7/31/2019 Immunology Lecture #2 (1)
1/19
53
2
Basic Concepts and Components of the
immune system
Amin Al-Baik
Ziad Al-Nasser
Monday, 4/7/2011
7/31/2019 Immunology Lecture #2 (1)
2/19
Lecture # 2, chapter 2
Date: Monday, 4/7/2011
Done by: Amin Al-Baik
Basic Concepts and Components of the immune system
Review for the first lecture ((Ch#1 mainly))
Everybody got the Idea about Immunology course, and yesterday we have startedtalking about some of the concepts and terminology that we have been using in the
science of Immunology.
We talked about Louis Pasteur (who created the first vaccine for rabies andanthrax)and the vaccination against rabies which give you thing that doesnt kil l
you, but makes you stronger.
and we talked aboutEdward Jenner who is considered as the father ofImmunology for his discovery of the vaccination against the smallpox; where he
noticed that shepherds, who got cowpox, they didnt get the smallpox, so he took
from the vesicles of cowpox (lesion has a fluid), he took from that fluid and injected
that to people, they expected to be getting the smallpox, but then they wereprotected.
I told you that vaccination starts with vaca which means (cows) in the Latinlanguage, so the terminology came from a cowpox vaccination byEdward Jenner,
and we started talking about the main divisions of our immune system and its
significance in defense; the nonspecific one = the innate , and the specific one = the
adaptive .
1
http://en.wikipedia.org/wiki/Vaccinehttp://en.wikipedia.org/wiki/Rabieshttp://en.wikipedia.org/wiki/Anthraxhttp://bword//!!09HMK27M2P,Jenner,%20Edward/http://bword//!!09HMK27M2P,Jenner,%20Edward/http://bword//!!09HMK27M2P,Jenner,%20Edward/http://bword//!!09HMK27M2P,Jenner,%20Edward/http://bword//!!09HMK27M2P,Jenner,%20Edward/http://bword//!!09HMK27M2P,Jenner,%20Edward/http://bword//!!09HMK27M2P,Jenner,%20Edward/http://en.wikipedia.org/wiki/Anthraxhttp://en.wikipedia.org/wiki/Rabieshttp://en.wikipedia.org/wiki/Vaccine7/31/2019 Immunology Lecture #2 (1)
3/19
And we said that:
1- The nonspecific (innate) is much faster, it is the one we are born with, (E.g physicalbarriers and mucus membranes), they make the bulk of the first line of defense. We
have the second line of defense, (e.g. serum and its constituents, WBC other than T
& b lymphocytes i.e. WBC which perform phagocytosis, and the complement
system), about cells (e.g. neutrophils, phagocytic cells, natural killer cells,
macrophages), all of them are nonspecific, and those cells can produce cytokines
which are components trigger the cells; they interact with each other, some are
upregulator (enhance) and some are downregulator (suppress).
2- Then we said on the other side about the specific of immune response, where wetalked about specificity, and we talked about memory at the same time, and we
talked about antigen-recognition moleculesreceptors and antigenic epitopes that
have to fit into those receptors, and we said that we were born with sets of
receptors on the surface of those T and B-cells, if those are there then we are
responders, and if they arent there then we are not responders.
So when we talk about T cells, B cells, major histocompatibility complex (MHC),
antibodies, memory cells, receptors and antigenic determinants (epitopes),
We talk about adaptive immune response
Then we talk about adaptive immune response, and we said also vaccination is theone of the successes of our immune system, and we will talk in details about it, andits program, and we will talk about transplantation, we have sometimes to
transplant a kidney or a cornea or even blood! , blood transfusion is considered as a
type of transplantation, and how we are going to keep that into perform the
function, so sometimes we need to suppress the immune system in order for our
body to accept that particular graft (the part which is transplanted), and also we
said that it is so important for you to understand the molecular interactions,
molecular reactions, biochemical pathways, which will take place, why?? Because if
any defect happened during that pathway, then we are going to have immune2
7/31/2019 Immunology Lecture #2 (1)
4/19
deficiency, or we can manipulate those by drugs to suppress the immune system. So
we said sometimes in hereditary diseases, the enzyme could be defective, and loss
enzymes expressed by genes, so in order to replace those genes we could do gene
therapy and we will talk about it later..
