Immunology | Immune System: Overview

Summary

This educational video offers a comprehensive overview of the human immune system, focusing on both innate and adaptive immunity. It explains the innate response to bacterial invasion, including inflammation and the release of cytokines, and delves into the adaptive response involving T and B cells, antigen presentation, and the production of antibodies. The video also touches on the roles of phagocytes, complement proteins, interferons, and the distinction between humoral and cell-mediated immunity.

Takeaways

• 😀 The innate immune system responds to damage caused by pathogens, such as bacteria, by releasing endotoxins and inflammatory cytokines.
• 🔥 Inflammatory cytokines cause vasodilation, increased permeability, and pain, leading to the cardinal signs of inflammation: swelling, pain, heat, and redness.
• 🚀 Histamines and other chemicals can increase the production of cell adhesion molecules, enhancing the margination response and allowing cells to migrate to the site of injury.
• 🌡️ Inflammatory cytokines like IL-1 and TNF-alpha can cause fever, produce C-reactive protein, and trigger leukocytosis, indicating active inflammation.
• 💊 Phagocytes, such as neutrophils and macrophages, play a crucial role in the innate immune response by engulfing and breaking down bacteria through phagocytosis and lysosomal action.
• 🔄 The complement system, activated by pathogens, undergoes cascades that enhance inflammation, promote opsonization, and initiate bacterial lysis.
• 🌐 Interferons, produced in response to viral infections, activate nearby cells to produce antiviral peptides and enhance the immune response against viruses.
• 🔬 Toll-like receptors (TLRs) recognize different types of pathogens and trigger the production of signaling proteins, interferons, and pro-inflammatory cytokines.
• 🌀 Adaptive immunity involves the presentation of antigens by macrophages and dendritic cells to T cells, leading to activation and proliferation of T and B cells.
• 💉 Humoral immunity is characterized by the production of antibodies by B cells in response to antigens, leading to neutralization, precipitation, lysis, and agglutination reactions.
• 🛡️ Cell-mediated immunity involves cytotoxic T cells that target and kill cells infected by viruses or cancer, utilizing mechanisms like perforin and granzymes to induce cell death.

Q & A

What is the primary function of the innate immune system?

The innate immune system acts as the first line of defense against pathogens, responding quickly to infections. It involves the release of inflammatory cytokines, which cause vasodilation, increased blood flow, heat, redness, and pain. It also triggers the production of cell adhesion molecules to enhance the margination response and the migration of immune cells to the site of injury.

What are the four cardinal signs of inflammation?

The four cardinal signs of inflammation are swelling, pain, heat, and redness. These are caused by the action of inflammatory cytokines on smooth muscle cells and endothelial cells, leading to vasodilation, increased permeability, and fluid leakage.

How do inflammatory cytokines like leukan 1 and leukan 6 affect the body?

Inflammatory cytokines like leukan 1 and leukan 6 can cause fever by acting on the hypothalamus, trigger the liver to produce C-reactive peptide (an indicator of active inflammation), and stimulate the bone marrow to produce more leukocytes through leukocytosis.

What is the role of phagocytes in the immune response?

Phagocytes, such as neutrophils and macrophages, play a crucial role in the immune response by engulfing and destroying pathogens through a process called phagocytosis. They also expose antigens on their cell membrane with MHC II molecules, which helps in the activation of the adaptive immune response.

What is the purpose of the complement system in the immune response?

The complement system enhances the immune response by undergoing specific cascades when activated. It helps in the lysis of bacteria through the membrane attack complex, enhances opsonization by C3b, and boosts the inflammatory response through C3a and C5a.

How do interferons contribute to the immune response?

Interferons, such as alpha, beta, and gamma, are produced in response to viral infections. They activate nearby healthy cells to produce antiviral peptides, enhance the activity of natural killer cells, and stimulate macrophages to proliferate and increase their expression of class I and class II molecules.

What is the role of toll-like receptors (TLRs) in the immune system?

Toll-like receptors (TLRs) are involved in recognizing different types of pathogens and initiating an immune response. They trigger the production of signaling proteins for chemotaxis, interferons, and pro-inflammatory cytokines, which enhance the inflammatory response and help eliminate foreign pathogens.

