Immunology & Pathophysiology

Innate vs. Adaptive Immunity

Innate is non-specific and rapid; adaptive is specific, acquired, and develops memory.

Humoral vs. Cellular Immunity

Humoral relies on B cells and antibodies; cellular relies on T cells (CD4 and CD8).

Active vs. Passive Immunity

Active is created by the host's immune response; passive is transferred from another source.

Neutrophils

Granulocytes that destroy bacteria and fungi via phagocytosis and release cytokines.

Eosinophils

Granulocytes that destroy parasites and large pathogens via cytotoxic proteins.

Dendritic Cells

Antigen-presenting cells (APCs) that link innate and adaptive immunity by activating T cells.

Complement System

Proteins that opsonize pathogens, perforate cell membranes, and summon phagocytes.

Coagulation System

Clotting proteins that wall off injury, stop bleeding, and trap antigens.

Kinin System

Bradykinin enhances vasodilation, vascular permeability, and stimulates pain receptors.

Antibody Functions

Bind/inactivate toxins, block pathogen receptors, cause agglutination, and act as opsonins.

IgG

Most abundant antibody; tags antigens, triggers complement, and crosses the placenta.

IgA

Resides in mucosal tissues, saliva, tears, and breast milk to tag antigens.

IgM

First antibody on the scene during acute infection; agglutinates pathogens.

IgE

Involved in allergic reactions and parasitic defense by triggering histamine release.

Inflammatory Mediators

Histamine, prostaglandins, leukotrienes, and bradykinin cause vasodilation and increased permeability.

Cardinal Signs of Inflammation

Redness, heat, swelling, pain, and loss of function.

Type I Hypersensitivity

IgE-mediated allergic response causing mast cell and basophil degranulation.

Type II Hypersensitivity

Antibody-mediated (IgG/IgM) direct attack on cellular or tissue antigens.

Type III Hypersensitivity

Immune complex-mediated reaction where antigen-antibody complexes lodge in tissues.

Type IV Hypersensitivity

T-cell mediated, delayed reaction causing tissue destruction (e.g., contact dermatitis).

Hypersensitivity Examples

Type I: Allergies; Type II: Blood transfusion reactions; Type III: Lupus; Type IV: Poison ivy.

Anaphylactic Shock Treatment

Epinephrine is the first-line medication treatment.

HIV Target Cells

Selectively attacks CD4 T lymphocytes, leading to immune vulnerability.

What is the difference between primary and secondary lymphoid organs?

Primary lymphoid organs (bone marrow and thymus) are where lymphocytes form and mature, while secondary lymphoid organs (lymph nodes and spleen) are where mature lymphocytes encounter pathogens.

What are Natural Killer (NK) cells and how do they function?

Innate lymphoid cells that destroy virus-infected cells and tumor cells by inducing apoptosis without prior sensitization.

What is the primary function of IgD antibodies in the immune system?

They act primarily as antigen receptors on the surface of naive B lymphocytes to help initiate B cell activation.

What distinguishes central tolerance from peripheral tolerance?

Central tolerance eliminates self-reactive lymphocytes during maturation in primary organs, while peripheral tolerance neutralizes or suppresses self-reactive cells in peripheral tissues.

How do the primary and secondary antibody responses differ following antigen exposure?

The primary response is slow with a low IgM and later IgG peak, whereas the secondary response is rapid and massive, dominated by high-affinity IgG due to memory cells.

Innate Immunity

Fast, non-specific immediate response to pathogens utilizing physical, physiological, and chemical barriers, cells (like phagocytes), and protein systems.

Adaptive Immunity

Highly specialized, slower-developing specific immune response utilizing T and B lymphocytes to recognize, attack, and remember specific antigens.

Active Immunity

Immunity developed when the host's own immune system is challenged by an antigen and creates a memory response (e.g., natural infection or vaccination).

Passive Immunity

Temporary immunity transferred from an outside source containing pre-formed antibodies (e.g., mother to fetus across placenta, or Rabies Immune Globulin).

Humoral Immunity

Adaptive immune response mediated by B lymphocytes, plasma cells, and antibodies circulating in body fluids to combat extracellular pathogens.

Cellular Immunity

Adaptive immune response mediated by T lymphocytes (CD4 and CD8 cells) attacking intracellular pathogens, foreign tissues, or cancer cells.

Neutrophils

The most abundant granulocytes that destroy antigens (especially bacteria and fungi) via phagocytosis and release cytokines, redox enzymes, and proteases.

