lymphatic system consists of several structures and organs that contain lymphatic tissue, bone marrow, and a fluid called lymph that flows within lymphatic vessels (often drawn in green). doesn't have to be an organ, just have a lymph function

lymphatic vessels begin as lymphatic capillaries (microscopic), which are closed on one end. lymphatic vessels (lymphatics) **return interstitial fluid and leaked plasma proteins back to blood. ~3L/day of excess fluid collected. once interstitial fluid enters lymphatics, called lymph

from lymphatic vessels, lymph passes through lymph nodes and then into lymph ___. lymph ___ include the lumbar, intestinal, bronchomediastinal, subclavian, and jugular trunks. lymph trunks then merge to form either the thoracic __ or the right lymphatic __

two major ducts in thoracic cavity

drains stuff in - rest of the body: left side face and head, thoracic cavity, left upper extremity, abdominal cavity, both lower extremities. bigger and drains larger area. drain into left subclavian vein and down into superior vena cava, brachiocephalic vein, etc

drains stuff in-right side of face/head, right side of thoracic cavity, right upper extremity. drain into right subclavian vein just before it empties into brachiocephalic and superior vena cava

interstitial fluid --> lymph capillaries --> lymph vessels --> lymph trunks --> lymph ducts --> subclavian veins

lymph propelled by:

milking action of skeletal muscle, pressure changes in thorax during breathing, valves to prevent backflow, pulsations of nearby arteries, contractions of smooth muscle in walls of lymphatics. similar to venous return-against gravity. follows same rules/mechanisms

primary lymphatic organs are organs related to immune system where immune cells become immunocompetent. after cells have differentiated in bone marrow, go to thymus for further education and become immunocompetent

where B cells lymphocytes become immunocompetent

where T cells lymphocytes become immunocompetent

where immature immune cells are going to become trained like a military school where they're going to learn to recognize antigens and not attack our own cells * learn to recognize our own tissue so don't develop autoimmunity

Thymus:

some lymph organs have an ___ capsule. ___ portion is made of trabecula which is made of CT and reticular fibers, etc. mostly filled with developing T cells

secondary lymphatic organs and tissues include

principal lymphoid organs of body. embedded in CT, in clusters along lymphatic vessels. near body surface in inguinal (groin), axillary, and cervical regions of body. where 1st contact happens between lymphocytes and pathogens - they're supposed to identify and destroy. not where lymphocytes are developing, but where they all hang out. when fight infection, proliferate (make copies of selves, causing them to swell)

afferent vessels - where lymph will flow from lymph vessels into lymph node

efferent vessels - where it flows out. as passes through, comes in contact with T cells and B cells and they become activated or not

there are way more afferent than efferent lymph node vessels

encapsulated because inside is very delicate

largest lymphoid organ. in LUQ just under ribs. normal lymphatic organ functions - investigate, identify, etc. also recycling and breakdown of old RBCs as well as storage of some blood. served by splenic artery (brings blood in) and vein (blood out), which enter and exit at the hilum

functions: 1. site of lymphocyte proliferation and immune surveillance and response. 2. cleanses blood of aged cells and platelets, macrophages remove debris (liver does this, too). 2 distinct areas of tissue: white pulp and red pulp

spleen tissue. around central arteries- mostly lymphocytes on reticular fibers; involved in immune functions (surveillance for immune activation)

spleen tissue. in venous sinuses and splenic cords. majority of tissue. rich in RBCs and macrophages for disposal of worn-out RBCs and bloodborne pathogens/debris. composed of splenic cords and sinusoids (capillaries with a lot of openings)

like lymph nodes but without the capsule. houses and provides proliferation site for lymphocytes. surveillance vantage point for lymphocytes and macrophages. largely reticular CT - type of loose CT. two main types: diffuse lymphoid tissue and lymphoid follicles. in mucosa of other structures and organs. activation of immune system

not the same as lymph nodes. these are masses of lymphatic tissue that are NOT surrounded by a capsule. they're scattered throughout the lamina propria of mucous membranes lining the GI, urinary, reproductive tracts and the respiratory airways. in these areas, also referred to as mucosa-associated lymphatic tissue (MALT). diffuse lymphatic tissue. right under mucosa in all the areas so it reacts quickly

lymphoid tissues in mucous membranes throughout body. protects from pathogens trying to enter body. largest collections of ___ in tonsils, Peyer's patches, appendix. also in mucosa of respiratory, urinary, and genitourinary organs; rest of digestive tract. seek and destroy anything that managed to get through

immunity:

resistance to disease-pathogens, parasites, bacteria, viruses, etc AND repair itself from damage.

