NSG6101 Week 2 Focus Points Immunity Flashcards

Comprehensive 100-card question-and-answer review of Chapter 2 Immunity concepts for NSG6101 focus points.

What are the two primary actions through which the immune system defends the body?

Defending against microbes/toxins and attacking damaged or cancerous cells to remove them.

How does innate immunity differ from adaptive immunity regarding onset, specificity, and memory?

Innate immunity is immediate, nonspecific, and has no memory; adaptive immunity takes $7\text{--}10\,\text{days}$, is antigen-specific, and creates memory.

How is an antigen defined in the Chapter 2 lecture notes?

Any substance the body recognizes as foreign, including microorganisms, drugs, transplanted tissue, and environmental substances.

What is an antibody (immunoglobulin)?

A protein used by the immune system to identify and neutralize foreign agents.

What is an autoantibody?

An antibody that mistakenly attacks the person's own proteins.

Where is the thymus located, and what is its dual role in immunity?

It is located in the anterior superior mediastinum; it is the site where T cells mature and where thymosins are produced.

What functions are served by lymphatic tissue?

It transports immune cells, antigen-presenting cells (APCs), and fatty acids/fats, and filters body fluids.

What is the birthplace of all blood cells, and where do B cells mature?

The bone marrow.

Which cell type acts as the first responder to infection and phagocytizes microorganisms?

Neutrophils.

What are band cells (baby bands)?

Immature neutrophils released early from the bone marrow during an active infection.

What does a 'shift to the left' on a complete blood count (CBC) indicate?

An increase in immature bands/neutrophils, which signals an acute bacterial infection.

Which cell type binds IgE and releases histamine in inflammatory reactions?

Basophils.

Which immune cells are primarily involved in allergic reactions and fighting parasites?

Eosinophils.

What is the pathway and function of circulating monocytes?

They circulate in the blood, replenish macrophages/dendritic cells, and migrate to inflamed tissue where they convert into macrophages or dendritic cells.

What are macrophages and what function do they perform as APCs?

They are tissue-based phagocytes differentiated from monocytes that engulf pathogens and stimulate other immune cells.

Where are mast cells located, and what substances do they release during inflammation?

Located in the skin, GI tract, and respiratory tract; they release histamine, heparin, hyaluronic acid, slow-reacting substance of anaphylaxis, and serotonin.

Which immune cells mature in the bone marrow and drive humoral immunity?

B cells (B lymphocytes).

What are the roles of memory B cells and plasma cells?

Memory B cells remember specific antigens to trigger rapid re-exposure responses; plasma cells develop from B cells to produce large volumes of specific antibodies.

Where do T lymphocytes mature, and what type of immunity do they drive?

T cells mature in the thymus and drive cellular immunity.

Which CD surface marker identifies killer (cytotoxic) T cells, and how do they destroy targets?

Marked by CD8+; they destroy virus-infected cells by releasing lymphokines that degrade cell walls.

Which CD marker identifies helper T cells, and what role do they play in HIV infection?

Marked by CD4+; helper T cells activate B cells to produce antibodies and serve as the receptor targeted and attacked by HIV.

What are the specific functional roles of Th1 vs Th2 helper T cells?

Th2 activates B cells to make antibodies; Th1 drives inflammation and macrophage activation.

How do Natural Killer (NK) lymphocytes differ from T lymphocytes?

NK cells are part of innate immunity and destroy cancer cells, foreign cells, and virus-infected cells without needing prior sensitization or antigen memory.

What is considered the number-one (first-line) physical barrier of innate immunity?

The skin (dermis).

How does keratin in the outer skin layer contribute to physical immunity?

Dead outer keratin cells create a waterproof layer while shedding bacteria.

Which body passageways are lined by mucous membranes?

The respiratory, GI, and genitourinary (GU) tracts.

What mechanical innate defenses help expel toxins and microbes from passageways?

Mucociliary clearance, coughing, and vomiting.

What chemical enzyme is present in tears and saliva to break down bacterial walls?

Lysozyme.

Which antimicrobial peptides present in chemical barriers also stimulate adaptive immunity?

Cathelicidins and defensins.

How does normal flora (the microbiome) protect against pathogenic microorganisms?

Resident bacteria and fungi compete with incoming pathogens for space and nutrients.

What triggers the inflammatory response, and what are its key defining characteristics?

Triggered by any cell or tissue injury (microbes, chemicals, hypoxia, trauma); it is nondiscriminatory and has no memory.

What are the sequential steps of the vascular response during inflammation?

Arterioles briefly constrict to limit bleeding, then vasodilate to increase blood flow and deliver neutrophils, nutrients, and oxygen.

What causes edema during an inflammatory reaction?

Increased capillary permeability allowing fluid and phagocytes to leak into interstitial tissue.

What are the four cardinal signs of acute inflammation?

Erythema (redness), edema (swelling), heat, and pain.

Define margination, transmigration (diapedesis), and phagocytosis.

Margination is leukocytes lining up along vessel walls; transmigration/diapedesis is leukocytes squeezing into interstitial tissue; phagocytosis is engulfing/digesting debris and pathogens.

