Anatomy 2 Exam 2

Functions of the Lymphatic System

Drains excess interstitial fluid and returns it to the bloodstream; transports fats and lipid‑soluble vitamins via lacteals

Interstitial Fluid → Lymph

Fluid enters blind‑ended lymphatic capillaries and becomes lymph

Lymphatic System Structure

One‑way system toward the heart composed of capillaries → vessels → trunks → ducts

Lymphatic Capillaries

Blind‑ended vessels interlaced with blood capillaries; absorb interstitial fluid and dietary fats (via lacteals)

Lacteals

Lymphatic capillaries in villi of the small intestine that absorb fats and lipid‑soluble vitamins

Chyle

Fat‑rich lymph formed from triglycerides combined with proteins in the small intestine

Lymphatic Vessels

Larger vessels with valves (more numerous than veins) that carry lymph toward trunks

Lymphatic Trunks

Formed by merging lymphatic vessels; drain large regions of the body

Right Lymphatic Duct

Drains right side of head, and into right subclavian vein

Left Lymphatic Duct

Drains the rest of the body into the left subclavian vein; arises from the cisterna chyli

Cisterna Chyli

Sac-like chamber below the diaphragm that receives lymph from lumbar and intestinal trunks

Lymphocytes

Primary cells of adaptive immunity; include T cells and B cells

B Cells

Produce antibodies and differentiate into plasma cells when activated

T Cells

Destroy infected cells and coordinate adaptive immune responses

Primary Lymphoid Organs

Bone marrow (B‑cell maturation

Bone Marrow ( Primary Lymphoid Organ )

Site of hematopoiesis; red marrow produces blood cells

Thymus ( Primary Lymphoid Organ )

Organ where T cells mature; largest in childhood and shrinks after puberty ( involution )

-Bilobed and contains thymocytes, macrophages, and dendritic cells ( phagocytes )

Secondary Lymphoid Organs

Sites where immune responses are mounted

Lymph Nodes

Filter lymph and mount immune responses against pathogenic antigens

- contain cortex ( germinal centers housing B and T cells deeper within )

- medulla ( medullary cords, and clusters of lymphatic tissue with B, T, and plasma cells )

Spleen

Largest lymphoid organ; Mounts immune response to blood-borne pathogens

- filters blood ( removes microbes, dying RBCs, etc. )

- Site of lymphocytic proliferation

Red Pulp (Spleen)

Region that removes old or damaged red blood cells

White Pulp ( Spleen )

Region of spleen rich in lymphocytes that fight infections

Lymphoid Nodules

Clusters of lymphocytes without a fibrous capsule

ex. Tonsils: develop immunity to oral pathogens

MALT

Mucosa‑Associated Lymphoid Tissue

-found in digestive mucosa: ex. Peyer’s patches, appendix, tonsils, etc.

BALT

Bronchus‑Associated Lymphoid Tissue

-lymphoid follicles found in bronchi; protects against inhaled pathogens

Immune Cell Formation

arise from hematopoietic stem cells in bone marrow and continuously differentiate to replace old or damaged cells

Phagocytic Cells

Neutrophils and monocytes / macrophages that ingest and destroy pathogens

Lymphocytes

Cells that coordinate the adaptive immune response

Granulocytes

Immune cells with cytoplasmic granules that respond to parasites and intracellular pathogens ex. viruses

B Cells

Generates diverse antibodies

T Cells

Secretes chemical messengers to regulate immune responses

Plasma Cell

Activated B cell that secretes antibodies

NK Cell

Destroys virally infected cells by inducing apoptosis ( programmed, orderly cell death )

First Line of Defense

Non-specific barrier defenses that physically prevent pathogen entry

Second Line of Defense

Innate immune response that is rapid and non-specific

Third Line of Defense

Adaptive immune response that is slower but highly specific and controlled by lymphocytes

Barrier Defenses

Physical defenses against pathogens

-Skin- dead keratinized cells → too dry for bacteria

-Sweat/secretions - lower pH, toxic lipids → wash bacteria away

-Saliva - contains lysozymes which ingest cell wall of of bacteria

-Mucus membranes - trap microbes + debris for removal

Phagocytosis

Process where macrophages and neutrophils engulf pathogens using phagosomes and lysosome digestive enzymes

Macrophages

Phagocytes found in tissues that participate in both innate and adaptive immunity

Neutrophils

Fast-acting phagocytes recruited to infection sites via chemotaxis

Natural Killer Cells

Lymphocytes that kill infected or cancerous cells using fas ligand or perforin/granzyme pathways

fas ligand

ligand bands to fas molecule receptor on infected cell surface and sends signal for apoptosis

perforins

create pores in infected cell that granzymes from granules can travel through to trigger apoptosis

Pattern Recognition Receptors

detect pathogen-associated molecules through characteristic features and damaged cell signals

-Limited # of receptors so they must be effective against wide variety

Cytokines

Short-distance signaling molecules that change cell physiology during immune responses

-ex. IL-4 induces B-cells to switch from producing IgM antibodies to producing IgE antibodies

Chemokines

Signaling molecules similar to cytokines that attract immune cells over longer distances (chemotaxis)

Interferons

Early induced proteins originating from infected cells that help nearby cells produce antiviral proteins