and some of the failureof the immune system other than immune suppression ,lack of these cells that we talked about, enzymes , genes and so on, sometimes our
immune system could go over reactive and this result in hypersensitivity or
Allergies; they could kill people; so we have to identify that, also we said one of the
major specific function of the adaptive immune system is to recognize self from
nonself, and we said this occurs in the major lymphoid organs, in the thymus gland,
and in the bone marrow, any defect in this normal process, then we will have
autoimmune disease , and these autoimmune diseases (e.g. systemic lupus
erythematosus, rheumatoid arthritis), they could lead to death, we will see how to
treat those later on.
For example look to this patient who hashepatitis B infection, it is chronic hepatitis
caused by Hepatitis B virus, and these patients
have jaundice. (Figure #1)
look to the *sclera here(figure #1), you can see
yellowish discoloration of the sclera. So, one of
the causes of jaundice is hepatitis B, and classical
causes of hepatitis , hepatitis A , hepatitis B ,
hepatitis C.
Hepatitis C is the mostserious one, it could infect the health care workers , and killsa lot of people all over the world, in USA it kills more than one MILLION every year,
they die by hepatitis.
*Sclera:
is a white fibrous membrane
which covers the eye.
3
7/31/2019 Immunology Lecture #2 (1)
5/19
We need to have precautions and vaccination, because some of the health care
workers could be infected when they are dealing with the patient with hepatitis,
and everybody who comes to the hospital should be vaccinated with Hepatitis B,
also hepatitis B could lead to liver failure , chronic hepatitis, hepatocellular
carcinoma and death, this disease is sexually transmitted disease. Also we talked
about influenza, and that its viruses are so evasive (they have ability to change their
antigenic structure), so we could be infected with one of them frequently, and there
is another example for the evasive viruses: Herpes Viruses which suppresses the
production of major histocompatibility antigens, which are the major role in
defense. However, Influenza could disguise with normal tissue covering itself with
mucus plug, so we should know all the pathogens, their evasive mechanism and our
counter measures to get rid of them. About influenza we told you that we use
upgraded vaccine every year.
This is the sneezing and cough, they are the wayby which we get rid of respiratory particles,
which next go into the air, floor, chair, and
hands, then you shake hands with someone,
and then pathogens will be transmitted to him
and so on, this is the droplet of transmission.
The most two important features of adaptive immune system are: specificityand memory. For example how we can modify our immune system in order to
increase the number of memory cells; then will be protected against these
organisms, and the classical example is the use of hepatitis B vaccination, we
give three doses (sometimes we give two doses), between the first and the
second dose there is a period of around one to two months, and the time
between the second and the third dose is four to six months, so we give morethan one dose, in order to increase number of memory cells.
4
7/31/2019 Immunology Lecture #2 (1)
6/19
the primary immune response is the response comes after first dose untilsecond dose, in this period the antigen will be recognized (recognitive phase),
the antigens bind through the receptors, the receptors through the clonal
selection theory, you must have cells that will develop into clones, the clones
will differentiate and proliferate increasing in number, and memory cells will
develop and immunoglobulins.
After second dose (secondary immune response), there is an increase in
immune response, and the period for the immune response to take place will
be much shorter i.e. it is faster, because memory cells have already developed.
And the type of the immunoglobulins that will develop is different, they are
with high affinity binding, so strong, neutralizing antibodies.
After third dose, the response will be much much higher, we will have huge
amount of immunoglobulins in few months.