immune system - 2 intrinsic systems: innate (nonspecific) defense system to prevent/detect any pathogen/invader into body system, and adaptive (specific) defense system where mount defense against a very specific pathogen/antigen, but also where create MEMORY- much more prepared to deal with it quickly and efficiently next time

immunity present at birth and includes defense mechanisms that provide general protection against invasion by a wide range of pathogens

immunity that involves activation of specific lymphocytes that combat a particular pathogen or other foreign substance. immunological memory created during this response

body system that carries out immune responses is

has two lines of defense:

first - external body membranes - physical barrier (skin and mucous membranes).

second- antimicrobial proteins, phagocytes, and other cells. if something does get through a tissue. inhibits spread of invaders. inflammation most important mechanism, as it's a set of conditions that makes/enhances the body's ability to get rid of pathogens

specific. #3 line of defense attacks particular foreign substances. takes longer to react than innate system because have to identify and make antibodies that will attack antigens. *create memory cells - don't participate in 1st infection, but for the ones after

1. surface barriers - skin and mucous membranes

2. internal defenses - phagocytes, natural killer cells, inflammation, antimicrobial proteins, fever

specific. 3. humoral immunity (B cells - fluids. extracellular antigens)

cellular immunity (T cells - intracellular antigens)

surface barriers ward off invading pathogens. skin, mucous membranes, and their secretions. physical barrier to most microorganisms. keratin resistant to weak acids and bases, bacterial enzymes, and toxins. mucosae provide similar mechanical barriers

1st line - surface barriers. protective chemicals inhibit or destroy microorganisms. acidity of skin and secretions - acid mantle - inhibits growth. enzymes - lysozyme of saliva, respiratory mucus, and lacrimal (tears) fluid - kill many microorganisms. defensins - antimicrobial peptides - inhibit growth. other chemicals - lipids in sebum, dermicidin in sweat - toxic, gastric juice

1st line - surface barriers. respiratory system modifications. mucus-coated hairs in nose. cilia of upper respiratory tract sweep dust and bacteria-laden mucus toward mouth. if surface barriers breached by nicks or cuts - second line of defense must protect deeper tissues

2nd line - internal defenses: cells and chemicals. necessary if microorganisms invade deeper tissues: phagocytes, natural killer (NK) cells (lymphocyte nonspecific-will destroy anything it sees as abnormal or foreign), antimicrobial proteins (interferons and complement proteins), fever, inflammatory response (macrophages, mast cells, WBCs, and inflammatory chemicals)

complement system is part of inflammation and is activated by the pathogen itself or previous cells or adaptive immune system sets stage for destroying pathogens

2nd line - internal defenses: phagocytes.

1st on scene: neutrophils - most abundant but die fighting. very effective. become phagocytic on exposure to infectious material.

macrophages develop from monocytes (in blood) - chief phagocytic cells - big - robust and permanent cells. free macrophages wander through tissue spaces (ex: alveolar macrophages). fixed macrophages permanent residents of some organs (ex: stellate macrophages in liver and microglia in brain)

2nd line - internal defenses: phagocytes must adhere to particle - some microorganisms evade adherence with capsule. opsonization marks pathogens - coating by complement proteins or antibodies (adaptive immune system). cytoplasmic extensions bind to and engulf particle in vesicle called phagosome. phagosome fuses with lysosome --> phagolysosome

2nd line - internal defenses: natural killer (NK) cells. nonphagocytic large granular lymphocytes that check ID. attack cells that lack "self" cell-surface receptors. induce apoptosis (cell suicide) in cancer cells and virus-infected cells. secrete potent chemicals that enhance inflammatory response

2nd line - internal defenses: inflammatory response. this is the bridge between the innate and adaptive immune systems. triggered whenever body tissues are injured. prevents spread of damaging agents. disposes of cell debris and pathogens. alerts adaptive immune system* so can build an army and create memory. sets the stage for repair

2nd line - internal defenses: inflammatory response. cardinal signs of acute inflammation: 1. redness 2. heat 3. swelling 4. pain (sometimes 5. impairment of function - joints). #1-3 - increase in circulation because WBCs, etc. #1-4 are major ones.

