection and initiating microbial killing. 1. Fibrinogen enters tissues and forms clots that trap pathogens in place. 2. Heparin prevents clotting at the exact injury site, keeping pathogens in a fluid pocket surrounded by clotting edges. 3. Neutrophils arrive first, performing phagocytosis and releasing toxic chemicals through the respiratory burst. They also secrete cytokines to recruit additional neutrophils and macrophages. 4. Macrophages and T cells release colony-stimulating factors to increase leukocyte production (leukopoiesis) in the bone marrow.

Answer 9

The final phase of inflammation focused on removing pathogens, debris, and dead cells to allow tissue repair. 1. Monocytes arrive 8–12 hours after onset, differentiate into macrophages, and become the primary agents of cleanup by phagocytosing bacteria, debris, and dead neutrophils. 2. Edema increases lymphatic drainage and decreases venous return, helping flush bacteria, antigens, and waste products out of the tissue. 3. Pus forms from accumulated tissue fluid, cellular debris, dying neutrophils, and microbes at the infection site.

Answer 10

1. Platelets and endothelial cells release PDGF (platelet-derived growth factor), which stimulates fibroblasts to multiply and produce collagen for tissue reconstruction. 2. Hyperemia (increased blood flow) delivers oxygen, nutrients, and heat to support cell activity and accelerate metabolism. 3. Fibrin clot provides a structural scaffold that supports tissue regrowth and helps organize repair. 4. Pain, mediated by bradykinin, restricts movement of the injured area to protect the tissue and promote healing.

Answer 11

1. Promotes interferon activity, boosting antiviral defenses. 2. Accelerates metabolic rate and tissue repair by increasing enzymatic activity. 3. Inhibits pathogen reproduction by raising temperature beyond their optimal range. 4. Triggered by **interleukin-1** (a pyrogen) released by macrophages, which stimulates the hypothalamus to secrete **prostaglandin E (PGE)** and reset the body’s temperature set point. 5. High fevers (>105°F/40°C) may cause delirium; very high fevers (111–115°F or 44–46°C) may lead to coma or death. 6. Follows three stages: onset (rising temp), stadium (plateau), and defervescence (return to normal).

Answer 12

Foreign molecules that can trigger an immune response, typically due to their structural complexity and distinctiveness. 1. Complex molecules: Must be >10,000 amu with unique shapes. Include proteins, polysaccharides, glycoproteins, and glycolipids. 2. **Epitopes**: Also called antigenic determinants, they are the specific regions of an antigen recognized by immune receptors and responsible for stimulating a response. 3. **Haptens**: Small molecules (<10,000 amu) that are not immunogenic alone; they must bind to host macromolecules to become antigenic. Often involved in allergic reactions.

Answer 13

Cell surface proteins that present antigen fragments to T cells and help the immune system distinguish self from non-self. 1. MHC I: Found on all nucleated cells (except red blood cells). Displays intracellular antigens (e.g., viral proteins) to CD8⁺ cytotoxic T cells. 2. MHC II: Found only on antigen-presenting cells (macrophages, dendritic cells, B cells, thymic epithelial cells). Displays extracellular antigens to CD4⁺ helper T cells. 3. Function: Allows immune cells to detect infection or abnormal proteins. Loss or downregulation of MHC I can trigger NK cell-mediated destruction; presence of foreign antigen on MHC II activates adaptive immunity.

Answer 14

Cells that process and present foreign antigens on MHC II molecules to activate helper T cells and initiate adaptive immunity. 1. Include **macrophages**, **dendritic cells**, **B cells**, and **thymic epithelial cells** (reticular cells). 2. Use **MHC II** to present **extracellular antigens** to CD4⁺ helper T cells. 3. Also express **MHC I**, like all nucleated cells, to present intracellular antigens (self or viral) to CD8⁺ cytotoxic T cells. 4. Link **innate and adaptive immunity** by activating naive T cells through antigen presentation. 5. Act as “ID tags” using MHC molecules to allow T cells to distinguish self from non-self.

Answer 15

1. **B cells** bind intact antigens in extracellular fluid via membrane-bound antibodies (BCRs). This can trigger activation directly (**T cell–independent**) or require help from a CD4⁺ helper T cell (**T cell–dependent**) to fully activate and initiate class switching and memory formation. 2. **T cells** recognize only processed antigen fragments presented on MHC molecules: - **CD8⁺ cytotoxic T cells** bind antigens on **MHC I**, found on all nucleated cells → leads to targeted cell killing. - **CD4⁺ helper T cells** bind antigens on **MHC II**, found only on antigen-presenting cells → stimulate B cells, macrophages, and other T cells. 3. Without MHC presentation, **T cells cannot recognize antigen**, whereas **B cells can bind free-floating antigens** but often require T cell help to mount an effective response.

