Chapter 7 – Immunity: Key Vocabulary

Immune System – General Overview

• Responsible for body defenses against all forms of injury or invasion.
• Nonspecific (innate) defenses – always present, respond immediately. -The skin is the most important part (the largest anatomical barrier)
• Examples: phagocytosis, inflammation.
• Specific (adaptive) defenses – require prior exposure and recognition.
• Involve production of antibodies or sensitized lymphocytes directed at unique antigens.

Major Structural Components - the skin is the most important part

• Lymphoid organs & tissues
• Lymph nodes – cervical, axillary, intestinal, inguinal (filter lymph, house lymphocytes).
• Spleen – blood filtration, immune surveillance.
• Tonsils – palatine & pharyngeal (adenoids) – protect upper respiratory tract.
• Intestinal lymphoid tissue – e.g., Peyer patches safeguard GI tract.
• Thymus – maturation of T-lymphocytes; largest in childhood.
• Bone marrow – origin of all immune cells, site of B-cell maturation.
• Lymphatic circulation – transports immune cells & antigens.

• Immune cells
• Lymphocytes – T & B populations plus natural killer (NK) cells. (thesse kill the germs)
• Macrophages – tissue phagocytes derived from monocytes; initiate responses. (largest cell) eats the pathogen or germ

• phagocytes- look for the cause of the infection and then die

• Chemical mediators
• Histamine, interleukins, monokines, cytokines – regulate or amplify immunity/inflammation.

Antigens (Immunogens) can make antibodies responsible for killing the germs

• Self-antigens (chickenpox for example once had cant catch it again
• Human leukocyte antigen (HLA) proteins label each person’s cells.
• Recognized as “self” ⇒ normally ignored (self-tolerance).
• Non-self antigens
• Usually exogenous cell-surface molecules (proteins, polysaccharides, glycoproteins).
• Recognition ⇒ specific, targeted response.
• Memory cells ensure faster secondary responses.

Key Immune Cells – Functions & Interactions

• Macrophages
• Part of mononuclear phagocyte system; present in virtually all tissues.
• Phagocytose foreign material → display processed antigen with MHC-II.
• Secrete cytokines (e.g., monokines, interleukins) that activate T cells.

• T-Lymphocytes (cell-mediated immunity)
• Originate in bone marrow → mature in thymus.
• Types:
• Cytotoxic (CD8) killer T cells – destroy virus-infected/cancer cells.
• Helper T (CD4) cells – coordinate both B & T responses.
• Memory T cells – ensure rapid recall.
• Suppressor (regulatory) T cells – dampen excess responses.

• B-Lymphocytes (humoral immunity)
• Mature in bone marrow → migrate to spleen/lymph nodes.
• Upon antigen + helper T stimulation:
• Differentiate into plasma cells → secrete antibodies (immunoglobulins).
• Produce B memory cells for recall.

Developmental Pathways

• Cell-mediated pathway

1. Lymphoblasts (bone-marrow stem cells) → thymus maturation.

2. Sensitized T cells circulate: helper, cytotoxic, suppressor, memory subtypes.
   • Humoral (antibody-mediated) pathway

3. B cells remain in marrow for maturation.

4. On antigen + macrophage presentation + helper T cytokines → clonal expansion → plasma & memory B cells.

5. Antibodies secreted into blood/lymph.

Immunoglobulins – Classes & Roles

• IgG – most abundant in serum; crosses placenta; secondary responses.
• IgM – pentamer; first antibody produced in primary response.
• IgA – secretory; in tears, saliva, mucous membranes, colostrum.
• IgE – bound to mast cells/basophils; triggers histamine release → allergy & inflammation.
• IgD – membrane-bound on B cells; initiates B activation.

Complement System

• C1 \rightarrow C9 – inactive plasma proteins.
• Activated by antigen–antibody complexes containing IgG or IgM.
• Cascade leads to membrane attack complex, cell lysis, and amplified inflammation.

Chemical Mediators

• Histamine – vasodilation, capillary permeability.
• Cytokines/Interleukins – cell signaling, fever induction, leukocyte chemotaxis.
• Excess mediator release → edema, tissue damage.

Diagnostic & Laboratory Tests

• Titer (\text{titre} ) – quantitative serum immunoglobulin levels. - blood work to tell if you hsve been exposed
• Indirect Coombs test – detects Rh incompatibility.
• ELISA – screens for HIV antibodies, many other pathogens.
• MHC/HLA typing – tissue matching prior to transplantation.

Immune Memory & Responses

• Primary response – first encounter; 1–2 weeks before antibody reaches effective level.
• Secondary response – subsequent exposure; antibody rises within 1–3 days, higher & longer.

Categories of Immunity

• Innate (natural, nonspecific)
• Species specific; gene related (e.g., certain ethnic resistances).