The different between the primary and secondary immune response is that the
primary takes longer period of time ends up with development of memory
cells, but the secondary, the type of immunoglobulin of which is much better
than the primary, they last longer, and the binding of them is so strong (high
affinity), and we call the secondary immune response another name which is
anamnesia which is in contrast to amnesia, anamnesia is the reaction that
remembers, so develops memory cells.
this patient has renal failure (figure 1.8, p5, ch1) , and you know when kidneysfail, there is no way to recover it except to do kidney transplantation, and
kidney transplantation needs donor to give and the patient which is recipient,
and we must have tissue match, in order the recipient to accept the donors
kidney.
5
7/31/2019 Immunology Lecture #2 (1)
7/19
and the role of histocompatibility antigens , each of us has sets of haplotype, Iinherit half of genes from my father and half from my mother, this is called
dominant type of expression , and those genes are the ones that stimulate the
immune response and genes, and antigens which will respond immunologically
, so if we have the same setup genes , that means same antigens = no immune
response = graft will be accepted and vice versa, until now there is no way to
reach 100% match, so we are going to do suppression of the immune response
(by using immune suppressor drugs), so patient will accept graft, there is a lot
of organs to make transplantation , e.g. cornea transplantation is the most
successful types of transplantation .
There are some similarities anddifferences between adaptive and
innate immune response :
- Innate is non-specific andadaptive is very specific.
- Innate is fast (minutes), whileadaptive needs time to develop so
it is slow (days).
- Innate is without memory, unlike adaptive which is with memory.- The innate include natural killer phagocytes and secreted molecules; the
adaptive has lymphocytes (B & T cells) and also secreted molecules.
- There are few pattern-recognition molecules in the innate (they develop aspattern for group of antigens) like a polysaccharide, and there are many
Antigen-recognition molecules in the adaptive.
6
7/31/2019 Immunology Lecture #2 (1)
8/19
Chapter #2: Basic concepts and components of the immune system
About interactions between twoimmune systems look at the figurehere : > >
- You require Antigen-presenting cell(APC) for the specific immune
response or what we call thymus
dependant antigens. However, About APC E.g. dendritic cells, interdigitating
cells, B cells itself, and Macrophages could detect the antigens, process it andthen present it with class 1 and class 2 of MHC.
- This process (presenting & Processing antigens) is required for the B and Tlymphocytes to be activated, and requires complement chemotaxis and
phagocytic process I.e. we will see that 1st line, 2nd line ,3rd line of defense and
primary immune response all of those mechanisms will help each other in
order to make the defense.
- For example , if you get a bacterial infection , then those bacteria will be takenby the APC , it is processed and then presented to T and B cells, and you know
we have different types of T cells , and the most important one is T helper
(the main (or the orchestrating) cell in our immune system).
- CD4 cells, is the T cell which has CD4+ antigen. Note: Orchestra means:band composed of musicians of many different
instruments. and we said that about T helper cell coz it produces cytokines
which manipulate, activate, suppress, and regulate the rest of other T cells
or B cells, the B cell without the cytokines which produced by T helper cell
will not produce immunoglobulin as much as when the cytokines is present,
so the importance of the APC is for activation of T and B cells, and
production of immunoglobulin.
7
7/31/2019 Immunology Lecture #2 (1)
9/19
- We talked that, Immunoglobulins when they develop, this is what we callhumoralimmune response, and this is required for neutralizing viruses,
toxins and pass through the placenta... etc.
- sometimes we require to kill in cell , and this is what we call cell mediatedimmune response , if you have a viral infection for example , and the target
cell is infected , and the virus is inside the cell , so we need to activate T cells to
kill that virally infected cell.
- Part of cell-mediated immunity is done by adaptive immune response, and thecells which are involved we call it T cytotoxic cells, and the other part by the
innate we call them natural killer cells. The mechanism of the killing in both is
the same , but the difference comprise the recognition of the particles , i.e. the
T cytotoxic cells recognize particles by the receptors that present on the
surface of it , while natural killer cells do that by different mechanisms like
antibodies that are going to bind receptors.
