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Immune System - Eternity Vasquez p6 - Coggle Diagram
Immune System - Eternity Vasquez p6
Immune System
function
: provides resistance to disease
made up of 2 intrinsic systems:
Innate (nonspecific) defense system
first and Second line of defenses
first
: external body membranes ( sin and mucosae)
second
: antimicrobial proteins, phagocytes, & other cells<- inhibits the spread of invaders; inflammation
have
specific pathways
for certain substances (<- moves a specific way)
innate responses release
proteins that alert cells
of adaptive system to foreign molecules
adaptive (specific) defense system
third
: attacks particular foreign substances ( <- takes longer to react than innate )
First Line of Defense
:
surface barriers
surface barriers are
skin
and
mucous membranes
skin and mucous membrane produce productive chemicals that
inhibit or destroy microorganisms
:
Acid:
acidity of skin, and some mucous secretions
inhibits growth:
called acid mantle
Enzymes:
.lysozyme of saliva, respiratory mucus, and lacrimal fluid kills many microorganisms; enzymes in stomach
kill
many microorganisms
Mucin:
stick mucus that lines digestive and respiratory tract
traps
microorganisms
surface area breaches by nicks or cuts trigger the interal second internal line of defenses that protect deeper tissues
Second Line of Defense
:
cells and chemicals
if microorganisms
invade deeper tissue:
Phagocytes
Natural Killer (NK) cells
Inflammatory Response ( macrophages, mast cells WBCs, inflammatory chemicals )
Antimicrobial Proteins ( interferon and complement proteins )
Fever
cells have
pattern recognition receptors
: recognize and bind to structures-> disarming them before harm is done
Phagocytes
:
Phagocytes
: WBCs that ingest and digest foreign invaders
Neutrophils
: most abundant phagocytes, die fighting; become phagocytic on exposure to infectious material
Macrophages
: develop from monocytes and are chief phagocytic cells; most robust phagocytic cell
Natural Killer Cells (NK):
nonphagocytic, large granular lymphocytes that
police blood and lymph
attacks cells that lack self cell-surface receptors
kill by apoptosis in cancer cells and virus infected cells
secrete potent chemicals that enhance inflammatory response
Inflammation: Tissue Response to Injury
triggered whenever body tissues are injured
benefits of inflammation:
prevents spread of damaging agents
disposes of cell debris and pathogens
alerts adaptive immune system
set stage for repair
four cardinal signs of acute inflammation:
redness
heat
swelling
pain
Stages of Inflammation:
inflammatory chemical release
vasodilation and increased vascular permeability
phagocytes mobilization
inflammatory chemical release:
chemicals are released into ECF by injured tissues or immune cells
example: histamine released by mast cells is key inflammatory chemical
Chemicals
Histamine
: increases blood flow to injured area, increases permeability of local capillaries. induce pain
Kinins
: prompt neutrophils to release lysosmal enzymes. induce neutrophils chemotoxis
Prostaglandis
: induce pain
Second Line of Defense
:
Innate cellular and chemical defenses
Phagocytes
: engulf and destroy pathogens
Natural Killer (NK) cells
: promote apoptosis (cell suicide), attacking virus infected or cancerous body cells
Antimicrobial Proteins:
Interferons
: are released by virus infected cells, chemical messenger to protect uninfected tissue cells from viral takeover
Complement
: bloodborne proteins that, when activated, lyse microorganisms, enhance phagocytes by oponization
Fever
: initiated bu pyrogens; high body temp inhibits microbes
Imbalance of Immune System
Pus
: creamy yellow mixture of dead neutrophils, tissues/cells, and living/dead pathogens
abscess
: collagen fibers are laid down, walling off sac of pus; may need to be surgically drained
bacteria, such as
tuberculosis bacilli
, resist digestion by macrophages and remain alive inside
form tumor like growths called
granulomas
- area of infected macrophages surrounded by uninfected macrophages and outer capsule
Adaptive Defenses
function
: eliminates almost any pathogen or abnormal cell in body
Characteristics
of adaptive immunity:
Specific
: recognizes and targets specific antigens
Systemic
: not restricted to initial site
memory
: mounts an even stronger attack to "known" antigens (second and subsequent exposures)
Two branches:
1. Humoral (antibody mediated) immunity:
antibodies, produced by lymphocytes, circulate freely in body fluids
bind temporary to target cell <- mark for destruction
2. Cellular Immunity (cell mediated):
lymphocytes act against target cell
directly
: by killing infected cells
indirectly
: by releasing chemicals that enhance inflammatory response; or activating other lymphocytes or macrophages
Antigens
antigens
: substances that can mobilize adaptive defenses and provoke an immune response
targets of all adaptive immune responses
characteristics
of antigens:
can be a
complete
antigens or
hapten
(incomplete)
contain
antigentic determinants
can be
self antigen
Self- Antigens
:
MHC Proteins
self antigens
: all cells are
covered with variety of proteins
located on surface that are not antigenic to self; may be antigenic to others in transfusions or grafts
one set of important self-proteins are group of glycoproteins called