2nd line - internal defenses: inflammatory response. begins with chemicals released into ECF by injured tissues, immune cells, blood proteins. macrophages and epithelial cells of boundary tissues bear TLRs that recognize classes of infecting microbes. activated TLRs trigger release of cytokines (chemicals - local hormone) that promote inflammation

2nd line - internal defenses: inflammatory response. inflammatory mediators. kinins, prostaglandins (PGs), and complement. dilate local arterioles (hyperemia-increased bloodflow). causes redness and heat of inflamed region. make capillaries leaky - increased intercellular space in BVs and leads to edema (swelling). many attract leukocytes to area (chemotaxis)

2nd line - internal defenses: inflammatory response: edema. increased capillary permeability --> exudate to tissues. fluid containing clotting factors and antibodies. causes local swelling (edema). swelling pushes on nerve endings --> pain. pain also from bacterial toxins, prostaglandins, and kinins (trigger nociceptors and feel pain). moves foreign material into lymphatic vessels. delivers clotting proteins (contain damage/infection to an area) and complement (help destroy microorganisms)

2nd line - internal defenses: inflammatory response. clotting factors form fibrin mesh: scaffold for repair. isolates injured area so invaders cannot spread

2nd line - internal defenses: phagocyte mobilization. neutrophils lead; macrophages follow. as attack continues, monocytes arrive. 12 hrs after leaving bloodstream--> macrophages. these "late arrivers" replace dying neutrophils and remain for cleanup prior to repair. if inflammation due to pathogens, complement activated; adaptive immunity elements arrive

2nd line - internal defenses: steps for phagocyte mobilization: 1. leukocytosis: release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells. 2. margination: neutrophils cling to walls of capillaries in inflamed area. 3. diapedesis of neutrophils. 4. chemotaxis: inflammatory chemicals (chemotactic agent) promote positive chemotaxis of neutrophils

2nd line - internal defenses: antimicrobial proteins. include interferons and complement proteins - trigger another pt of immune system (adaptive immune system). some attack microorganisms directly. some hinder microorganisms' ability to reproduce

neutrophils enter blood from bone marrow. attracted through chemotaxis

neutrophils cling to capillary wall

neutrophils flatten and squeeze out of capillaries. increase leaking of capillaries

neutrophils follow chemical trail

2nd line - internal defenses: interferons. family of immune modulating proteins. have slightly different physiological effects. viral-infected cells secrete IFNs (IFN alpha and beta) to "warn" neighboring cells. IFNs enter neighboring cells --> produce proteins that block viral reproduction and degrade viral RNA, preventing them from dividing and affecting other cells. IFN alpha and beta also activate NK cells

2nd line - internal defenses: complement system (complement) - always ready to go. idling like a car - don't want to press on gas unless have to. ~20 blood proteins that circulate in inactive form. major mechanism for destroying foreign substances and alerting adaptive immune system. our cells contain complement activation inhibitors that suppress it

2nd line - internal defenses: complement. unleashes inflammatory chemicals that amplify all aspects of inflammatory response. non-specifically kills bacteria and certain other cell types by cell lysis (destroy the cell). enhances both innate and adaptive defenses

2nd line - internal defenses: complement activation. 3 pathways to activation. classical pathway, lectin, and alternative

complement activation pathway where: antibodies bind to invading organisms and to complement components. called complement fixation. first step in activation. adaptive immune system. produced by B cells when exposed to a specific antigen

complement activation pathway where: activated spontaneously, lack of inhibitors on microorganism's surface allows process to proceed. activated by pathogen itself. common

2nd line - internal defenses: complement activation. each pathway involves activation of proteins in an orderly sequence. each step catalyzes the next. each pathway converges on C3, which cleaves into C3a and C3b. common terminal pathway initiated that. enhances inflammation, promotes phagocytosis, causes cell lysis

2nd line - internal defenses: complement activation. cell lysis begins when C3b binds to target cell --> insertion of complement proteins called membrane attack complex (MAC) into cell's membrane; MAC forms and stabilizes hole in membrane --> influx of water --> lysis of cell. C3b also causes opsonization. C3a and other cleavage products amplify inflammation. stimulate mast cells and basophils to release histamine. attract neutrophils and other inflammatory cells

2nd line - internal defenses: fever. abnormally high body temp. systemic response to invading microorganisms. leukocytes and macrophages exposed to foreign substances secrete pyrogens. pyrogens act on body's thermostat in hypothalamus, raising body temp. helps immune system be more effective