What is the process of antigen presentation in the adaptive immune system?

In the adaptive immune system, antigen-presenting cells like macrophages and dendritic cells present antigens to T cells in the lymph nodes. This process involves the binding of antigens to MHC II molecules, which are then recognized by T cell receptors (TCRs) on T helper cells, leading to their activation.

What are the key differences between humoral immunity and cell-mediated immunity?

Humoral immunity involves the production of antibodies by B cells in response to antigens, while cell-mediated immunity involves the action of cytotoxic T cells that target and kill cells infected by viruses or cancerous cells. Humoral immunity is primarily focused on neutralizing and eliminating extracellular pathogens, whereas cell-mediated immunity targets intracellular pathogens.

How do natural killer (NK) cells contribute to the immune response?

Natural killer (NK) cells are part of the innate immune system and contribute to the immune response by killing virus-infected cells and cells with abnormal MHC I molecules. They recognize the absence or abnormality of MHC I molecules and release perforin and granzymes to destroy the target cells.

Outlines

00:00

🛡️ Innate Immune System Overview

This paragraph introduces the innate immune system, focusing on its response to bacterial damage. Endotoxins released by bacteria trigger a massive release of inflammatory cytokines, leading to vasodilation, increased blood flow, heat, redness, and pain. Fluid leakage from blood vessels causes swelling and discomfort. The immune response also involves the production of cell adhesion molecules, enhancing the margination response and facilitating the migration of immune cells to the site of injury. Inflammatory cytokines like leukan 1, manic rhotic factor-alpha, and leukan 6 induce fever, liver production of C-reactive peptide, and increased leukocyte production. Phagocytes, such as neutrophils and macrophages, engage in phagocytosis, breaking down bacteria with lysosomal action. The complement system, activated by various pathways, enhances inflammation and promotes bacterial lysis or opsonization.

05:01

🌡️ Inflammatory Response and Adaptive Immunity

The second paragraph delves into the inflammatory response and the transition to adaptive immunity. It discusses the role of interferons in antiviral defense, where infected cells produce interferons that activate nearby healthy cells to produce antiviral peptides. Gamma interferons, secreted by immune cells like macrophages and natural killer cells, enhance the inflammatory response and activate other macrophages. The paragraph also covers the role of toll-like receptors in pathogen recognition and the production of signaling proteins that enhance chemotaxis and inflammation. The adaptive immune response is initiated when antigens are presented to lymphocytes in the lymph node, leading to activation and proliferation of B and T cells. Interleukins play a crucial role in this process, with interleukin 4 converting naive T cells into Th2 cells, which are essential for humoral immunity.

10:03

🧬 Humoral and Cell-Mediated Immunity

This paragraph explores the concepts of humoral and cell-mediated immunity. Humoral immunity involves B cells producing antibodies in response to antigens. These antibodies can neutralize, precipitate, lyse, or agglutinate foreign antigens, facilitating their removal. Memory B cells are also produced, which can quickly respond to future encounters with the same antigen. Cell-mediated immunity is primarily carried out by cytotoxic T cells, which target cells that have been infected by viruses or are cancerous. These T cells recognize and kill infected cells by releasing perforins and granzymes. Natural killer cells, part of the innate immune system, also contribute to cell-mediated immunity by killing cells that lack MHC class I molecules or display abnormal MHC molecules. The paragraph concludes with a comprehensive overview of the adaptive and innate immune systems.

Keywords

💡Innate Immune System

The innate immune system is the body's first line of defense against pathogens, providing a rapid, nonspecific response. It includes physical barriers, cells, and proteins that defend against a wide range of pathogens without the need for prior exposure. In the video, it is discussed how this system responds to damage caused by bacterial cells, releasing endotoxins and inflammatory cytokines, which trigger the cardinal signs of inflammation such as heat, redness, swelling, and pain.