Which cell type is the primary trigger of the inflammatory cascade?

Mast cells.

What effects are produced when histamine binds to H1 and H2 receptors?

H1 receptor binding causes vasodilation, increased vascular permeability, and bronchial/smooth muscle contraction; H2 receptor binding increases gastric secretion.

What is the function of heparin as a preformed mast cell mediator?

It acts as an anticoagulant and promotes angiogenesis (new vessel growth).

Which preformed mediator affects the kinin pathway to produce bradykinin?

Chondroitin sulfate.

What effects are produced by the release of tryptase from mast cells?

Inactivates fibrinogen, recruits eosinophils, and increases IL-8 (neutrophil chemotactic factor).

List three newly synthesized inflammatory mediators.

Leukotrienes, platelet-activating factor, and prostaglandins.

Which newly synthesized mediator is tied directly to pain and complement activation?

Prostaglandins.

How do Nonsteroidal Anti-inflammatory Drugs (NSAIDs) relieve pain and inflammation?

By blocking prostaglandin synthesis.

What are interferons, and how do they defend against viral infections?

Proteins released by virus-infected cells that warn neighboring healthy cells, interfere with viral replication, and signal NK cells and macrophages.

How many plasma proteins make up the complement system cascade?

Approximately $30$ plasma proteins ($C1\text{--}C9$).

What are the three primary actions of the activated complement system?

Opsonization (flagging pathogens), chemotaxis (attracting phagocytes), and forming the Membrane Attack Complex (MAC) to lyse pathogen membranes.

How does the complement system bridge innate and adaptive immunity?

It can be triggered directly by pathogens (innate link) or by antigen-antibody complexes (adaptive link).

How do the acute and chronic phases of inflammation differ in duration and function?

Acute begins immediately, lasts hours to days to clear threats; chronic lasts weeks to months, handling persistent threats, with healing/repair occurring here.

What is a granuloma and which conditions trigger its formation?

A collection of macrophages and lymphocytes walling off persistent pathogens that cannot be cleared; seen in tuberculosis, syphilis, leprosy, and brucellosis.

How does a granuloma differ from granulation tissue?

A granuloma walls off chronic infections, whereas granulation tissue (new blood vessels, fibroblasts, collagen) is part of normal wound repair.

Which human chromosome contains the genes for the Major Histocompatibility Complex (MHC/HLA)?

Chromosome 6.

Which cell types are presented antigens by Class I MHC versus Class II MHC?

Class I MHC presents to CD8+ cytotoxic T cells; Class II MHC presents to CD4+ helper T cells.

What is the primary function of suppressor T cells?

To turn off or down-regulate antibody production once an infection or threat is cleared.

What specific targets does cellular immunity protect against?

Viruses, fungi, parasites, intracellular bacteria, and cancer cells; it also drives hypersensitivity reactions and transplant rejection.

How quickly can antibody production begin after initial exposure in humoral immunity?

Within $72\,\text{hours}$ of first exposure.

Which immunoglobulin is the main defense against bacteria and crosses the placenta?

IgG.

Which immunoglobulin serves as a marker of long-term immunity that stays positive for life?

IgG.

Which immunoglobulin is the first produced in response to a new antigen and signals acute infection?

IgM.

Which is the first antibody synthesized independently by a fetus?

IgM.

Where is IgA located, and what protection does it provide?

Found in mucosal secretions (respiratory/GI tracts, tears, saliva, mucus, colostrum) to provide local surface immunity.

Which immunoglobulin binds mast cells and basophils, driving Type I hypersensitivity?

IgE.

What is the location and function of IgD?

Present in small amounts in serum; sits on B-cell surfaces as an antigen receptor to help anchor the cell membrane.

What mnemonic memory trick differentiates IgM from IgG?

IgM means the immune system is making 'Memory' (acute infection); IgG means the infection is 'Gone' (long-term immunity).

What mechanism defines natural active immunity, and does it produce memory?

Natural exposure to a live antigen causing illness and self-produced antibodies; YES, it produces memory.

Give an example of artificial active immunity.

Administering a vaccine (polio, measles) so the body makes its own antibodies without serious illness.

What mechanism defines natural passive immunity, and what is its duration?

Direct transfer of maternal antibodies across the placenta or via breastmilk; provides short-term protection (lasting up to $\sim 1\,\text{year}$) with NO memory.

Give examples of artificial passive immunity.

Injecting preformed antibodies or immunoglobulins (e.g., gamma globulin for ITP, rabies immunoglobulin, hepatitis A/B immunoglobulin).

Why does passive immunity fail to create long-term memory?

Because the individual's immune system did not produce the antibodies itself.

Why are live, attenuated vaccines contraindicated in immunocompromised patients?

Because the weakened live pathogen can replicate and cause active disease in an immunocompromised individual.

List four examples of live, attenuated vaccines.

MMR (measles, mumps, rubella), varicella, BCG (TB), and oral typhoid.

Why do inactivated (killed) vaccines often require multiple doses or boosters?

Because they cannot replicate, mainly stimulate a humoral response, and produce a less robust cellular response.