Answer 16

T cells mature in the thymis Ensures developing T cells are MHC-restricted and self-tolerant before entering circulation. 1. **Positive selection** (in cortex): T cells must bind **MHC** on **reticular epithelial cells** in the thymus to survive. Those that fail die by apoptosis.- > ensures can responde to foreign antigen 2. **Negative selection** (in medulla): T cells must **not strongly bind self-antigens**. Those that react undergo: - **Clonal deletion** (apoptosis) - **Anergy** (survive but permanently inactive) 3. Successful cells become **immunocompetent but naive**, form clones with identical receptors for a specific antigen, and exit the thymus for peripheral circulation. *Only ~2% of T cells survive both selection processes.*

Answer 17

Occurs entirely in the **red bone marrow**, where B cells are both generated and selected for self-tolerance. 1. **Negative selection**: B cells that bind **self-antigens** undergo: - **Clonal deletion** (apoptosis) - **Anergy** (remain alive but unresponsive) 2. **Self-tolerant B cells** survive, synthesize **B cell receptors (BCRs)**, and proliferate into clones of **immunocompetent** but naive B cells. 3. These cells exit the bone marrow and migrate to lymphoid tissues, ready for antigen exposure.

Answer 18

Cytokines that mediate communication between **leukocytes**. Coordinate **inflammation**, **immune activation**, and **antibody class switching**. Secreted by **lymphocytes**, **macrophages**, and **APCs**. 1. **IL-1**: Secreted by **macrophages**. Triggers **chemokine production**, induces **fever** by stimulating hypothalamus to release **PGE₂**, and promotes **IL-2 release** by activating T cells. 2. **IL-2**: Secreted by **activated Th1 cells**. Drives **clonal expansion** of **CD4⁺** and **CD8⁺ T cells**. Supports **inflammation** by amplifying T cell responses and enhancing **IFN-γ** and **cytotoxic activity**. 3. **IL-3**: Secreted by **T cells**. Stimulates **bone marrow** to increase production of leukocytes → enhances **inflammatory cell supply**. 4. **IL-4**: Secreted by **Th2 cells**. Induces **B cell class switching to IgE**, promotes **mast cell** activation → key in **allergic inflammation**. 5. **IL-5**: Secreted by **Th2 cells**. Promotes **class switching to IgA**, stimulates **eosinophil proliferation** and activation → important for **mucosal inflammation** and **parasite defense**.

Answer 19

T cells must recognize antigens presented on **MHC molecules** and receive **costimulatory signals** to become fully activated. Both CD4⁺ and CD8⁺ T cells require **antigen recognition** + **cytokine costimulation** for clonal selection and effector function. --- **CD8⁺ Cytotoxic T Cell Activation** 1. **Antigen Recognition**: CD8⁺ T cells bind to foreign peptides presented on **MHC I** of a professional APC 2. **Costimulation**: Requires CD28–B7 binding and a cytokine signal (typically **IL-2**) secreted by an activated CD4⁺ helper T cell nearby 3. **Clonal Selection**: CD8⁺ T cell proliferates into clones with the same TCR → become cytotoxic T lymphocytes (CTLs) 4. **Effector Function**: CTLs induce **apoptosis** in infected, cancerous, or foreign cells lacking normal self-MHC --- **CD4⁺ Helper T Cell Activation** 1. **Antigen Recognition**: CD4⁺ T cells bind to foreign peptides presented on **MHC II** of **APCs** (dendritic cells, macrophages, B cells). 2. **Costimulation**: CD28 on CD4⁺ T cell binds to B7 on APC (second signal). 3. **Clonal Selection**: CD4⁺ T cell proliferates and differentiates 4. **Effector Function**: Coordinate immune response by secreting cytokines to activate other immune cells (CTLs, B cells, macrophages). *Note: IL-2 is a key cytokine produced by activated Th1 cells and is required for full activation of CD8⁺ cells.*