💡Inflammatory Cytokines

Inflammatory cytokines are signaling proteins that mediate and regulate immune responses, particularly inflammation. They are mentioned in the script as being released in response to damage and causing various effects such as vasodilation, increased permeability, and pain. Examples from the script include the release of these cytokines leading to the cardinal signs of inflammation and the activation of fever in the hypothalamus.

💡Vasodilation

Vasodilation is the widening of blood vessels, which increases blood flow and is part of the body's inflammatory response. The script describes how inflammatory cytokines act on smooth muscle cells to cause vasodilation, leading to heat and redness at the site of injury or infection.

💡Phagocytosis

Phagocytosis is the process by which certain cells of the immune system, such as macrophages and neutrophils, engulf and destroy pathogens or debris. In the script, phagocytosis is explained as the action of phagocytes taking bacteria into their phagosomes, which then combine with lysosomes to break down the ingested material.

💡Complement System

The complement system is a part of the immune system that enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells, promotes inflammation, and attacks the pathogen's cell membrane. The script discusses how complement proteins, when activated, can enhance inflammation, promote opsonization, and lead to the lysis of bacteria.

💡Interferons

Interferons are proteins released by host cells in response to the presence of pathogens, such as viruses. They have antiviral activities and also regulate the immune response. The video script explains the role of alpha, beta, and gamma interferons in activating nearby cells to produce antiviral peptides and enhancing the inflammatory response.

💡Toll-Like Receptors (TLRs)

Toll-like receptors are a class of proteins that play a key role in the innate immune system by recognizing pathogen-associated molecular patterns. The script mentions that TLRs respond to different types of pathogens and result in the production of signaling proteins and cytokines that enhance the inflammatory response.

💡Adaptive Immunity

Adaptive immunity is a more specific and targeted immune response that involves the recognition of specific pathogens and the development of immunological memory. The video script describes how adaptive immunity involves the presentation of antigens by macrophages and dendritic cells to T cells, leading to the activation and proliferation of B cells and the production of antibodies.

💡Humoral Immunity

Humoral immunity is the aspect of adaptive immunity that involves the production of antibodies by B cells to neutralize or destroy pathogens. The script explains how B cells, upon activation, differentiate into plasma cells that produce antibodies, which can neutralize, precipitate, lyse, or agglutinate foreign antigens.

💡Cell-Mediated Immunity

Cell-mediated immunity is the aspect of adaptive immunity that involves T cells, particularly cytotoxic T cells, which can directly kill infected or cancerous cells. The script describes how cytotoxic T cells recognize cells with abnormal MHC class I expression or foreign peptides presented by MHC class I molecules and then kill these cells through the release of perforins and granzymes.

💡Natural Killer Cells

Natural killer (NK) cells are a type of lymphocyte that is part of the innate immune system and plays a role in defending the body against both tumor cells and virally infected cells. The script explains that NK cells can kill target cells by recognizing the absence or alteration of MHC class I molecules or the presence of foreign antigens bound by IgG antibodies, using mechanisms similar to cytotoxic T cells.

Highlights

The innate immune system's response to bacterial damage and endotoxins release, leading to inflammation.

Inflammatory cytokines' effects on smooth muscle cells causing vasodilation, heat, and redness.

Endothelial cells' contraction leading to increased permeability and pain due to fluid leakage.

The four cardinal signs of inflammation: swelling, pain, heat, and redness.

Chemokines' role in enhancing the margination response of white blood cells.

Phagocytosis process by phagocytes and the breakdown of bacteria within phagosomes.

Neutrophils' use of oxidative burst and release of chromatin for bacterial destruction.

Macrophages exposing antigens on the cell membrane with MHC II molecules.

Complement proteins' activation and their role in enhancing inflammation and pathogen destruction.

Interferons' production in response to viral infections and their antiviral activities.

Toll-like receptors' function in the innate immune system and their response to different pathogens.

Adaptive immunity involving antigen presentation by macrophages and activation of T cells.

The process of clonal expansion of B cells and their differentiation into memory or plasma cells.

Humoral immunity's role in producing antibodies in response to exogenous antigens.

Cell-mediated immunity involving cytotoxic T cells and their response to virally infected or cancerous cells.