• Active immunity – host actively produces antibodies -can be natural or artifiial naturlal is catching the disease and recovering, artifical is vaccines
• Natural: infection leads to lifelong/long-term protection.
• Artificial: vaccination (live, attenuated, toxoid); boosters maintain titer.

• Passive immunity – ready-made antibodies transferred - Natural or passive (from breast milk if passive) (artifical would be rabies)
• Natural: maternal IgG via placenta & breast milk – protection first few months.
• Artificial: antiserum/immune globulin injections – rapid, short-term (e.g., rabies, tetanus).

Public-Health Considerations

• Herd immunity – high vaccination rates ↓ disease incidence.
• Declines in revaccination → measles, mumps outbreaks.
• Ongoing vaccine research: AIDS, malaria, tuberculosis; genetic/mRNA vaccines.
• Emerging diseases – newly identified; re-emerging – once-controlled but resurfacing (globalization, drug resistance).
• Bioterrorism threat – altered pathogens, limited vaccines, wide impact.

Transplantation & Rejection - A patient getting a transplant will always be on immunosuppresents

• Hyperacute – minutes to hours; pre-formed antibodies attack graft.
• Acute – weeks; activation of T cells vs. foreign MHC.
• Chronic – months/years; vascular damage & fibrosis.
• Management – immunosuppression (cyclosporine, azathioprine, prednisone) but ↑ opportunistic infection risk & nephrotoxicity.

Hypersensitivity Reactions

1. Type I (Immediate/Allergic)
   • Mechanism: allergen → IgE production → mast-cell sensitization → re-exposure → mediator release (histamine).
   • Manifestations: hay fever (rhinitis), food allergy (GI mucosa), atopic dermatitis, asthma.
   • Severe form: anaphylaxis.

2. Type II (Cytotoxic)
   • Antigen on cell membrane (intrinsic or extrinsic) + IgG → complement → cell lysis/phagocytosis.
   • Example: incompatible ABO transfusion.

3. Type III (Immune-Complex)
   • Soluble antigen–antibody complexes deposit in tissues/vessels → complement → inflammation & necrosis.
   • Examples: post-streptococcal glomerulonephritis, rheumatoid arthritis.

4. Type IV (Delayed/Cell-Mediated)
   • Sensitized T lymphocytes release lymphokines → macrophage activation → tissue destruction.
   • Examples: tuberculin (PPD) test, contact dermatitis (poison ivy), transplant rejection.

Anaphylaxis – Detailed Pathophysiology & Care

• Systemic, life-threatening Type I reaction.
• Pathology: widespread histamine → vasodilation (↓BP), bronchoconstriction, mucous secretion, edema.
• Triggers: latex, insect stings, nuts, shellfish, drugs.
• S/S: pruritus, tingling mouth, coughing, dyspnea, edema (eyes, lips, tongue), urticaria, hypotension, collapse.
• First aid: EpiPen, call 911.
• ER treatment: epinephrine, antihistamines, glucocorticoids, oxygen, fluids/pressors to stabilize BP.

Autoimmune Disorders - the body attacks itself (Lupus)

• Loss of self-tolerance → autoantibodies against own cells.
• May be organ-specific or systemic.
• Examples: Hashimoto thyroiditis, SLE, rheumatic fever, myasthenia gravis, scleroderma, pernicious anemia.

Systemic Lupus Erythematosus (SLE)

• Chronic multisystem inflammatory disease, primarily in young women (higher in African-American, Asian, Hispanic, Native American groups).
• Autoantibodies vs. DNA, platelets, RBCs → immumalarmplexes deposit in tissues → vasculitis, ischemia. This is how to determine if you have an autoimmue disease
• Classic sign: butterfly malar rash.
• Common manifestations (Table 7-7):
• Joints – polyarthritis/arthralgia.
• Skin – photosensitive rash, oral ulcers, alopecia.
• Kidneys – glomerulonephritis with marked proteinuria.
• Lungs – pleurisy, chest pain.
• Heart – pericarditis.
• Vessels – Raynaud phenomenon.
• CNS – depression, seizures.
• Hematologic – anemia, leukopenia, thrombocytopenia.
• Diagnosis: serum autoantibodies (ANA), LE cells, inflammatory markers.
• Treatment: rheumatology management; prednisone, NSAIDs, immunosuppressants as needed.

Immunodeficiency Syndromes

• Primary – congenital (e.g., DiGeorge, SCID) – developmental failure of components.
• Secondary (acquired) – due to infection, splenectomy, malnutrition, liver disease, immunosuppressive therapy, radiation, chemotherapy.
• Consequences: recurrent opportunistic infections, cancers; prophylactic antimicrobials often required.

Human Immunodeficiency Virus & AIDS

• HIV – retrovirus, subfamily lentivirus.
• HIV-1 – predominant in US/Europe.
• HIV-2 – predominant in central Africa.
• Transmission fluids: blood, semen, vaginal secretions

Antivirals are like a teenager with no cellphone they cant say to replicate