Lymphatics II

immune system

barriers, cells, and proteins involved in the defense of the human body

immune system phases

barrier defense

innate immune response

adaptive immune response

barrier defense

instantaneous prevention

innate immune response

rapid but nonspecific response

adaptive immune response

slower but specific and effective response

innate (non-specific) response time

immediate, pre-formed

innate (non-specific) range of targets

effective against a wide variety of targets

innate (non-specific) body structures

barrier to invasion (skin, mucous membrane)

chemicals

cells (phagocytes, NK cells)

adaptive (specific) response time

some delay

adaptive (specific) range of targets

selective

adaptive to each target

adaptive (specific) body structures

B lymphocytes

T lymphocytes

antigen presenting cells

barriers to infection

classed as “innate immunity” as it is immediate and non-specific

barriers to infection consists of

intact skin

mucous membrane

intact skin characteristics

30-50 rows of stratified keratinized epithelium

slightly acidic pH (3-5)

salty due to NaCl in sweat (discourages most bacterial growth)

relatively dry

skin secretions contain antibacterial chemicals (lysozyme, fatty acids)

mucous membrane characteristics

non-keratinized, stratified squamous epithelium

acidic pH (stomach, vagina during childbearing years)

hair, cilia, mucous which helps to trap foreign particles

saliva contains lysozome

normal flora compete with pathogens

innate internal defense

inflammatory response

phagocytes

natural killer cells

complement system

inflammatory response

process begins with tissue injury, which is recognized by mast cell and basophils

inflammatory response characteristics

heat

redness

pain

swelling

what does mast cell release?

histamines

leukotrienes

prostaglandins

heat

capillary widening

increased blood flow

redness

increased permeability

fluid release into tissues

swelling

inbetween redness and tenderness

what is tissue injury caused by?

physical/chemical agent or pathogenic microorganism

tenderness

attraction of leukocytes

extravasation of leukocytes to site of injury

pain

systemic response

fever and proliferation of leukocytes

inflammatory response stages

tissue injury

vasodilation

increased vascular permeability

recruitment of phagocytes

what do phagocytes include?

macrophages (derived from monocytes)

neutrophils

eosinophils (weakly phagocytic)

mast cells

phagocytes

these cells can perform phagocytosis

first event of phagocytosis

phagocyte adheres to pathogens or debris

second event of phagocytosis

phagocyte forms pseudopods that eventually engulf the particles forming a phagosome

third event of phagocytosis

lysosome fuses with the phagocytic vesicle, forming a phagolysosome

fourth event of phagocytosis

lysosomal enzymes digest the particles, leaving a residual body

fifth event of phagocytosis

exocytosis of the vesicle removes indigestible and residual material

phagocytosis

the process of using cytoplasmic extensions to pull and engulf pathogens toward it

what happens during phagocytosis?

adherence

opsonisation

adherance

phagocytes must adhere to microbes

can be done by carbohydrates on the pathogen’s surface via opsonisation

opsonisation

the coating of a pathogen with antibodies or complement proteins

natural killer cells

a group of lymphocytes

they lyse and kill cancer cell and virus infected cells by releasing perforins and granzyme B

natural killer cells function

create defects in the plasma membrane and nuclear membranes of pathogens (perforins poke holes)

stimulates apoptosis (programmed cell death)

complement system

proteins made in the liver that are found in the plasma

what activates the complement system?

the innate immune response via thte alternative pathway

the adaptive immune response in the classical pathway

what can the complement system do once activated?

bind to pathogens for opsonization

act as chemotactic agents to attract more phagocytes/inflammation

form damage pores in plasma membrane in pathogens called “membrane attack complex”

c reactive protein

acute phase protein made by the liver

it binds to surfaces of pathogens and damaged body cells and then binds to C1, activating complement in the classical pathway

interferons

produced by a variety of cell types

α (alpha) IFN

β (beta) IFN

γ (gamma)

α (alpha) IFN

produced by all leukocytes except lymphocytes

β (beta) IFN

produced by fibroblasts (beta, blasts)

γ (gamma) IFN

produced by lymphocytes

interferon stages

antiviral effects

activate microphages

activate natural killer cells

first interferons step

virus enters cell

second interferons step

interferon genes switch on

third interferons step

cell produces interferon molecules

fourth interferons step

interferon binding stimulates cell to turn on genes for antiviral proteins

fifth interferons step

antiviral proteins block viral reproduction

antiviral effects

blocks viral replication

what do body cells infected with virus secrete?

interferon (IFN)

how is Protein Kinase R (PKR) synthesized?

interferon diffuses to nearby healthy cells and induces them

what does PKR do?

blocks the production of proteins the virus needs to replicate

types of adaptive immunity

humoral

cell-mediated

cell-mediated immunity

mostly managed by t cells that develop in the thymus

defend against infected cells, transplant tissues, cancers

2 types of cell-mediated immunity

helper t cells (Th)

cytotoxic t cells (Tc)

helper t cells (Th)

CD4 molecules on them

they release cytokines to activate macrophages, other t cells, and b cells

cytotoxic t cells (Tc)

CD8 molecules on them

these kill target cells via apoptosis, similar to NK cells, but can kill multiple at once

humoral immunity

b cells develop in the bone marrow, each one is specialized to recognizing a specific antigen

if it is activated by its antigen, it develops into a plasma cells

plasma cells secrete antibodies into body fluids

what happens when antibodies form complexes with antigens?

activate complement (classical pathway)

neutralize the antigen

immobilize the antigen by precipitation or agglutination

what do b cell become

memory cells—so we can mount a faster response if we see that pathogen again

antibodies (immunoglobins)

IgG

IgM

IgA

IgD

IgE

IgG

highest opsonization and neutralization activities

classified into four subclasses

subclasses of IgG

IgG1

IgG2

IgG3

IgG4

IgM

produced first upon antigen invasion

increases transiently

IgA

expressed in mucosal tissues

forms dimers after secretion

IgD

unknown function

IgE

involved in allergy