Natural killer cells' mechanisms for identifying and killing abnormal or infected cells.

Overview of the innate and adaptive immune systems and their coordinated response to pathogens.

Transcripts

all right ninja nerds so the goal of

this video is to cover an entire

adaptive in an innate overview and again

I get a prize if I win if I do this

under 20 minutes so we're definitely

trying to make this kind of quick good

overview here so again starting with

innate immune system right with the

innate there was some type of damage

right because of this bacterial cell it

caused the release of endotoxins caused

what a massive release of inflammatory

cytokines right such as all of these

ones that we've already talked about

here what is the overall results of

these guys one thing that they're gonna

do is is they're gonna act on smooth

muscle cells and cause vasodilation

which increases the blood flow and

causes heat and redness they're also

gonna act on the endothelial cells cause

contraction right which is gonna cause a

lot of fluid to leak out increasing

permeability and a lot of fluid leaking

out can compress on the pain receptors

and variety kinase can activate Prine

pain receptors inducing pain and that

fluid exudate that leaks out can cause

swelling so that covers swelling pain

heat and redness which are the four

cardinal signs of inflammation right and

if there's a really really bad form of

inflammation like you burn your hand to

third-degree burn around your hand it

actually can cause a lot of inflammation

around this joint

to where you can't move it right it's

not your joint in mobility what else can

happen

these histamines and all these other

chemicals they can also cause the

production of certain types of cell

adhesion molecules and we've already

talked about these in great detail

there's no need to go over them again

these things could be like pee selectins

ISA lectins eye cams and v cams and what

is their whole purpose to enhance the

margination response in other words

cling to the edge of the capillary bed

and rolling on the surface right then as

it rolls it can move through the actual

endothelial cells by Dionysos which is

that amoeboid motion and then what i can

actually migrate to the site of injury

where all these bacterial molecules are

due to these inflammatory chemicals and

it's gonna move towards that area by

positive chemotaxis right so that's the

overall result there what else can

happen though a lot of these

inflammatory cytokines that's also being

released like

Lucan one to manic rhotic factor-alpha

and her Lucan six what can they do let's

follow it up here look what they can do

they can cause fever within the

hypothalamus right they can cause the

liver to produce C reactive peptide

which is a good indicator of active

inflammation and they can trigger the

bone marrow to make more leukocytes via

leukocytosis that's the entire

inflammatory response for the vascular

and some of the cellular effects right

so it's not that bad right now what else

can happen

well once these phagocytes get out here

into this area and they start fighting

with this bacteria what can be the

result phagocytosis they eat the

bacteria right so they take the bacteria

in through their pseudopods I'll just

call phagocytosis and remember they form

the phagosome combined with the lysosome

form the lysosome break them down

through the lysosomal action but

neutrophils sometimes depend upon how

intense the bacteria or form a microbe

may be it might have to do free radical

reactions called oxidative burst or

release it's chromatin out into the

extracellular space to tag bacterial

molecules for destruction from from like

for example cut deep Sanji what else can

happen the macrophages they can

phagocytose those actual bacteria and

actually what expose those antigens on

the cell membrane with MHC 2 molecules

major histocompatibility put complex

type 2 but remember all nucleated cells

all nucleated cells in your entire body

expressed what's called MHC 1 molecules

so that's important and we'll talk about

when we get to adaptive all right so

that's one mechanism there what else can

happen remember you also have complement

proteins your livers are constantly

making these complement proteins and

they're circulating within our plasma in

the inactive form and whenever they're

in the inactive form what can happen

whenever they actually act it they're

become activated due to certain types of

chemotaxis or due to the increased

permeability or due to the FC portion of

antibodies so on and so forth what

happens you activate these proteins and

they undergo specific Cascades like the

classical pathway which is antibody

mediated right so as to be antibody

meated then it starts with c1 and it

goes all the way to c9 producing c3 and

c5 a which enhance inflammation

alternative is not antibody meted it's

directly binding c3b with the foreign

pathogen and that caused that whole

process again right and then lectin you

just need a man''ôs and electon binding

Manos to trigger this entire cascade

