Slide1 l.jpg
This presentation is the property of its rightful owner.
Sponsored Links
1 / 54

Introduction to the immune system Innate immunity the “front line” of defense non specific Acquired immunity mechanisms- antigen specificity PowerPoint PPT Presentation


  • 98 Views
  • Uploaded on
  • Presentation posted in: General

Introduction to the immune system Innate immunity the “front line” of defense non specific Acquired immunity mechanisms- antigen specificity immunological memory principles of vaccination. Important features of the immune system Must be able to distinguish foreign antigens from

Download Presentation

Introduction to the immune system Innate immunity the “front line” of defense non specific Acquired immunity mechanisms- antigen specificity

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -

Presentation Transcript


Slide1 l.jpg

Introduction to the immune system

Innate immunity

the “front line” of defense

non specific

Acquired immunity

mechanisms- antigen specificity

immunological memory

principles of vaccination


Slide2 l.jpg

Important features of the immune system

Must be able to distinguish foreign antigens from

self antigens (what is an antigen?)

Must have memory (responds slowly to first

exposure, but more rapidly to subsequent

exposures TO THE SAME ANTIGEN)


Slide3 l.jpg

What does the immune system actually do?

Phagocytes- kill and remove foreign or

damaged cells

Antibodies- “tag” invading cells or viruses for

destruction

Cytotoxic cells- killed altered cells

Regulate the immune response


Slide4 l.jpg

What/where is the immune system?

Barriers

Circulating blood cells

Tissue-fixed cells

Lymphatic system


Slide5 l.jpg

p. 375, physical barriers to infection


Slide6 l.jpg

p. 377, origin of lymphoid cells


Slide7 l.jpg

Cells with immune function (p. 378)

Granulocytes

Neutrophils

most common leukocyte (50-70%)

most potent phagocyte

Eosinophils (2-4%)

probably phagocytic

involved in allergic responses, parasitic infections

Basophils (0-1%)

mostly found in tissues (mast cells)

release inflammatory molecules


Slide8 l.jpg

Agranulocytes

Monocytes (5-10%)

more common in tissues

In tissues:

macrophages- phagocytes; help regulate

immune response (“antigen presenting cells”)

dendritic cells- present antigen to lymphocytes

Lymphocytes (20-40%)

B cells- make antibodies

T cells- some are cytotoxic, some are regulatory


Slide9 l.jpg

Where are the lymphoid cells?

In the blood

In the tissues

In the lymphoid system

Can be recruited to site of injury or infection


Slide10 l.jpg

p. 396, the lymphoid system


Slide11 l.jpg

The lymphoid system parallels the circulatory

system

Primary lymphoid organs- where lymphoid cells

develop

bone marrow (ALL blood cells)

thymus- T cells mature there (become

cytotoxic or helper T cells) and then

circulate


Slide12 l.jpg

Secondary lymphoid organs

Purpose: to trap antigen and present it to lymphocytes

Most lymphocytes actually reside in these tissues

Lymph nodes- “filter” antigen from lymph

Spleen- “filters” antigen from blood

Lymphoid tissue in mucosa, gut and skin


Slide13 l.jpg

Innate defenses

If they are “non-specific” how are they actually

activated-appropriately??

Barriers

skin

antimicrobial chemicals

lysozyme (in tears and saliva

stomach acid

oxygen metabolites

normal flora (“healthy competition”)


Slide14 l.jpg

If barrier is breached- then what?

Pattern recognition- something is perceived as

abnormal

Damaged tissue

Structures associated with bacteria (peptidoglycan,

LPS, etc.)

toll-like receptors on phagocytes, endothelial

cells- some recognizes viruses, too

Cell is then activated in response


Slide15 l.jpg

Toll-like receptors, p. 381


Slide16 l.jpg

Complement proteins- circulate in blood

Are normally inactive, but become active when

binding to antigen, or antigen-antibody

complexes

What happens next?

