Lymphatic System A&P2

3 functions of the lymphatic system

Fluid balance (returns interstitial fluid to blood), lipid absorption (via lacteals), and defense against disease.

Lymph

Fluid derived from interstitial fluid that lymphatic vessels carry; same composition as plasma minus plasma proteins.

Lymphatic capillaries

Close-ended, thin-walled (simple squamous epithelium) tubes; have flap-like valves allowing easy entry of tissue fluid and proteins.

Lacteals

Lymphatic capillaries in the small intestine that absorb dietary fats and transport them to the bloodstream.

Thoracic duct

Longer, wider lymphatic collecting duct; begins as the cisterna chyli; drains most of the body; empties into the left subclavian vein.

Right lymphatic duct

Smaller duct that drains the upper right portion of the body; empties into the right subclavian vein.

Cisterna chyli

The sac-like beginning of the thoracic duct.

Edema

Accumulation of excess tissue fluid; normally prevented because lymphatic capillaries drain interstitial spaces.

Lymph flow — 3 driving forces

Skeletal muscle contraction, respiratory movements, and smooth muscle in larger lymphatic vessels; semilunar valves prevent backflow.

Lymph node functions

Filter harmful particles from lymph; immune surveillance via macrophages and lymphocytes; center for lymphocyte production.

Locations of lymph nodes

Cervical, axillary, supratrochlear, inguinal regions, pelvic cavity, abdominal cavity, and thoracic cavity.

Thymus function

Houses lymphocytes and differentiates thymocytes into T lymphocytes; located in mediastinum posterior to upper sternum.

Spleen function

Macrophages remove foreign particles, damaged RBCs, and cellular debris from blood; contains lymphocytes; acts as blood reservoir; in upper left abdomen.

MALT

Mucosa-associated lymphoid tissue; unencapsulated lymphoid tissue in digestive, respiratory, urinary, and reproductive tracts; includes tonsils and appendix.

Peyer's patches

Aggregates of lymphatic nodules found in the small intestine; part of MALT.

Innate (nonspecific) defenses

General defenses that protect against many types of pathogens; include mechanical barriers, inflammation, chemical barriers, NK cells, phagocytosis, and fever.

First line of defense

Skin and mucous membranes — mechanical barriers that block pathogen entry.

Second line of defense

All other innate defenses: inflammation, chemical barriers (interferons, defensins, complement), NK cells, phagocytosis, and fever.

Interferons

Chemical barriers that block viral replication, act against tumor growth, and stimulate phagocytosis.

Defensins

Peptides produced by neutrophils and other granulocytes that cripple microbes by making openings in cell membranes or walls.

Collectins

Proteins that protect against many bacteria, yeast, and some viruses.

Complement system

Group of plasma proteins that interact in a cascade; stimulate inflammation, attract phagocytes, and enhance phagocytosis.

Natural killer (NK) cells

Small lymphocyte population that uses activating/inhibitory receptors to detect threats; secretes perforins to lyse virally infected or cancerous cells.

Perforins

Cytolytic substances secreted by NK cells and cytotoxic T cells that lyse the cell membrane of target cells.

Chemotaxis

The process by which chemicals from damaged tissue attract phagocytic cells (neutrophils, monocytes) to the site of injury.

Monocytes vs. macrophages

Monocytes are the most active phagocytic cells in the blood; when they leave the blood they become macrophages in the tissues.

Mononuclear phagocytic system

Consists of monocytes and macrophages throughout the body; removes particles from blood and lymph.

Fever mechanism

Infection → lymphocytes proliferate → secrete interleukin-1 (IL-1, endogenous pyrogen) → raises thermoregulatory set point → inhibits microbial growth, increases phagocytic activity.

Inflammation steps

Vasodilation → increased capillary permeability → WBC invasion → possible pus formation → fibrin clot → fibroblasts form connective tissue sac → phagocytes remove debris → cells divide to replace damaged ones.

Adaptive (specific) defenses

More precise defenses targeting specific antigens; carried out by lymphocytes that recognize specific foreign molecules.

Antigen

Molecule (protein, polysaccharide, glycoprotein, or glycolipid) recognized by lymphocytes as non-self; most effective when large and complex.

Hapten

Small molecule not antigenic alone; becomes antigenic when combined with a large body molecule.