what's the overall effect of these these

pathways right here to produce the

membrane attack complex to initiate a

lysis of the bacteria or to enhance

opsonization by the c3b

or to enhance the inflammatory response

to c3 a and C 5 a so that's the

complement system still in the innate

now what else we also said what if we

have these cells here are macrophages

are general tissue cells what if they're

infected by a virus so they're infected

by some type of viral molecules right if

they're infected by the virus so this is

these cells are infected by a virus what

can happen they can activate genes to

produce specific types of molecules

called interferons like alpha beta and

gamma

what do alpha and beta do they activate

what they come over here to a nearby

healthy cell and tell those nearby

healthy cells to produce antiviral

peptides for example protein kinase r

what does that do it actually destroys

the actual virus or prevents the virus

from attaching right and prevents this

virus from causing damage in these

tissue cells what does gamma interferons

do well the only one who really secrets

gamma interferon is because we have them

over here remember alpha and beta

interferons are produced by tons of

cells a lot of different cells beta

interferons are usually specific to

making platelets though a front they're

made by platelets right Gami

interference are made by specific types

of cells like your natural killer cells

your lymphocytes your macrophages

what are those gamma interferons do we

already showed it over here right these

gamma interferon x' is secreted by

macrophages or natural killer cells or

lymphocytes they come over activate

other macrophages and then do what

caused these macrophage to proliferate

get bigger get hungrier and increase the

expression of class 1 and class 2

molecules all designed to enhance the

inflammatory response right then what

else alpha and beta they can also cause

the activation of natural killer cells

who can come in and start killing some

of these virus infected cells so it's a

beautiful thing right and that is a part

of our innate immune system still now

lasting for our need immune system

we have these toll-like receptors in

these toll-like receptors we have 11

different types right so many different

types but there's 10 that we're only

talked about here because we don't know

the function of toll-like receptor 10

what is the overall result of all these

because they're all responding to

different types of pathogens the overall

result is the production of specific

types of signaling proteins for

chemotaxis right or the production of

interference like alpha beta and gamma

interference and the production of tumor

necrotic factor alpha interleukin-1 beta

and interleukin 18 and remember these

guys have to be acted on by caspases to

become in their active form because then

they're their preformed right now or

their proform what do all these guys do

they enhance the inflammatory response

enhance chemotaxis and tried to be able

to eliminate de foreign pathogens from

the body right that's the desire now

then we go into the adaptive immunity

what was the adaptive effect you

remember we took these macrophages with

the MHC 2 molecules and we also took

these free antigens and we take them

into a lymph node well what was the

effect here so again what do we do we

take this macrophage and we take these

free antigens and we bring them aside

lymph node right because we already went

through the phagocytosis process and we

know that the neutrophils exocytosed

what those free antigens the macrophages

are good antigen presenting cells those

as well as lymphocytes and specifically

antigen sorry dendritic cells they come

in and what happens let's see if we

follow the free antigens first the free

antigens are the exhaustion as antigens

bind onto a naive B lymphocyte

activating that by a B lymphocyte right

that B lymphocyte then can bring in the

receptor mediated endocytosis bring that

antigen in and produce MHC 2 molecules

against it right and expose it on the

membrane surface but that activated

lymphocyte which also has all these BCR

receptors specific to that antigen he

can't get stimulated to proliferate yet

why because he needs some type of

stimulation from other cells so what's

those other cells remember the

macrophage the macrophage is going to be

coming over here it's having its MHC 2

and the foreign antigen it brings it to

a naive T cell T helper cell right that

T helper cell will have cd4 positive

proteins it will have a TCR our t-cell

receptor

Pacific to that foreign antigen which

will interact when they interact it

activates a cd3 molecule which sends

this primary signal into the nucleus

there also be Kiko stimulation signals

between b7 and cd28 and then there also

be the secretion of interleukin 1 what

does this do interleukin 1 that third

signal will activate this T helper cell

to produce interleukin 2 and there also

be the production of interleukin 4 from

other cells which will bind onto this