Opsonization

Process where proteins coat pathogens to enhance phagocytosis

Complement System

Plasma proteins synthesized mainly by the liver that trigger opsonization

Classical Complement Pathway

Adaptive pathway activated by antigen-antibody complexes

Alternative Complement Pathway

Innate pathway triggered directly by pathogen surfaces through spontaneous C3 hydrolysis

membrane attack complex

pokes hole in pathogen plasma membrane

-C3 protein fragments attract phagocytes, while C5 fragments create this complex

Complement System Action Summary

1. Opsonin bind to the cell membrane of the pathogen that activates it, labeling it for phagocytosis ( opsonization )

2. Diffuses away from the pathogen and act as chemotactic agents to attract phagocytic cells to the site of inflammation

3. Form damaging pores in the plasma membrane of the pathogen (MAC)

What is Inflammation

signals phagocytic cells to damaged area to clear cellular debris and start process of wound repair

- helps isolate the infected/damaged site to limit the spread of the pathogen/injury

Inflammation characteristics

-heat

-redness

-pain and swelling

Inflammatory response #1

Tissue injury: injured cells release contents that stimulate release of mast cell granules and associated mediators

Histamine

Mediator released by mast cells that causes vasodilation and increased capillary permeability

- leads to swelling

Leukotrienes

Mediators that attract neutrophils to infection sites via chemotaxis

Inflammatory response #2

Vasodilation: Increases blood flow → heat + redness

Inflammatory response #3

Increased vascular permeability: causes leaking of fluid into interstitial space (swelling/edema)

Inflammatory response #4

Recruitment of phagocytes: Leukotrienes are especially good at this

Prostaglandins

Mediators causing vasodilation ( through muscle relaxation ) and pain; inhibited by NSAIDs

Adaptive Immunity Benefits

Specificity

-Antigens (markers associated w/pathogens) are recognized by receptors on surface of B & T lymphocytes

Primary Adaptive Response

First exposure to pathogen; slower and more severe

Secondary Adaptive Response

Faster and stronger response due to memory cells

Self Recognition

Ability of immune system to distinguish self from non-self; failure leads to autoimmunity

Antigens

Molecules on pathogens recognized by B and T cell receptors

Memory Cells

Long-lived T or B cells that enable rapid secondary responses

Antigen-Presenting Cells (APCs)

Cells that process antigens and present them on MHC molecules to T cells ( only way T cells can ID antigens )

Antigen Processing

Cleaving antigens into fragments that bind MHC molecules for presentation

MHC Class I

Found on most cells; presents intracellular antigens to cytotoxic T cells for destruction of cell and pathogen within ex. important for viruses

MHC Class II ( Professional APCs )

Only on cells of immune system

-Found on macrophages, dendritic cells, and B cells

Macrophages ( APC Role )

Stimulate T cells to release cytokines and enhance phagocytosis

-Found in lining of mucosal surfaces ( nasopharynx, lungs, stomach, intestines )

Dendritic Cells ( APC role )

Bring antigens to regional draining lymph nodes

-where most T-cells mount response against pathogens in the interstitial tissues

B Cells ( APC Role )

Presents antigen to helper T cells and stimulate antibody production

T cell tolerance

When T-cells are produced, many of them are eliminated to prevent them from attacking your own cells

T Cell Development Step 1

Thymocytes from bone marrow enter cortex of thymus

T Cell Development Step 2 ( Positive selection )

Epithelial cells of thymus present MHC proteins to thymocytes. Ones that successfully bind move to next step and ones that don’t undergo apoptosis

-receive both CD4 and CD8

T Cell Development Step 3 ( Negative selection )

Selected thymocytes move to medulla of thymus where they encounter APCs that present self-antigens from other body cells

-Thymocytes that bind -> apoptosis, ones that don’t → survive

T Cell Development Step 4

As a result of cell signaling, self-tolerant thymocytes express either CD4 or CD8 receptor, not both

-CD4= T-helper cells (T_H)

-CD8= Cytotoxic T-cells (T_c)

CD4 Helper T Cells

Secrete cytokines that help enhance other immune responses

- Th1 cytokines regulate immune activity and T cell development

- Th2 cytokines promote B cell differentiation into plasma cells

CD8 Cytotoxic T Cells

Kill infected cells inducing apoptosis, through fas ligand or perforins and granzymes

Regulatory T Cells (Treg) aka Suppressor T Cells

Have both CD4 as well as CD25 and FOXP3

-Function still being investigated, but known to suppress other T-cell immune responses → controls “population”

Clonal Expansion (T Cells)

Rapid division of activated T cells to strengthen immune response

Clonal selection ( T cells )

process of antigen binding on T-cells that have receptors specific to that antigen

Memory T Cells

Long-lived cells that respond rapidly upon re-exposure to antigen

Antibodies

Proteins that are secreted

-act as receptors

-circulate to tag pathogens

IgM

First antibody produced in primary response; can class-switch to: IgG, IgA, or IgE

IgG

Major antibody of late primary and secondary responses

IgA

Found in mucosal secretions and colostrum of newborns; protects mucosal surfaces

IgE

Associated with allergies and anaphylaxis

B Cell Differentiation

Occurs in bone marrow; includes central tolerance ( destruction/inactivation of B cells that recognize self-antigens )

B Cell Activation

Occurs after antigen binding; activated B cells become plasma cells or memory B cells

-Plasma cells usually leave secondary lymphoid organs and migrate back to bone marrow where differentiation process is started

Memory B cell

results from clonal expansion of activated B cell

-similar to memory T cells: have a stronger & faster secondary response

Clonal Selection (B Cells)

Expansion of B cells with receptors specific to an encountered antigen

Primary B Cell Response

Delayed by several days, takes time for B cell clones to expand and differentiate into plasma cells

-Slow initial antibody production

Secondary B Cell Response

Rapid and strong antibody production upon re-exposure

Active Immunity

Immune response generated by the body (infection or vaccination)

Passive Immunity

Antibodies transferred without immune activation ( maternal IgG / IgA or injections )

T-Dependent Antigens

Require Helper T cells to activate B cells