- We will talk to you about the Major histocompatibility antigens and its majorrole, and the expression of those antigens on the surface of those cells will
determine whether T cytotoxic cells will take an action and kill or the natural
killer cells will do that, we can see that we have so many alternatives for
getting rid of invading micro-organisms.
- Again, there are similarities and differences between the innate and the adaptiveimmune response:
7/31/2019 Immunology Lecture #2 (1)
10/19
Innate immune response:-
The response time is fast. The pathogen (non-self) recognition mechanisms are few. There is no memory. There is no improvement, unlike the adaptive.Adaptive immune response:-
The response time is slow. The pathogen (non-self) recognition mechanisms are so many. It has memory. It has improvement by changing of the type of immunoglobulin that they will develop
and this development will change even a binding affinity.
Innate immune response
1. Phagocytosis and MBL(mannan binding lectin) of the C(complement) system whichis non specific, we will tell you more about that.
2. cells that are involved in non-specific :-a)Neutrophils : those are the major cells that are involved in Phagocytosis, they are
developed on daily basis , they have short half life ,they are present in huge number,
neutrophils live less than 24 hours, and then it will expire, they are called by process
called Chemotaxis, and chemotaxis require cytokines to be expressed or secreted, sothey (cytokines) will call those cells (neutrophils) to come in the area, mainly they are
called upon when I have bacterial type of infection, so when I see lots of neutrophils;
I know this is what we called pyogenic infection, when the process is finished they
turn to pus cells, they get expired by the act , and they have so many killing
mechanisms we will talk about them later.
b) Macrophages: they differ from neutrophils, Macrophages are larger, they last longer,
but they are not high efficient; coz their number is less, they can phagocyte once,
twice, and third. They dont expire by the act, unlike the neutrophils.c) Naturalkiller cells (NK): non- specific cells, they kill virally-infected cells and tumor
cells, and they are the main surveillance cells of our body, they keep circulating in
our body, I will tell u more how they kill later.
8
7/31/2019 Immunology Lecture #2 (1)
11/19
Morphologically, when we look to them under the microscope they look like
lymphocytes but the difference between NK cells and the lymphocytes that NK dont
have specific receptors against Antigens. In fact they are used to be large granular
lymphocytes, but in reality they are not granular: they are not lymphocytes, they look
like lymphocytes and they develop from the progenitor cell of lymphocytes.
Mechanism of killing: the initiation is difference, but the outcome is the same, both ofthem produce substances we call them cytotoxins and cytolysins that they will kill
virally infected cell, they kill the virally infected cell or the tumor cell by convincing
the cell to commit suicide we call that apoptosis.
3. Interferon: one of the most important cytokines produced from many cells. AlphaInterferon (), beta Interferon () and gammaInterferon (); gamma type is
produced from T-helper cell. Alpha from WBC, beta from tissue, and the interferons
provide protection of cells mainly against viral infection .they are excreted from cells
which are infected with viruses mainly and provide protection to others against viral
infection, I.e. the outcome is the destruction of the messenger RNA of the viruses.
So, remember that the Innate and the Adaptive immune response are interconnected
through the cytokines, they perform dual function, they help each other and they
work as a team.
Adaptive immune response
The adaptive Is specific , distinguishes self from non-self , it has Diversity of antigenrecognition molecules and so many genes that are produced so, this is why your
new response is different from mine ; it depends on the gene that you have inherited
from your parents and gene that I have inherited from my parents which is going to
determine the receptors on the surface of the lymphocytes so, if you have the same
receptors as the ones I do, then you will react the same, if you have more than me,
you will react better.
More genes you have inherited from your parents more lymphocyte cell surface
receptor more efficient reaction with antigen
The importance of diversity to you is to have more genes more receptorsmoredifferent cells than mine, to encounter all the different pathogens that we could be
exposed.- Which determines the diversity of genes is the inheritance of your parents.
the ones they have what we call Intersanguineous marriages ; if my
9
7/31/2019 Immunology Lecture #2 (1)
12/19
mother and father they are so related to each
other, then the types of genes that Im going
to get from my father and mother they are
going to be the same .they arent going to be
diverse as such compared if may mother and
father are not related to each other, then the polymorphism and the diversity, they
are going to be enormous So, I will have better chance of responding to pathogens
and foreign cells than the Intersanguineous marriages.
