anatomy chapter 22

secondary lymphoid structures house

t- and b- lymphocytes, macrophages, dendritic cells, and NK cells

macrophages location

select organs, may be residents of organ or migrating

dendritic cells location

epithelial layers of skin and mucosal membranes

mast cells location

connective tissue

cytokines

small proteins that regulate immune activity

cytokines function

chemical messengers released from one cell that bind to receptors on target cell, can be autocrine, paracrine, or endocrine

innate immunity

present at birth, nonspecific, includes barriers of skin and nonspecific cellular and molecular internal defenses, responds immediately

adaptive immunity

response to antigen involving specific t- and b- lymphocytes, specific, takes several days to be effective

first line of defense

skin and mucosal membranes

second line of defense

internal processes- immune cells, chemicals, physiological processes

skin defense

physical barrier, releases antimicrobial substances from sweat and sebaceous glands

antimicrobial substances released from skin

dermicidin, lysozyme, sebum, defensins

mucous membranes defense

produce mucus and release antimicrobial substances (defensins, lysozyme, IgA)

commensal microflora

nonpathogenic microorganisms on body surface that interfere with attachment of potentially pathogenic organisms

nonspecific internal defenses

selected immune cells, antimicrobial proteins, inflammation, fever

phagocytic cells

neutrophils, macrophages, dendritic cells

neutrophils and macrophages

destroy engulfed particles, lysosome enzymes break down unwanted substances, residue is released by exocytosis

dendritic cells

destroy particles and present fragments, antigens presented on surface to t-lymphocytes, necessary for adaptive immunity

basophils and mast cells

promote inflammation through chemotaxis chemicals histamine and heparin, release eicosanoids from their plasma membrane that also increase inflammation

natural killer cells

perform immune surveillance, destroy unwanted cells using cytotoxic chemicals perforin and granzymes

perforin

creates a transmembrane pore in unwanted cell

granzymes

enter pore made by perforin and cause apoptosis of cell

eosinophils

attack multicellular parasites by degranulating and releasing enzymes and other toxic substances, also engage in phagocytosis of antigen-antibody complexes

antimicrobial proteins

molecules that function against microbes

interferons

class of cytokines that nonspecifically interferes with spread of intracellular pathogens

complement system

group of over 30 plasma proteins that work along with complement antibodies, synthesized by liver in inactive form

classical pathway

antibody attaches to foreign substance, then complement binds to antibody

alternative pathway

complement binds to polysaccharides of bacterial or fungal cell wall

complement effect on inflammation

enhanced, activates mast cells and basophils, attracts neutrophils and macrophages

complement effect on opsonization

complement protein (opsonin) binds to pathogen, enhances likelihood of phagocytosis of pathogenic cell

complement effect on cytolysis

complement triggers splitting of target cell, forms membrane attack complex that creates channel in target cell membrane

complement effect on elimination of immune complexes

complement links anitgen-antibody complexes to erythrocytes, cells move to liver and spleen where complexes are stripped off

inflammation

local, nonspecific response of vascularized tissue to injury or infection, major response of innate immunity

first event of inflammation

injured tissue, basophils, mast cells, and infectious organisms release chemicals that initiate response (histamine, leukotrines, prostaglandins, chemotactic factors)

second event of inflammation

released chemicals cause vascular changes (vasodilation, increased capillary permeability, increased endothelial expression of molecules for leukocyte adhesion)

margination of leukocytes

adherence of leukocytes to endothelial cell-adhesion molecules (CAMs)

diapedesis of leukocytes

cells escape blood vessel walls

chemotaxis of leukocytes

leukocytes migrate toward chemicals released from damaged, dead, or pathogenic cells

third event of inflammation

delivery of plasma proteins to site- immunoglobulins, complement, clotting proteins, and kinins

kinins function

stimulate pain receptors, increase capillary permeability, increase production of CAMs by capillary cells

effects of inflammation

fluid, protein, immune cells moved to infected area promoting healing, vasodilation brings blood to area, increased capillary permeability, loss of plasma proteins

cardinal signs of inflammation

redness, heat, swelling, pain, loss of function in severe cases

fever (pyrexia)

abnormal body temperature elevation 1C or more from normal (37C), results from release of pyrogens from immune cells or infectious agents

events of fever

pyrogens circulate through blood, target hypothalamus which releases prostaglandin E2, raises temperature set point

fever onset

temperature rises, hypothalamus stimulates constriction of dermal blood vessels (less heat loss), shivering of muscle generates more heat

fever stadium

elevated temperature is maintained, metabolic rate increases to promote elimination of harmful substance, liver and spleen binds zinc and iron slowing microbial reproduction

fever defervescence

temperature returns to normal, hypothalamus no longer stimulated by pyrogens, prostaglandin release decreases, hypothalamus stimulates mechanisms to release heat