MHC Proteins
Lymphocytes and Antigen - Presenting Cells
3 crucial types of cells
two types
of lymphocytes
B lymphocyte (B cells) - humoral immunity
T lymphocytes (T cells) - cellular immunity
Antigen Presenting Cells (APCs)
do not respond to specific antigens
play essential auxillary roles in immunity
Lymphocytes
lymphocytes developments, maturation and activation
five general steps:
1. Origin
: both lymphocytes originate in red bone marrow
2. Maturation
Immunocompetence
: lymphocytes must be able to recognize only 1 specific antigen
self tolerance
: lymphocytes must be unresponsive
3. Seeding secondary lymphoid organs and circulation
immunocompetent B and T cells not yet exposed to antigen are called
naive
exposed from primary lymphoid organs (bone marrow and thymus) to seed (colonize)
secondary lymphoid organs
(lymph nodes, spleen)
4. Antigen encounter and activation
naive lymphocyte's first encounter with antigen triggers lymphocyte to develop further
lymphocyte is selected to differentiate into active cell by binding to its specific antigen
correct signals are present; lymphocyte will complete its differentiation into active cell
5. Proliferation and Differentiation
once selected and activated, lymphocyte proliferates
clones become effector cells that fight infectors
a few remain as
memory cells
B and T memory cells are effector T cells circulate continuously
Antigen Receptor diversity
genes, not antigens, determine which foreign substances the immune system will recognize
huge variety of receptors: gene segments are shuffled around, resulting in many substances
Lymphocyte Education during Maturation
T cells mature in thymus under negative and positive selection pressures ("tests")`
Antigen Presenting Cells (APCs)
3 major types:
dendritic cells:
act as mobile sentinels of boundary tissues
most effective antigen presenter known
key line between innate and adaptive immunity
macrophages:
widely distributed in CT and lymphoid organs
present antigens to T cells, which not only T cell, but further activates macrophage
B lymphocytes:
do not activate naive T cells
present antigens to helper T cell to assist their own activation
Humoral Immune Response
when b cells encounters target antigen, it provokes humoral immune response
antibodies specific for that particular antigen are the produced
Activation and Differentiation of B cells
Be cells are activated when antigens
bind to surface receptor,
cross linking them
triggers receptor - mediated endocytosis of cross-linked antigen receptor complexes (clonal selection), leading proliferation and differentiation of B cell into effector cells
most clone cells become
plasma cells
, antibody secreting effector cells
clone cells that
do not become plasma cells
become
memory cells
mount an immediate response to future exposures to same antigen
provide immunological memory
Immunological Memory
Primary immune response
cell proliferation and differentiation upon exposure to antigen for first time
lag period: 3 to 6 days
peak levels of plasma antibody are reached in 10 days
antibody levels then decline
Secondary immune response
re- exposure to same antigen gives faster, more prolonged more effective response
responds within hours, not days
antibody levels peak in 2 to 3 days at much higher levels
antibodies bind with greater affinity
antibody level can remain high for weeks to months
Active and Passive Humoral Immunity
active humoral immunity
occurs when B cells encounter antigens and produce specific antibodies against them
Naturally acquired
: formed in response to actual bacterial or viral infection
Artificially acquired:
formed in response to vaccine of dead or attenuated pathogens
passive humoral immunity
: occurs when ready made antibodies are introduced into body
Naturally acquired:
antibodies delivered to fetus
Artificially acquired:
injection of serum,
Antibodies
aka immunoglobulins, Igs: proteins secreted by plasma cells
basic antibody structure
T or Y shaped antibody monomer consists of four looping polypeptide chains linked by disulified bonds
four chains consist of:
two identica
l heavy (H) chains
with hinge region at middles
two identical
light (L) chains
variable (V) regions:
end of each arm combine to form two identical
antigen-binding sites
antibody classes
: IgM, IgA, IgG, and IgE
antibody targets and functions:
antibodies do not destroy antigens; they inactivate and tag them (<- form antigen- antibody (immune) response)
Defensive mechanisms used by antibodies
Neutralization
one of the most important mechanisms
antibodies block specific sites on viruses or bacterial explosions
prevent antigens from binding to receptors on tissue cells
antigen antibody complexes undergo phagocytosis
Agglutination
allows for antigen- antibody complexes to become cross linked into large lattic like clumps (process referred to as agglutination)
Precipitation
complexes precipitate out of solution
soluble molecules (instead of cells) are cross linked into complexes
precipitated complexes are easier for phagocytes to engulf
complement fixation and activation
main antibody defense against cellular antigens
when several antibodies are bound close together on same antigen, complement binding sites on their stem regions are aligned
Summary of antibody actions
antigen antibody complexes do not destroy antigens; they prepare them for destruction by innate defenses