- Then always we said : (()) *We will keep talking about that when we cometo the genetics of immunoglobulin and
its diversity B-cell, T-cell receptor diversity.
Somatic mutation: the change that occurs at the binding site of that immunoglobulinand what we call a better fit of an immunoglobulin compared to a weak fit. The
nature of immunoglobulin will develop, so the somatic hypermutation occurs in the
secondary immune responsei.e. after primary immune response; cuz primaryresponse is just to recognize, and the mutation in secondary is for make the binding
sites better fit.
Receptors prior exposure to antigens: this is what I want you remember we haveborn with receptors on cells, those receptors do not develop when antigens enter
our body. I want u to remember this important information: receptors they arealready there, they are determined with set of genes that we inherit from our
parents, so when we are exposed to antigen; if you have the cells then interact, if you
do not have, they will not interact.
Receptors of antigen are determined by genes that we have inherited from our
parents, and arent determined by antigen that is going to enter our bodies"
Clonal expansion:will take place. This what we call clonal selection theory, we mean by clonal selection
theory that We are born with cells which have already receptors there, and the clone
that is selected is going to be activated, and proliferated.
Self receptors must be deleted or inactivated: why?? All the progenitor cells thatthey come from the bone marrow, they go to the thymes glandin order to develop
into what we call T-cells ( T from thymes) or in the bone marrow into B-cell (B frombone marrow), the main function to those progenitor cell to do into thymes gland ( T-
cell) or in the bone marrow (B-cell)is to get rid of the self reactive cells ; the cells that
are supposed to react against self antigen should be deleted . If this process fail for
*)) ((--
7/31/2019 Immunology Lecture #2 (1)
13/19
one reason or another we are going
to have an autoimmune phenomena.
I will tell u more about this autoimmune
diseases, and how they develop and
all the theories and what I mean by
tolerance, and how the tolerance is
broken out.
This is what I was talking about, you have
so many different B-cells we are born
with; with much different
specificities, i.e. in one cell we have
one type of specificity.
When we are exposed to non-self, so
non-self it has to find its match , if the
match is there, it is going to bind, this
is going to expand, this clone will
develop, proliferate and immune
response going to take place.
If non-self doesnt find the match, no immune response going to take place, and Im
considered as an immune compromised.
These are the antigen- recognition molecules and the specificity that is involved inadaptive immune response and in the innate immune response.
innate immune response: we dont have many genes that are involved, thats whywe dont have the specificity of the adaptive or specific immune response .
Ancestralgenemodern gene pattern recognition molecule
11
7/31/2019 Immunology Lecture #2 (1)
14/19
So, you can see on the surface of the macrophage a receptor, this receptor for so many
antigens at the same time, this what we call it pattern recognition molecule .for
example; antigen recognition molecule will recognize the lipopolysaccharides in all
gramvebacteria .
While in adaptive immune response, so many genes are involved that we inherit fromour parents , and those will be selected one at the type its so interesting, ones that
are selected one at the type will end up on the surface of those cells for the clonal
selection theory which we have talked about.
Ancestral genesgene duplicationmodern genespecializationantigen
recognition molecule.
major histocompatibility complex antigen : that will give u major histocompatibility
proteins, when we talk about major histocompatibility, we talk about class and class
; class :locus a , b and c ,and we have two allelic forms, that are present on every
cell in our body: ones come from father and the 2 nd come from mother so, if the
mother and father are related to each other , for example ; a1 from father and
mother has a1 as well we end up with a1, but if mother and father they are not related
a1 and a2 then I will have a1 and a2 at the same time .