Answer 20

Once activated, cytotoxic T cells directly destroy infected or abnormal cells. They use mechanisms similar to natural killer (NK) cells, but require antigen-specific recognition via MHC I. --- **Lethal Hit Sequence:** 1. **Target Recognition**: CD8⁺ T cell docks on infected or abnormal cell displaying a foreign peptide on MHC I. 2. **Cytotoxic Granule Release**: - **Perforin** forms pores in target cell membrane. - **Granzymes** enter through pores → activate caspase cascad* → trigger **apoptosis**. 3. **Cytokine Secretion**: - Interferons (e.g., IFN-γ): → Inhibit viral replication in surrounding cells → Activate nearby macrophages to enhance phagocytosis - Tumor Necrosis Factor (TNF-α): → Induces apoptosis in tumor cells → Recruits and activates macrophages --- *Only CD8⁺ T cells directly kill target cells. NK cells kill similarly but do not require MHC I–antigen specificity.*

Answer 21

Helper T cells are the **central coordinators of adaptive immunity**, linking **humoral** and **cellular responses** by releasing interleukins and other cytokines. --- **Mechanism of Action:** 1. **Recognize Antigen on MHC II**: CD4⁺ T cells are activated by antigen-presenting cells (e.g., **macrophages, dendritic cells, B cells**) that display foreign antigen fragments on **MHC II**. 2. **Cytokine Secretion (esp. Interleukins)**: Once activated, they secrete **interleukins** that: - **Recruit and activate phagocytes** (e.g., neutrophils, macrophages, NK cells) → enhances **inflammation** and pathogen clearance. - **Stimulate B cell clonal expansion and maturation** → promotes **antibody production** (humoral immunity). - **Stimulate cytotoxic T cell (CD8⁺) activation** → supports **cellular immunity** by enabling Tc clonal selection. 3. **Coordinate Immunity**: Helper T cells function as an **interface between innate and adaptive immunity**, and between **humoral and cellular arms**. --- *Without CD4⁺ T cell help, both antibody production and cytotoxic T cell responses are impaired.*

Answer 22

Formed after **clonal selection** during a primary immune response, **memory T cells** are long-lived lymphocytes that persist in the body to provide rapid, robust protection upon re-exposure to a previously encountered antigen. --- **Key Features:** - Derived from activated **CD4⁺ or CD8⁺ T cells** after infection or vaccination - **Longer lifespan** and **greater numbers** than naïve T cells - Reside in lymphoid tissues, circulation, and peripheral tissues --- **T Cell Recall Response:** - Upon **re-exposure** to the same antigen: 1. Memory T cells rapidly proliferate and differentiate into effector cells 2. Mount a **faster and stronger** immune response 3. Often eliminate pathogen **before symptoms occur** This accelerated response forms the basis for long-term cellular immunity.

Answer 23

Mediated by **B lymphocytes** and **antibodies**, humoral immunity targets **extracellular pathogens** and toxins in body fluids. --- **Recognition Phase** 1. **Stationary B cells** use surface receptors to **bind antigen** directly 2. B cell **endocytoses**, processes, and presents antigen fragment on **MHC-II** 3. A **helper T cell (CD4⁺)** binds to the MHC-II–antigen complex 4. Helper T cell secretes **interleukins** (e.g., IL-4, IL-5) to provide **costimulation** --- **Clonal Expansion and Differentiation** - Stimulated B cell proliferates and differentiates into: - **Plasma cells** → secrete large amounts of **specific antibodies** (high RER activity) - **Memory B cells** → persist for long-term immunity --- **Attack Phase** - **Antibodies** bind to antigen → neutralize pathogen or mark for destruction (opsonization, complement activation, etc.) --- **Memory** - **Memory B cells** respond rapidly upon re-exposure, ensuring quicker and stronger antibody production

Answer 24

1. **Neutralization** - Antibodies (especially **IgG**, **IgA**) bind to and mask pathogenic regions (epitopes) of antigens → prevent pathogen attachment to host cells 2. **Complement fixation** - **IgM** and **IgG** bind antigens → undergo conformational change → initiate classical complement pathway - Leads to opsonization, inflammation, cytolysis 3. **Agglutination** - **IgM** (pentamer) and **IgA** (dimer) have multiple antigen-binding sites - Bind multiple enemy cells → clump them together → immobilization 4. **Precipitation** - Antibodies (often **IgG**) bind soluble antigens → form insoluble antigen-antibody complexes - Complexes precipitate → **phagocytized by eosinophils** or macrophages 5. **Opsonization** - **IgG** and **C3b** (from complement) coat pathogen surface - **Fc receptors** (for IgG) or **complement receptors** (for C3b) on macrophages and neutrophils bind these opsonins → enhances phagocytosis

Lymph / Immune - Lecture Flashcards

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