antibodies go after extracellular pathogens; they do not invade solid tissue unless lesion is present
Cellular Immune Response
function: defense against intracellular antigens
some T cells directly kill cells; others release chemicals that regulate immune response
T cells are more complex than B cells both in classification and function
Two populations of T cells
CD4 cells
usually become helper T cells (Th) that can activate B cells, other T cells, and macrophages; direct adaptive immune response
some become regulatory T cells, which moderate immune response
CD8 cells
become cytotoxic T cells (Tc) that are capable of destroying cells harboring foreign antigen
can become memory T cells
Help, cytotoxic and regulatory T cells are activated T cells
Naive T cells are simply termed CD4 or CD8 cells
MHC Proteins and Antigen Presentation
T cells respond only to processed fragments of antigens displayed on surfaced of cells by major-histocompatibility complex (MHC) proteins
antigen presentation is vital for activation of naive T cells and normal functioning of effector T cells
Activation and Differentiation of T cells
T cells can be activated only when antigen is presented to them
Activation is a two step process
Step 1; Antigen Binding
T cell antigen receptor (TCRs) bind to antigen MHC complex on APC surface
TCR must recognize both MHC and foreign antigen it displays
binding of TCR to complex triggers multiple intracellular signaling pathways that start T cell activation
Step 2; Co- Stimulation
complete T cell activation requires T cell to bind to one or more co-stimulating signals on surface of APC
Profileration and Differentiation
T cells activated enlarge and proliferate in response to cytokines
primary T cell response peaks within a week
T cell apoptosis occurs between days 7 to 30
memory T cells remain and mediate secondary responses
Cytokines
chemical messengers of immune system
mediate cell development, differentiation, and responses
include interferons and interleukins
Roles of Specific Effector T cells
Helper T (Th) Cells
play central role in adaptive immune response
activate both humoral and cellular arms
once primed by APC presentation of antigen, helper T cells:
induce T and B cell profileration
help activate B cells and other T cells
secrete cytokines that recruit other immune cells
Without Th there is no immune system
Activation of B cells
helper T cells interact directly with B cells displaying antigen fragments bound to MHC IL receptors
stimulate B cells to divide more rapidly and begin antibody formation
Activation of CD8 Cells
CD8 cells require TH cell to become activated into destructive cytotoxic T cells
cause dendritic cells to express co stimulatory molecules required for CD8 cell activation
Amplification of innate defenses
amplify responses of innate immune system
activate macrophages leading to more potent killers
mobilize lymphocytes and macrophages and attract other types of WBCs
Cytotoxic T (Tc) cells
directly attack and kill other cells
activated Tc cells circulate in blood and lymphoid organs in search of body cells displaying antigen they recognize
activated Tc cells target
virus infected cells
cells with intracellular bacteria or parasites
cancer cells
foreign cells (transfusions or transplants)
cytotoxic T cells deliver lethal hit using two mechanisms
Tc cell releases perforins and granzymes
Tc cell binds specific membrane receptor on target cell and stimulate apoptosis
Regulatory T (TReg) cell
important in preventing autoimmune reactions
Organ Transplants and prevention of Rejection
success depends on similarity of tissues
After surgery
patient treated with immunosuppressive therapy
many of therapies have severe side effects
Immunodeficiencies
immunodeficiency:
congenital or acquired conditions that impair unction or production of immune cells or molecules
Severe combined immunodeficiency syndrome
(SCID):
genetic defect marked deficit in B and T cells
treatment:
bone marrow transplants
Hodge's disease
: an acquired immunodeficiency that causes cancer of B cells, which depresses lymph node cells and this leads to immunodeficiency
AIDS:
Human Immunodeficiency virus (HIV):
cripples immune sys by interfering with activity of helper T cells
Autoimmune Disease
autoimmune disease
: system loses ability to distinguish self from foreign
autoimmunity
: production of autoantibodies and sensitized Tc cells that destroys body tissues
Rheumatoid arthritis:
destroy joints
Myasthenia gravis:
impairs nerve muscle connections
Multiple sclerosis
: destroy white matter myelin
Grave's disease:
causes hyperthyroidism
Type 1 diabetes mellitus:
destroy pancreatic cells
Systemic Lupus erythematosus (SLE): affects multiple organs
Glomerulonephritis:
damages kidney
Treatments
: suppress entire immune system
Hypersensitivities
immune responses to perceived (otherwise harmless) threat that cause tissue damage
immediate hypersensitivity
aka acute (type 1) hypersensitivities (allergies); begin in seconds after contract with allergen, antigen causes allergic reaction
initial contact with allergen is asymptomatic but sensitivities person
activated in IgE against antigen binds to mast cells and basophils
later encounter with same allergen causes floor of histamine release from IgE result induced inflammatory response