T lymphocytes (T cells)

Specialize in the thymus; make up ~70% of lymphocytes; involved in cellular immune response; become helper, cytotoxic, memory, or regulatory T cells.

B lymphocytes (B cells)

Released from bone marrow; make up 20–30% of blood lymphocytes; make antibodies; involved in humoral immune response.

Helper T cells (CD-4)

Activate other immune cells by secreting cytokines; stimulate B cells to produce antibodies and activate cytotoxic T cells; critical — damage destroys immunity.

Cytotoxic T cells (CD-8)

Attack virally infected or cancerous cells; secrete perforin to lyse target cells.

Memory T cells

Long-lived T cells that provide rapid immune protection upon future exposure to the same antigen.

Regulatory T cells

Suppress immune responses after a pathogen is defeated; lower the chance of developing an autoimmune disease.

MHC Class I antigens

Present on all nucleated cells; display intracellular antigens (viral proteins, tumor antigens); activate cytotoxic T cells to kill the cell.

MHC Class II antigens

On antigen-presenting cells (dendritic cells, macrophages); APC phagocytizes antigen and displays it on surface; activate helper T cells.

Antigen-presenting cell (APC) process

Macrophage phagocytizes bacterium → bacterial antigens displayed on surface with MHC proteins → T cell determines self vs. foreign.

Plasma cells

Differentiated B cells that produce and secrete antibodies; involved in the humoral immune response.

Memory B cells

Long-lived B cells that respond rapidly to subsequent exposures; basis of secondary immune response.

Primary vs. secondary immune response

Primary: antibodies appear 5–10 days after first exposure. Secondary: antibodies appear within 1–2 days due to memory B and T cells.

Polyclonal response

Multiple types of antibodies created against a single microbe or virus; results from different B cell clones responding to different antigens on the pathogen.

Antibody structure

Y-shaped; 4 chains (2 light, 2 heavy) linked by disulfide bonds; variable regions at ends form antigen-binding sites (idiotypes).

IgG

Most abundant antibody (~80%); acts against bacteria, viruses, and toxins.

IgA

~13% of antibodies; found in exocrine gland secretions (saliva, tears, breast milk).

IgM

~6% of antibodies; acts on antigens in foods and bacteria; first antibody produced in primary response.

IgD

Less than 1% of antibodies; found on B cell surfaces; common in infants.

IgE

Less than 1% of antibodies; found in exocrine gland secretions; involved in allergic (Type I hypersensitivity) reactions.

Naturally acquired active immunity

Exposure to live pathogens stimulates an immune response with disease symptoms; long-lasting.

Artificially acquired active immunity

Exposure to a vaccine (weakened/dead pathogens or components); stimulates immune response without disease symptoms.

Naturally acquired passive immunity

Antibodies passed from pregnant woman to fetus, or via colostrum/breast milk; short-term, no immune response stimulated.

Artificially acquired passive immunity

Injection of antiserum with specific antibodies or antitoxin; short-term immunity without stimulating an immune response.

Type I hypersensitivity (allergy)

IgE produced against allergen → IgE attaches to mast cells/basophils (sensitization) → subsequent exposure triggers rapid release of histamine and other mediators.

Type II hypersensitivity

Antibody-dependent cytotoxic reaction; phagocytosis and complement-mediated lysis of antigen-bearing cells. Example: mismatched blood transfusion.

Type III hypersensitivity

Immune complex reaction; phagocytosis cannot clear antigen-antibody complexes. Example: autoimmunity.

Type IV hypersensitivity

Delayed reaction; T cells and macrophages release chemical factors into skin. Example: contact dermatitis.

Tissue rejection

Recipient's immune cells recognize donor MHC antigens as foreign and destroy transplanted tissue; severity increases with greater MHC mismatch.

Graft-versus-host disease (GVHD)

Transplanted immune cells recognize recipient's tissues as foreign and attack them.

4 types of transplants

Isograft (identical twin), autograft (self), allograft (same species), xenograft (different species).

Autoimmunity

Immune system fails to distinguish self from non-self; produces autoantibodies and cytotoxic T cells that attack own tissues. Examples: Type 1 diabetes, multiple sclerosis, rheumatoid arthritis, lupus.