A series of reactions, resulting in:

destruction of antigen

inflammation

enhanced phagocytosis of antigen


Slide17 l.jpg

Complement system, p. 382


Slide18 l.jpg

Phagocytosis; how do the cells know whence to

engulf?

detectors of microbes and/or damaged cells

(pattern recognition)

response to cytokines (produced by damaged

cells and other immune cells

complement receptors

What happens in phagocytosis?


Slide19 l.jpg

Process of phagocytosis, p. 384


Slide20 l.jpg

Neutrophils are more potent killers, but die

quickly

Macrophages can present antigen; amplify

immune response

can prolong activity by regenerating

lysosomes

Both contribute to inflammatory response to

infection and/or damage


Slide21 l.jpg

What is the inflammatory process?

What triggers the inflammatory process?

What are the outcomes of inflammation?

What is apoptosis, and how does it prevent

inflammation?


Slide22 l.jpg

Inflammatory process, p. 387


Slide24 l.jpg

Inflammation is triggered by infection or injury

Purpose: to contain damage (and response)

repair damage

“Cardinal signs of inflammation”:

swelling, redness, heat, pain


Slide25 l.jpg

Why swelling?

Chemical signals are released by damaged tissue

Neutrophils, monocytes recruited to the site and

enter tissues

fluid enters tissues, too

Why redness?

Chemicals promote vasodilation

Blood vessel walls relax; more blood (and

therefore more blood cells) can be

brought to the region


Slide26 l.jpg

Why heat?

Chemicals raise temperature at the spot

(pyrogens)

Increased temperature kills microbes

phagocytes are more active

more cells are formed

Effect can be systemic (fever)

Why pain?

Chemicals effect free nerve endings (pain

receptors)

Pain inhibits mobility; can help localize

damage


Slide27 l.jpg

Inflammation can cause a lot of “bystander

damage”

Ideally, damaged is confined to the site of injury

Some sites are more sensitive to damage than

others

Damage can be systemic (septic shock, due

to blood infections: loss of blood volume,

tissue damage, excess clot formation


Slide28 l.jpg

Not all cell death causes inflammation

Apoptosis: programmed cell death

Under genetic control

(In immune response a large number of cells are

formed to fight the infection- what happens to

them after the infection is cleared?)


Slide30 l.jpg

Summary

Innate defense consists of barriers, phagocyte

surveillance, and mechanisms to detect

infection or damage

Inflammation is the first line response to infection

Lymphocytes may be activated during this process

which will respond more rapidly and inten-

sively to subsequent infections


Slide31 l.jpg

Adaptive immunity

Specificity

Memory

Distinguishes self from non-self

Components of adaptive immunity:

Humoral

Cell-mediated

Principles of vaccination

Immune deficiency and its consequences


Slide32 l.jpg

Adaptive immunity takes several days to

develop (to first exposure to antigen)

Cells proliferate

Antibodies are produced

Cytokines (signaling molecules) are produced

Meanwhile, innate mechanisms act

Adaptive mechanisms respond if infection has

not been eliminated


Slide33 l.jpg

What are the adaptive mechanisms?

Humoral immunity against “extracellular”

antigens (bacteria, free viruses,

toxins, etc.)

antibodies and other molecules

Cell-mediated against “intracellular” antigens

(virus-infected cells; tumor cells)

Responses are orchestrated by helper

T cells


Slide34 l.jpg

p. 395 (be sure to come back to this slide)


Slide35 l.jpg

How does humoral immunity work?

B cells proliferate (in lymphatic tissues) and

make antibodies

Antibodies circulate and bind to antigen

Neutralization; immobilization

Immune complexes

Facilitates phagocytosis

Facilitates complement-mediated lysis

B cells are activated clonally


Slide36 l.jpg

p. 401

How antibodies work


Slide37 l.jpg

Clonal selection theory

In bone marrow

In the system

Applies to T cells, too (p. 403)


Slide38 l.jpg

Antibodies have certain features in common

but different classes (isotypes) have

different properties.

p. 398


Slide39 l.jpg

Variable region is unique, because each binds

to a different antigen

Constant regions fall into five classes

(table 16.1, p. 399)


Slide41 l.jpg

What happens in the primary response that

leads to antibody production?