2nd line - internal defenses: benefits of moderate fever. causes liver and spleen to sequester iron and zinc (needed by microorganisms to reproduce). increases metabolic rate of immune cells and body in general --> faster repair

adaptive immune (specific defense) system. protects against infectious agents and abnormal body cells. amplifies inflammatory response. activates complement. must be primed by initial exposure to specific foreign substance. priming takes time - produces memory. much quicker on subsequent exposures than on 1st

specific - recognizes and targets specific antigens. systemic - not restricted to initial site because memory throughout body. have memory- stronger attacks to "known" antigens. two separate, overlapping arms: humoral- (antibody-mediated) immunity=B cells. cellular (cell-mediated) immunity=Tcells - intracellular pathogens, cancerous cells, etc

humoral immunity. antibodies, produced by B lymphocytes, circulating freely in body fluids looking for particular antigen. bind temporarily to target cell. temporarily inactivate. mark for destruction by phagocytes or complement. opsonization - completely coat the pathogen and target it for phagocytosis. humoral immunity has EXTRAcellular (fluid) targets

cellular immunity. T-lymphocytes act directly against target cell. directly - by killing infected cells. indirectly - by releasing chemicals that enhance inflammatory response; or activating other lymphocytes or macrophages. cellular immunity has INTRAcellular targets

substances that can mobilize adaptive defenses and provoke an immune response. targets of all adaptive immune responses. most are large, complex molecules not normally found in body (nonself)

important functional properties: immunogenicity -ability to stimulate proliferation of specific lymphocytes to mount an immune response; reactivity- ability to react with activated lymphocytes and antibodies released by immunogenic reactions. ex: foreign protein, polysaccharides, lipids, and nucleic acids

something can incorporate into body from outside. small molecules (think half an antigen) that are not immunogenic by themselves. ex: peptides, nucleotides, some hormones. may be immunogenic if attached to body proteins and combination is marked foreign. ex: poison ivy, animal dander, detergents, and cosmetics

only certain parts (epitopes) of entire antigen are immunogenic. antibodies (B - humoral) and lymphocyte (T - cellular) receptors bind to them like an enzyme binds to its substrate. most naturally occurring antigens have numerous ___ that: mobilize several different lymphocyte populations; form different kinds of antibodies against them. large, chemically simple molecules (ex, plastics) have little or no immunogenicity

self-antigens: MHC proteins - protein molecules (self-antigens) on surface of cells not antigenic to self but antigenic to others in transfusions or grafts. lymphocytes recognize as self and don't respond to it. ex: MHC glycoproteins: coded by genes of major histocompatibility complex (MHC) and unique to individual (self-signal); have groove holding self or foreign antigen. T lymphocytes can only recognize antigens that are presented on MHC proteins

cells of the adaptive immune system- 3 types of cells. 2 types of lymphocytes

lymphocyte development, maturation, and activation. 5 general steps:

both B and T lymphocyte precursors originate in red bone marrow

lymphocyte precursors destined to become T cells migrate in blood to thymus and mature there. B cells mature in bone marrow. during maturation lymphocytes develop immunocompetence (graduation) and self-tolerance

immunocompetent but still naive lymphocytes leave thymus and bone marrow. they "seed" the secondary lymphoid organs and circulate through blood and lymph. not yet activated

when a lymphocyte's antigen receptors bind its antigen, that lymphocyte can be activated

activated lymphocytes proliferate (multiply) and then differentiate into effector cells and memory cells. memory cells and effector T cells circulate continuously in blood and lymph and throughout the secondary lymphoid organs

"educated" to become mature; B cells in bone marrow, T cells in thymus. 1. immunocompetence - lymphocyte can recognize one specific antigen by binding to it. B or T cells display only one unique type of antigen receptor on surface when achieve maturity - bind only one antigen. 2. self-tolerance. lymphocytes unresponsive to own antigens

mature in thymus under negative and positive selection pressures ("tests"). positive selection: selects __ cells capable of recognizing self-MHC proteins (MHC restriction); failures destroyed by apoptosis. negative selection: prompts apoptosis of __ cells that bind to self-antigens displayed by self-MHC. ensures self-tolerance

mature in red bone marrow. positively selected if successfully make antigen receptors. those that are self-reactive are eliminated by apoptosis (clonal deletion)

immunocompetent, self-tolerant B and T cells not yet exposed to antigen called naive. exported from primary lymphoid organs (bone marrow and thymus) to "seed" secondary lymphoid organs (lymph nodes, spleen, etc). increases chance of encounter with antigen when in lymph tissues

clonal selection. naive lymphocyte's first encounter with antigen --> selected for further development. if correct signals present, lymphocyte will complete its differentiation