Basophils

Granulocytes representing

Eosinophils

Granulocytes that destroy parasites and large pathogens too big for phagocytosis; they release cytotoxic proteins or trigger basophils to release histamine.

Monocytes

Precursors to macrophages and dendritic cells that circulate in blood, migrate to tissues, engulf antigens, and release cytokines.

Macrophages

Large phagocytes that remove antigens and apoptotic cells, release inflammatory cytokines, and can act as antigen-presenting cells (APCs).

Dendritic Cells

White blood cells known as the primary Antigen-Presenting Cells (APCs) that link innate and adaptive immunity by capturing and presenting antigens to T cells.

Mast Cells

Granulocytes residing in environmental barrier tissues, often coated in IgE; allergen cross-linking triggers rapid degranulation and release of histamine.

Complement System Functions

A protein cascade that opsonizes pathogens (marking them for destruction), kills pathogens by perforation (MAC), summons phagocytes, and agglutinates pathogens.

Coagulation (Clotting) System Functions

A protein system that walls off injured areas, stops bleeding, traps antigens, and provides a physical framework for future wound healing.

Kinin System (Bradykinin)

An inflammatory mediator system that causes vasodilation, smooth muscle contraction, and vascular permeability; works with prostaglandins to stimulate pain.

Cardinal Signs of Inflammation

Calor (heat), Rubor (redness), Tumor (swelling), Dolor (pain/tenderness), and Loss of Function.

Calor (Heat) Physiological Cause

Capillary dilation resulting from increased local blood flow, driven by the release of histamine and bradykinin.

Rubor (Redness) Physiological Cause

Capillary dilation and increased blood flow to the injured site, initiated by vasoactive mediators like histamine.

Tumor (Swelling) Physiological Cause

Increased capillary permeability allowing protein-rich plasma to escape the bloodstream and accumulate in the surrounding tissue.

Dolor (Pain) Physiological Cause

Direct tissue destruction and irritation of nerve endings by inflammatory mediators like histamine, bradykinin, and prostaglandins.

Systemic Inflammatory Response (Acute Phase)

Widespread cytokine release (IL-1 to brain causing fever, IL-6 to liver producing CRP as an opsonin, and IL-8 recruiting neutrophils).

Anaphylactic Shock Pathophysiology

Systemic IgE-mediated histamine release causing widespread vasodilation (severe hypotension) and capillary leakage (fluid shift), leading to airway obstruction.

Epinephrine in Anaphylactic Shock

The first-line drug of choice because it reverses systemic vasodilation (raises blood pressure) and counteracts bronchoconstriction (opens airways).

Type I Hypersensitivity

IgE-mediated classic allergic response; allergen cross-links IgE on mast cells and basophils, triggering degranulation of histamine (e.g., anaphylaxis, hay fever).

Type II Hypersensitivity

Antibody-mediated/cytotoxic; IgG or IgM bind directly to cell-bound antigens, causing complement-mediated cell lysis (e.g., ABO transfusion reactions, Graves).

Type III Hypersensitivity

Immune complex-mediated; IgG or IgM form complexes with soluble antigens that circulate and deposit in tissues (like kidneys or joints), activating complement (e.g., SLE).

Type IV Hypersensitivity

T-cell mediated delayed reaction (12-72 hrs); sensitized CD4/CD8 cells recruit phagocytes and directly attack tissue (e.g., contact dermatitis, PPD skin test).

Autoimmunity

A breakdown of self-tolerance (central in bone marrow/thymus, or peripheral maintained by T-regulatory cells), leading the immune system to produce autoantibodies.

HIV Target and Mechanism

gp120/gp41 glycoproteins bind CD4 receptors on T-helper lymphocytes, macrophages, and dendritic cells; incorporates RNA into host DNA to replicate and destroy cells.

Untreated HIV Clinical Course

Early flu-like illness (antibody development) followed by a long latency period (8-10 years) of slow CD4 depletion, culminating in AIDS and opportunistic infections.

Newborn HIV Antibody False Positive

Maternal IgG is the only antibody that crosses the placenta. An uninfected newborn carrying maternal HIV IgG antibodies will test positive on antibody screenings.

Preventing Maternal-Fetal HIV Transmission

Taking antiretroviral therapy (ART) during pregnancy/delivery, giving birth via Cesarean section if viral load is high, and avoiding breastfeeding