Phys Lab M11

Innate Immunity Review

Innate immunity is the body's immediate, non-specific defense system. It includes physical barriers, phagocytic cells, natural killer (NK) cells, complement proteins, and the inflammatory response. :contentReference[oaicite:1]{index=1}

Barrier Defenses

The first line of defense includes skin, mucous membranes, sweat, sebaceous glands, saliva (lysozyme), stomach acid, mucus, and normal microbiota, all of which help prevent pathogens from entering or colonizing the body.

Phagocytosis

Phagocytosis is the process by which neutrophils and macrophages engulf and digest pathogens, dead cells, and debris. It is one of the primary defense mechanisms of innate immunity.

Macrophages vs. Neutrophils

Neutrophils are rapid first responders that quickly destroy pathogens, while macrophages arrive later, continue phagocytosis, remove dead tissue, release cytokines, and promote tissue repair.

Natural Killer (NK) Cells

NK cells recognize infected or abnormal cells and induce apoptosis (programmed cell death) without requiring prior exposure to a specific antigen.

Complement System

The complement system is a group of plasma proteins that enhances immune defense by promoting inflammation, coating pathogens for easier phagocytosis (opsonization), and directly lysing pathogens through the membrane attack complex (MAC).

Opsonization vs. Membrane Attack Complex (MAC)

Opsonization coats pathogens to make them easier for phagocytes to recognize and ingest, while the membrane attack complex (MAC) forms pores in microbial membranes, causing cell lysis.

Purpose of Inflammation

The inflammatory response eliminates pathogens, removes damaged tissue, and initiates healing. Its four classic signs are redness (rubor), heat (calor), swelling (tumor), and pain (dolor).

Complete Inflammatory Response Sequence

Injury or infection → macrophages and mast cells release cytokines and histamine → vasodilation and increased vascular permeability → neutrophils arrive first, followed by macrophages and lymphocytes → pathogens are destroyed through phagocytosis and antimicrobial substances → tissue repair begins → anti-inflammatory signals resolve inflammation.

Inflammatory Response Steps

1. Initiation → 2. Vascular phase → 3. Cellular phase → 4. Defense mechanisms → 5. Tissue repair → 6. Resolution.

Vascular Phase

Cytokines and histamine cause vasodilation and increased capillary permeability, allowing immune cells and plasma proteins to leave the bloodstream. This produces redness, heat, swelling, and pain.

Cellular Phase

Neutrophils arrive first to destroy pathogens and clear debris. Macrophages follow to continue phagocytosis, release cytokines, and recruit additional immune cells. Lymphocytes may later participate in a targeted adaptive response.

Tissue Repair & Resolution

Macrophages remove dead tissue and stimulate growth factors, fibroblasts produce collagen to rebuild damaged tissue, and anti-inflammatory cytokines suppress the immune response once healing is underway.Adaptive Immunity Review

Antigen Presentation

Dendritic cells and macrophages act as antigen-presenting cells (APCs). They engulf pathogens, digest them into antigenic peptides, attach those peptides to MHC proteins, and present them to T cells in the lymph nodes to initiate the adaptive immune response.

Helper T Cells (CD4⁺) vs. Cytotoxic T Cells (CD8⁺)

Helper T cells recognize antigens presented on MHC Class II molecules and coordinate the immune response by releasing cytokines. Cytotoxic T cells recognize antigens presented on MHC Class I molecules and directly kill infected cells by releasing perforins and granzymes.

MHC Class I vs. MHC Class II

MHC Class I presents intracellular antigens to CD8⁺ cytotoxic T cells and is found on nearly all nucleated cells. MHC Class II presents extracellular antigens to CD4⁺ helper T cells and is found primarily on professional antigen-presenting cells such as dendritic cells, macrophages, and B cells.

Five Steps of T Cell Activation

1. Antigen presentation by APCs → 2. T-cell receptor recognizes the antigen-MHC complex → 3. Costimulatory signals fully activate the T cell → 4. Clonal expansion and differentiation into effector and memory T cells → 5. Effector T cells carry out immune functions. :contentReference[oaicite:2]{index=2}

Recognition by T Cell Receptors (TCRs)

The T-cell receptor binds only to a specific antigen displayed on the appropriate MHC molecule. This antigen-MHC interaction provides the first signal required for T-cell activation.

Costimulation

Antigen recognition alone is not enough to activate a T cell. APCs must also provide costimulatory molecules, ensuring T cells respond only to legitimate threats.

Clonal Expansion & Differentiation

Once activated, T cells rapidly divide to produce many identical cells. Some become effector T cells that fight infection immediately, while others become memory T cells that provide faster protection during future exposures.

Effector vs. Memory T Cells

Effector T cells actively eliminate pathogens during the current infection, whereas memory T cells persist long-term and generate a faster, stronger immune response if the same antigen is encountered again.

Cell-Mediated Immunity

Cell-mediated immunity primarily involves T lymphocytes. Helper T cells coordinate immune responses through cytokines, while cytotoxic T cells directly destroy infected or abnormal body cells.

Putting Adaptive Immunity Together

Pathogen enters → APC engulfs and processes pathogen → antigen is displayed on MHC molecules → helper or cytotoxic T cells recognize the antigen → costimulation activates the T cell → clonal expansion occurs → effector cells eliminate infection while memory cells remain for future protection.