T cells respond to antigen; produce cytokines

These cause B cells to proliferate and become

plasma cells (antibody-producing cells)

They become more able to react with antigen

Class-switching (for appropriate response)

from IgM to IgA, IgG, IgE (unclear about IgD)

Memory cells- more of them; they respond faster

in subsequent responses


Slide42 l.jpg

p. 405


What about the memory cells l.jpg

What about the memory cells?

  • There are more of them in the circulation

  • Antigen specificity does not change

  • They have already gone through development so can become active right away (note the secondary response on previous slide)

  • Both T and B memory cells have been identified

  • Memory cells can live for years


Slide44 l.jpg

T cells also have an antigen-specific receptor

Receptor is NOT released

T cell must come in direct contact with antigen-

presenting cell

Major antigen-presenting cells:

macrophage

dendritic cell

B cell

How do these cells present antigen (and where)?


Slide45 l.jpg

What are the different types of T cells

CD4(helper) and CD8 (cytotoxic)

Both have antigen-specific receptors

CD4 and CD8 molecules help with antigen

presentation

CD4 cells “see” antigen + MHC Class II

(helper T cells)

CD8 cells “see” antigen + MHC Class I

(cytotoxic T cells)


Slide46 l.jpg

What is MHC? (major histocompatibility

complex)

Groups of cell- surface proteins, inherited

When cells process antigen they return fragments

(peptides) to the surface, bound to either

MHC Class I or Class II

MHC Class I is found on most cells

MHC Class II on antigen-presenting cells (and

levels can vary)


Slide47 l.jpg

How do cells present antigen?

Class II-bearing cells take up and “process” antigen,

then antigen is expressed on cell surface bound to

MHC Class II

Remember, only certain cell types express MHC

Class II- so not all cells can do this

Lots of antigen-presenting cells in lymphoid tissues!

Class I-bearing cells (remember, virtually all cells),

if infected or transformed, will express antigen bound

to MHC Class I


Slide48 l.jpg

When T cells are activated they proliferate

and produce cytokines

Dozens of cytokines have been identified

(and other cells can produce them, too)

Cytokines bind to neighboring cells and

activate them

Recall that immune response is characterized

by rapid proliferation and activation of

cells!

(And: you don’t want cells activated all the time)


Slide49 l.jpg

What do T cells actually do?

T helper cells- cytokine production

(Some are engaged in “delayed-type hypersen-

sitivity)

Cytotoxic T cells- cause apoptosis in targets

What about natural killer cells?

similar targets as CTLs

no antigen-specific receptor

no memory response

have antibody receptors

probably immune surveillance


Natural killer cells vs cytotoxic t cells l.jpg

Natural killer cells vs cytotoxic T cells

  • Natural killer cells part of innate immune system

  • Early protection against transformed cells or virus-infected cells (Same targets as cytotoxic T cells)

  • Cytotoxic T cells become activated if natural killer cells cannot eliminate these cells


Slide51 l.jpg

How DO immune cells avoid reacting with

self antigens?

Remember that T cells regulate the immune

response

Most self-reactive cells are eliminated in the

thymus

Antigen-presenting cells seem to be key


Slide52 l.jpg

APC: antigen presenting cell

Model of antigen presentation

Notice the APC has MHC Class

II and other molecules required

to present antigen


Slide53 l.jpg

Summary, p. 412


Slide54 l.jpg

Immune system responds to antigens that

enter body in course of infection

Vaccination: antigens are DELIBERATELY

introduced to body to generate a specific

immune response (and memory)

Immune system normally distinguishes “harmful”

antigens from self antigens or harmless

substances

What happens if it does not?

What happens if immune system is deficient?


  • Login