actual T helper cell then what will

happen whenever this interleukin 4 and

interleukin 2 bind it triggers the T

naive cell to start proliferating and

becoming specialized and differentiating

into its called th 2 lymphocytes because

remember enter Lucan 4 converts the

naive T cell into th two interleukin 12

converts the naive T cell into th 1 or T

helper 1 cells so now our teach two

cells are activated they're ready to

start producing specific types of

interleukins what are those interleukins

one of them is interleukin 4 and our

Lucan 5 and interleukin 6 and then Lucan

4 is the very signal that these

activated lymphocytes need to start

proliferating what does that

proliferation called it's called clonal

expansion and you're making all these

b-cells with the BCR specific to that

foreign antigen that we've started with

this whole process they expand

interleukin 5 stimulates these actual

activated B cells to undergo

differentiation so again what does this

step right here called this is actually

differentiation so differentiation right

here will convert these actual b-cells

into memory cells or plasma cells memory

cells will stay in our body for awhile

right with that specific b-cell receptor

specific to any foreign antigen the

plasma cells will respond to interleukin

5 and interleukin 6 and they'll produce

antibodies and what will those

antibodies do these antibodies what can

either do a couple different things

right we talked about it very briefly

they can bind with these foreign

antigens and cause the neutralization

reactions precipitation reactions lysis

and we also set agglutination reactions

to right so there's a lot of different

opsonization will go into more detail on

those in antibodies right alright so

again they can undergo the opsonization

reactions right now that whole thing

that we talked about is humoral immunity

what is humoral immunity it's the effect

again one more time of those at

exogenous antigens stimulating these

actual b-cells or these t-cells and the

overall response is to produce

antibodies in response to that right or

to produce memory b-cells and we can

also produce memory t-cells I didn't

talk about those enough but again these

are effector T cells but you also can

make as a response to this whenever they

proliferate you also can make memory th2

cells and those memory th two cells will

have a TCR specific to that foreign

antigen alright

whenever the MHC molecule comes back MHC

two molecule in the foreign antigen on

the macrophage comes to him again he'll

be ready for it alright

that's humoral immunity what is cell

mediated immunity cell mediated immunity

is due to the it's going to be exerted

by this cytotoxic T cells and the

cytotoxic T cells they're gonna act on

cells that have already been virally

infected so they've been infected by a

virus and there's no turning back or

they're cancerous what's the overall

result again one is it can actually down

regulate the class 1 molecules or it can

produce the expression of a viral

peptide that combined with our own self

peptide and then what happens our t

cytotoxic T cells recognize those either

foreign peptides or they recognize the

lack of class war molecules as there's

not that many and then what will they do

they'll produce perfer ins which would

create holes in the membrane and

granzymes which initiates this a

pathetic mechanism that we talked about

right

so that's killing the cell why is it

cell mediated though because the actual

infectious pathogen is already inside of

the cell it's not outside of the cell

it's inside of the cell and it's

affected it inside of the cell okay

that's the basis way or the basic way of

understanding cell mediated immunity we

also talked about natural killer cells

but remember just because I included

them with the adaptive immune system

that doesn't mean they are a part of

them they are not a part of the adaptive

immune system they're a part of our

innate immune system they're not

specific but they're mechanism is very

similar to the cytotoxic T cells how

they do this what do they do there's

three rep mechanisms one is they either

recognize that there is no MHC one

molecules present and if there's no

class 1 molecules present they perceive

it as form because all nucleated cells

have class 1 molecules and then what

it'll produce perforin and granzymes and

kill the cell it'll also recognize an

abnormal form of the MHC molecule right

and again we said MHC molecules have

alpha 1 alpha 2 alpha 3 chains as well

as a beta 2 microglobulin mica has no

beta 2 microglobulin so therefore he's

kind of like an image see if he's

recognized but the natural killer cells

he'll actually really spur friends and

granzymes

and kill him and then again if there's

any type of foreign antigen with IgG

antibodies bound the natural killer

cells release parens and granzymes and

kill him

again guys this pretty much gives us

everything we're going to need to know

about the entire overview of what the

adaptive and the innate immune system

all right ninja nerds