Why are pure polysaccharide subunit vaccines ineffective in children under $2\,\text{years}$ of age?

Because children under $2\,\text{years}$ have an immature immune system that cannot mount an effective response to un-conjugated polysaccharides.

How does a conjugate subunit vaccine improve immunogenicity compared to a polysaccharide vaccine?

It combines the bacterial capsule polysaccharide with a protein carrier.

Which vaccine category is produced via genetic engineering?

Recombinant vaccines (e.g., hepatitis B, HPV, some influenza vaccines).

How is hypersensitivity defined?

An inflated or inappropriate immune response to an antigen that causes inflammation and destruction of healthy tissue.

What key cells, antibodies, and mediators drive Type I hypersensitivity?

Mediated by IgE antibodies, mast cells, and basophils releasing histamine, serotonin, leukotrienes, and prostaglandins.

What is the onset timing and clinical examples of Type I hypersensitivity?

Immediate ($\le 30\,\text{min}$) or delayed (hours); examples include allergic rhinitis, asthma, and systemic anaphylaxis.

What cells, antibodies, and mediators drive Type II cytotoxic hypersensitivity?

IgG or IgM antibodies binding to antigens on RBCs or WBCs, activating complement; onset is $5\text{--}8\,\text{hours}$.

List two classic clinical examples of Type II hypersensitivity reactions.

Blood transfusion reactions and hemolytic disease of the newborn.

What mechanism causes Type III immune complex hypersensitivity?

IgG antibodies form circulating antigen-antibody complexes that deposit in host tissues, activating complement in $2\text{--}8\,\text{hours}$.

List four classic disease examples of Type III hypersensitivity.

Serum sickness, Arthus reaction, Systemic Lupus Erythematosus (SLE), and rheumatoid arthritis.

How does Type IV hypersensitivity differ fundamentally from Types I, II, and III?

Type IV is cell-mediated by T lymphocytes and cytokines, and is NOT antibody-mediated.

What is the onset time and list four clinical examples of Type IV hypersensitivity.

Delayed onset ($1\text{--}3\,\text{days}$); examples include contact dermatitis (poison ivy), TB skin test (PPD), transplant rejection, and Crohn disease.

What distinguishes immunologic anaphylaxis from non-immunologic (anaphylactoid) reactions?

Immunologic anaphylaxis involves IgE, IgG, or immune complexes; non-immunologic reactions occur without antibodies (e.g., vancomycin red man syndrome, cold urticaria).

What four pharmacological strategy concepts are used to treat Type I hypersensitivity?

Epinephrine, antihistamines, corticosteroids, and desensitization injections.

What is alloimmunity?

An immune response directed against tissue transferred from another person of the same species.

Define the four transplant types: allogeneic, syngeneic, autologous, and xenogeneic.

Allogeneic = same species (genetically non-identical); Syngeneic = identical twin; Autologous = self-donor; Xenogeneic = different species.

What are the three categories of transplant rejection timing, and what drives hyperacute rejection?

Hyperacute (minutes-hours), acute (days-weeks), chronic (months-years); hyperacute is driven by preformed antibodies.

What is autoimmunity?

A state where the immune system fails to recognize 'self' and produces autoantibodies against its own tissues.

Which hypersensitivity mechanism primarily drives Systemic Lupus Erythematosus (SLE)?

Type III immune-complex mediated hypersensitivity.

Which organ systems are most commonly injured by immune complex deposition in SLE?

Kidneys, joints, skin, and blood vessels.

What are the primary clinical features of Systemic Lupus Erythematosus (SLE)?

Malar ('butterfly') rash, joint pain/stiffness/swelling, fatigue, weight loss, photosensitivity, low-grade fever, oral ulcers, and lupus nephritis.

Which screening test is the hallmark for SLE, and which autoantibodies are most specific?

ANA (antinuclear antibody) is the primary screening test; anti-dsDNA and anti-Smith are most specific for SLE.

What happens to serum complement levels (C3/C4) during active SLE disease?

Complement levels (C3/C4) decrease because they are consumed by circulating immune complexes.

What is the hallmark clinical clue for any immunodeficiency state?

Frequent, recurrent, or severe infections.

How do primary and secondary immunodeficiencies differ?

Primary immunodeficiency is genetic/congenital (present from birth); secondary is acquired later due to an external cause (e.g., HIV, chemotherapy, steroids).

Which specific immune cell type is destroyed by HIV?

CD4+ helper T cells.

What are the 7 steps of the HIV life cycle in exact order?

1. Binding/Attachment, 2. Fusion, 3. Reverse transcription, 4. Integration, 5. Replication, 6. Assembly, 7. Budding.

What diagnostic thresholds establish a diagnosis of AIDS in an HIV-positive patient?

A CD4+ count $< 200\,\text{cells/mm}^3$ OR the presence of an AIDS-defining opportunistic infection.

What is the recommended first-line screening test for HIV, and how is a positive result confirmed?

Initial screening uses a 4th-generation Ag/Ab combination immunoassay; confirmation requires an HIV-1/HIV-2 antibody differentiation immunoassay.