Introduction to the immune system
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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

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Introduction to the immune system

Innate immunity

the “front line” of defense

non specific

Acquired immunity

mechanisms- antigen specificity

immunological memory

principles of vaccination

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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


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What does the immune system actually do?

Phagocytes- kill and remove foreign or

damaged cells

Antibodies- “tag” invading cells or viruses for


Cytotoxic cells- killed altered cells

Regulate the immune response

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What/where is the immune system?


Circulating blood cells

Tissue-fixed cells

Lymphatic system

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Cells with immune function (p. 378)



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

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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

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Where are the lymphoid cells?

In the blood

In the tissues

In the lymphoid system

Can be recruited to site of injury or infection

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The lymphoid system parallels the circulatory


Primary lymphoid organs- where lymphoid cells


bone marrow (ALL blood cells)

thymus- T cells mature there (become

cytotoxic or helper T cells) and then


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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

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Innate defenses

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




antimicrobial chemicals

lysozyme (in tears and saliva

stomach acid

oxygen metabolites

normal flora (“healthy competition”)

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If barrier is breached- then what?

Pattern recognition- something is perceived as


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

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Complement proteins- circulate in blood

Are normally inactive, but become active when

binding to antigen, or antigen-antibody


What happens next?

A series of reactions, resulting in:

destruction of antigen


enhanced phagocytosis of antigen

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Phagocytosis; how do the cells know whence to


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?

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Neutrophils are more potent killers, but die


Macrophages can present antigen; amplify

immune response

can prolong activity by regenerating


Both contribute to inflammatory response to

infection and/or damage

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What is the inflammatory process?

What triggers the inflammatory process?

What are the outcomes of inflammation?

What is apoptosis, and how does it prevent


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Inflammation is triggered by infection or injury

Purpose: to contain damage (and response)

repair damage

“Cardinal signs of inflammation”:

swelling, redness, heat, pain

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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

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Why heat?

Chemicals raise temperature at the spot


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


Pain inhibits mobility; can help localize


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Inflammation can cause a lot of “bystander


Ideally, damaged is confined to the site of injury

Some sites are more sensitive to damage than


Damage can be systemic (septic shock, due

to blood infections: loss of blood volume,

tissue damage, excess clot formation

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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?)

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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

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Adaptive immunity



Distinguishes self from non-self

Components of adaptive immunity:



Principles of vaccination

Immune deficiency and its consequences

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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

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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

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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

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p. 401

How antibodies work

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Clonal selection theory

In bone marrow

In the system

Applies to T cells, too (p. 403)

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Antibodies have certain features in common

but different classes (isotypes) have

different properties.

p. 398

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Variable region is unique, because each binds

to a different antigen

Constant regions fall into five classes

(table 16.1, p. 399)

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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

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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

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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:


dendritic cell

B cell

How do these cells present antigen (and where)?

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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


CD4 cells “see” antigen + MHC Class II

(helper T cells)

CD8 cells “see” antigen + MHC Class I

(cytotoxic T cells)

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What is MHC? (major histocompatibility


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)

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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

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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


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

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What do T cells actually do?

T helper cells- cytokine production

(Some are engaged in “delayed-type hypersen-


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

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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

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How DO immune cells avoid reacting with

self antigens?

Remember that T cells regulate the immune


Most self-reactive cells are eliminated in the


Antigen-presenting cells seem to be key

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APC: antigen presenting cell

Model of antigen presentation

Notice the APC has MHC Class

II and other molecules required

to present antigen

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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


What happens if it does not?

What happens if immune system is deficient?