benefits of fever

inhibits production of bacteria and viruses, promotes interferon activity, increases activity of adaptive immunity, accelerates tissue repair, increases CAMs on endothelium of capillaries in lymph nodes

low grade fever

100-101 F

intermediate grade fever

102 F

high-grade fever

103-104 F

irreversible brain damage if temperature above

106 F

death likely if temperature above 

108 F

cell mediated immunity involves

t-lymphocytes

antibody mediated immunity

involving b-lymphocytes, plasma cells, antibodies

antigen

substance that binds a t-lymphocyte or antibody, usually a protein or polysaccharide 

epitope

antigenic determinant, specific site on antigen recognized by immune system, each has a different shape, pathogenic organisms can have multiple

immunogen

antigen that induces an immune response 

immunogenicity

ability to trigger immune response, increases with antigen’s degree of foreignness, size, complexity, or quantity 

haptens

too small to function as an antigen alone, become immunogenic when attached to a carrier molecule 

receptor complexes

binds one specific antigen, t- and b- lymphocytes have unique ones, about 100,000 per cell

TCR

antigen receptor for t-lymphocyte

BCR

antigen receptor for b-lymphocyte

b-lymphocyte contact with antigen

direct

t-lymphocyte contact with antigen

antigen presented by another cell

helper t-lymphocytes

CD4+ cells

cytotoxic t-ylymphocytes

CD8+ cells

helper t-lymphocyte function

assist in cell-mediated, antibody-mediated, and innate immunity

cytotoxic t-lymphocytes function

release chemicals that destroy other cells

antigen presentation

cells display antigen on plasma membrane so t-cells can recognize it

antigen presenting cells (APCs)

immune cells that present to both helper t-cells and cytotoxic t-cells, include dendritic cells, macrophages, b-lymphocytes

major histocompatibility complex (MHC)

group of transmembrane proteins antigen must attach to for antigen presentation

MHC class 1 molecules

glycoproteins synthesized by rough er, display fragments of proteins that were bound in RER

MHC class 2 molecules

glycoproteins synthesized by rough er, fragments of exogenous antigens loaded onto this molecule within vesicle and bound to plasma membrane

positive selection

selects for ability of t-cells to bind thymic epithelial cells with MHC molecules, those that can bind survive

negative selection

tests ability of t-lymphocyte to avoid binding self antigens, self-tolerance

immunocompetent t-lymphocyte

able to bind to antigen and respond to it

naive t-lymphocyte

not yet exposed to antigens they recognize

regulatory t-lymphocytes (Tregs)

CD4+ cells formed from t-cells that bind self-antigens, inhibit immune response, function in tolerance outside of primary lymphoid structures (peripheral tolerance)

clonal selection

forming clones in response to an antigen, all formed cells have same TCR or BCR that matches specific antigen

antigen challenge

first encounter between antigen and lymphocyte

first signal of t-lymphocyte activation

direct contact with MHC molecule of APC, if lymphocyte recognizes antigen contact lasts several hours

second signal of t-lymphocyte activation

other receptors of APC and t-cell interact, helper t-cell releases IL2 stimulating itself or a cytotoxic t-cell, cells proliferate

first signal of b-lymphocyte activation

antigen binds to BCR. cross-linking 2 BCRs, b-cell engulfs, processes, and presents antigen to t-cell

second signal of b-lymphocyte activaiton

receptors between b-cell and t-cell interact, helper t-cell releases IL-4 stimulating b-cell

lymphocyte recirculation

after a period of time, a lymphocyte exits secondary lymphatic structure and circulates through blood and lymph for several days

effector response

mechanisms used by lymphocytes to help eliminate antigen

helper t-lymphocyte effector response

release IL-2 and other cytokines, regulate cells of adaptive and innate immunity

cytotoxic t-lymphocytes effector response

destroy unhealthy cells by apoptosis

plasma cells effector response

produce antibodies

antibody titer

circulating blood concentration of antibody against a specific antigen

variable region of antibody

located at end of arms, contain antigen-binding site, bind antigens through weak intermolecular forces

constant region of antibody

contains the Fc region which determines biological function, same in structure for antibodies of a given class

neutralization

antibody covers antigenic determinant of pathogen

agglutination

antibody cross-links antigens of foreign cells causing clumping

precipitaiton

antibody cross-links circulating antigens, forms antigen-antibody complex that becomes insoluble and precipitates out of body fluids

complement fixation

Fc region of IgG and IgM can bind complement for activation

opsonization

Fc region of certain antibody classes makes it more likely target cell will be seen by phagocytic cells

activation of NK cells

Fc region of some antibodies IgG trigger NK cells to release cytotoxins

IgG

make up 75-85% of antibodies in blood, can participate in all types of antibody actions, can cross placenta