activated lymphocyte proliferates --> exact clones. most clones --> effector cells that fight infections. few remain as memory cells - able to respond to same antigen more quickly second time. B and T memory cells and effector T cells circulate continuously

genes, not antigens, determine which foreign substances immune system will recognize. immune cell receptors result of acquired knowledge of microbes likely in environment. lymphocytes make up to a billion different types of antigen receptors: coded for by ~25,000 genes. gene segments are shuffled by somatic recombination

engulf antigens. present fragments of antigens to T cells for recognition. major types: dendritic cells in CT and epidermis; macrophages in CT and lymphoid organs; B cells

phagocytize pathogens, enter lymphatics to present antigens to T cells in lymph node. most effective antigen presenter known. key link between innate and adaptive immunity

widespread in lymphoid organs and CTs. present antigens to T cells to activate themselves into voracious phagocytes that secrete bactericidal chemicals

humoral immune response; secrete antibodies; extracellular pathogens; originate in red bone marrow and mature in red bone marrow; effector cells are plasma B cells; form memory cells

cellular immune response; do NOT secrete antibodies; intracellular pathogens; originate in red bone marrow and mature in thymus; effector cells are cytotoxic T (Tc) cells, Helper T (Th) cells, regulatory T cells; form memory cells

phagocytes. do not activate naive T cells. present antigens to helper T cell to assist in their own activation

uses lymphocytes, APCs, and specific molecules to ID and destroy nonself substances. depends on ability of its cells to recognize antigens by binding to them and communicate with each other so that whole system mounts a specific response

B cell activated when antigens bind to its surface receptors and cross-link them --> receptor-mediated endocytosis of cross-linked antigen-receptor complexes (clonal selection) --> proliferation and differentiation into effector cells (plasma cells that produce antibodies)

most clone cells become plasma cells. some become memory cells. secrete specific antibodies at rate of 2000 molecules per second for 4-5 days, then die. antibodies (Y shaped) circulate in blood or lymph. bind to free antigens and mark for destruction by innate or adaptive mechanisms

clone cells that do not become plasma cells become memory cells. provide immunological memory. mount an immediate response to future exposures to same antigen

primary immune response - cell proliferation and differentiation upon first antigen exposure. lag period: 3-6 days. peak levels of plasma antibody are reached in 10 days (why we feel sick for a while). antibody levels then decline

secondary immune response. re-exposure to same antigen gives faster, more prolonged, more effective response. sensitized memory cells respond within hours. antibody levels peak in 2-3 days at much higher levels. antibodies bind with greater affinity (makes more efficient). antibody level can remain high for weeks to months

when B cells encounter antigens and produce specific antibodies against them. 2 types of active humoral immunity:

active humoral immunity. response to bacterial or viral infection. infection; contact with pathogen. produce own antibodies from own activated cells

active humoral immunity. response to vaccine of dead or attenuated pathogens. vaccines: most of dead or attenuated pathogens. spare us symptoms of primary response because dead/weakened. provide antigenic determinants that are immunogenic and reactive. now have memory. produce own antibodies from own activated cells

readymade antibodies introduced into body. B cells are not challenged by antigens. immunological memory does not occur. protection ends when antibodies degrade. 2 types of passive humoral immunity:

passive humoral immunity. antibodies delivered to fetus via placenta or to infant through milk. from mom. given antibodies

passive humoral immunity. injection of serum, such as gamma globulin (immunoglobulins). protection immediate but ends when antibodies naturally degrade in body. injection of exogenous (produced outside) antibodies. given antibodies

AKA immunoglobulins (Ig) - gamma globulin portion of blood produced by plasma cells. activated B cells that are proteins secreted by plasma and memory cells and can be found in plasma. capable of binding specifically with antigen detected by B cells. grouped into one of 5 Ig classes

structure is T or Y shaped antibody monomer of four polypeptide chains linked by disulfide bonds. constant portion has 5 different types. 2 identical heavy (H) chains with hinge region at "middles". 2 identical light (L) chains. variable (V) regions at one end of each arm combine to form 2 identical antigen-binding sites. specific shape with many different types/combinations

antibodies structure. constant (C) regions of stem determine antibody class (IgM, IgA, IgD, IgG, IgE). serve common functions in all antibodies by dictating cells and chemicals that antibody can bind, and how antibody class functions to eliminate antigens

class of antibodies that is a pentamer (5 antibodies), which is larger than others; first antibody released. potent agglutinating agent. readily fixes and activates complement

class of antibodies that is secretory. monomer or dimer (1 or 2); in mucus and other secretions (saliva, sweat, milk, etc). helps prevent entry of pathogens

class of antibodies that is a monomer attached to surface of B cells. functions as naive B cell receptor

class of antibodies that is a monomer; most abundant. takes longer to be released but when are, most abundant. 75-85% of antibodies in plasma. from secondary and late primary responses. crosses placental barrier. activates complement by classic pathway. antigen-antibody complex

class of antibodies that is a monomer active in some allergies and parasitic infections. allergen=harmless substances. causes mast cells and basophils to release histamine --> inflammation

B cells can switch antibody classes but retain antigen specificity. IgM at first; then IgG - most abundant. almost all secondary responses are IgG

antibodies inactivate and tag (mark) antigens; do NOT destroy them. form antigen-antibody (immune) complexes. defensive mechanisms used by antibodies. neutralization and agglutination (the 2 most important). precipitation and complement fixation

commercially (in a lab) prepared pure antibody (1). specific for single antigenic determinant. proliferate indefinitely and have ability to produce single type of antibody. used in research, clinical testing, and cancer treatment

T cells provide defense against intracellular antigens. some T cells directly kill cells that have been infected already; others release chemicals that regulate immune response

cellular immune response has 2 populations of T cells based on which glycoprotein surface receptors displayed:

become helper T cells (TH); activate B cells, other T cells, macrophages, and direct adaptive immune response. can also become memory T cells

become cytotoxic T cells (TC). destroy cells harboring foreign antigens. also become memory T cells. helper, cytotoxic, and regulatory T cells are activated T cells. naive T cells simply termed CD4 or CD8 cells

T cells respond only to processed fragments of antigens displayed on surfaces of cells. antigen presentation is vital for activation of naive T cells and normal functioning of effector T cells that will become active in immune response

2 types of MHC proteins important to T cell activation. both types are synthesized at ER and bind to peptide fragments

displayed by all nucleated cells - not RBCs. bind with fragment of protein synthesized in the cell (endogenous antigen). endogenous antigen is self-antigen in normal cell; a nonself antigen in infected or abnormal cell. crucial for CD8 cell activation because this class binds here. inform cytotoxic T cells of microorganisms hiding in cells (cytotoxic T cells ignore displayed self-antigens). act as antigen holders; form "self" part that T cells recognize. think: 1-8. saying that it's self but it's been invaded and to kill me

displayed by APCs (antigen presenting cells) like dendritic cells, macrophages, and B cells. gobble up extracellular antigens. bind with fragments of exogenous (outside cell) antigens that have been engulfed and broken down in a phagolysosome. professional APCs. signal CD4 cells (TH) that help is required. think 2-4. saying it belongs to self but have captured a foreign invader and tells what it looks like - need help mounting defense against it

T cells that are activated enlarge and proliferate in response to cytokines and differentiate and perform functions according to their T cell class. primary T cell response peaks within a week. T cell apoptosis occurs between days 7-30. benefit of apoptosis: activated T cells are a hazard-produce large amount of inflammatory cytokines --> hyperplasia, cancer if accumulate. effector activity wanes as amount of antigen declines. memory T cells remain and mediate secondary responses

play central role in adaptive immune response. activate both humoral and cellular arms. once primed by APC presentation of antigen, they: help activate T and B cells, induce T and B cell proliferation, their cytokines recruit other immune cells. without them, there is no immune response

interact directly with B cells displaying antigen fragments bound to MHC II receptors. stimulate B cells to divide more rapidly and begin antibody formation. most antigens require TH co-stimulation to activate B cells: T cell-dependent antigens

CD8 cells require TH cell activation into destructive cytotoxic T cells. cause dendritic cells to express co-stimulatory molecules required for CD8 cell activation

directly attack and kill other cells. activated __ cells circulate in blood and lymph and lymphoid organs in search of body cells displaying antigen they recognize

targets: virus-infected cells, cells with intracellular bacteria or parasites, cancer cells, foreign cells (transfusions or transplants). bind to a self-nonself complex. can destroy all infected or abnormal cells

lethal hit - 2 methods: __ cell releases perforins and granzymes by exocytosis. perforins create pores through which granzymes enter target cell. granzymes stimulate apoptosis

natural killer cells- innate immunity. recognize other signs of abnormality: lack of class I MHC and antibody coating target cell. destroy cells by perforins and granzymes. use same key mechanisms as TC cells for killing their target cells (see above). not-specific - just a cell that's doing something abnormal is what they will go after