A1 will look different than a2, so here the chance that Im going to have to be exposed
to a varietyofantigenic determinants will be much higher. So, these are we call
specificity that comes by inheritance.
again locus a ,b ,and c for class and d, r ,p and q for class and we require two; one
from the father and one from the mother, so will end up with 6 minimum ; when
mother and father are related to each other and have the same set of genes , and
maximum 12, if the mother and father are different completely I will be more diverse.
The mother gives 6 and the father gives six also, so we will have 12 if there arent any
similarities (considered as maximum), if they are related, then there will be some
similarities, and this will make it less than 12, i.e. may be 10, 8, and 6 as minimum
The same thing in the T- cell receptors and Immunoglobulins, I will tell you what arethe type of those genes that is going to make which types of proteins of
immunoglobulin or the T or B cell receptors, so genes will determine specificity, if
that gene is selected, that protein will appear on the surface of cell and that type of
immunoglobulin is going to be excreted.
The T-cell receptors on T-cells and Immunoglobulins of B-cells, all of them are calledAntigen recognition molecules. There is single antigenic determinant or epitope
which can be recognized by one of those T-cells, B-cells or immunoglobulin as we are
12
7/31/2019 Immunology Lecture #2 (1)
15/19
going to see. This in adaptive while in
innate there is pattern recognition
molecule for the whole group of
bacteria, and so on.
This is how self reaction could fail: ifyou have B-cells for example, by one of
the mechanisms manage to escape the
deletion in the bone marrow or the T-
cells in the thymes gland and they
managed as you can see here with
many different specificities depends on
the antigenic determinant that we
have, and if we have self antigen could
react here as you can see with the B-cells, and the B-cells are going to react and
produce immunoglobulins and those immunoglobulin will attack our own tissue
,complement could be activated and that tissue is going to be destroyed. They think
this is foe, and they are going to have autoimmune disease, this could happen, it is
this unusual; it is a disease; I will tell you how this will develop and how we prevent
that from taking place.
The component of our immune system
Very important points regarding the adaptive immune system:-
1. Specificity: I mean by that the antigenic determinants and receptors.2. Diversity: so many types, so many receptors, so many antigenic determinants that
we have talked about, immunoglobulins and MHC antigens.
3. Memory: second time is not like the first time.We are talking about cells specific and non-specific ,
1. Specific cells:-are T cell and B-cell.2. Non- specific: - we are talking about macrophages, neutrophils, eosinophils,
basophils, mast cells and NK cells, each one has a deferent function.
And we talked about soluble molecules like cytokines, for example for cytokines:
interleukin and interferon, they are soluble mediator that the cells utilize and interact
with each other, all of those cells and their function should be know all the cells I
have mentioned that they play a role in our immune defense.
Cell mediated immunity: - involvement of virally infected cell and tumor cell
E.g. T-cytotoxic and NK cells.
Humoral immune response antibody mediated cell:-
It is the immune response that uses immunoglobulins for defense, antibodies, B-celland Plasma cell that are involved. And remember here the notion of antigen
presenting cells ~APC~ and their function, and this is mainly for thymes dependent
13
7/31/2019 Immunology Lecture #2 (1)
16/19
antigens, the function of T-helper cells which will never accept to participate in the
game unless the antigen is presented to her by APC.
You should know what these APC are.
APC:
E.g. 1)
interd
igitati
ng cells, 2) macrophages 3) and B-cell itself has dual function.
And remember secondary immuneresponse and primary immuneresponse that we
have talked about, and why we use what we call it boosterdose; dose two and dose
three , sometimes we give more than that, for example in poliowe give 5 doses at 2
months ,4 months ,6 months , one in half year pre-school. The main reason why we
give booster dose is to increase the number of memory cells and to have a better fit,
andbetter functioning immunoglobulin.
If we give booster doses continuously, Our immune system will figure out that this is
not needed and instead of having and activation of immune response, our immune
system through the signals - we will talk about that later in the regulation of immune
response -will give a suppression signals to T-cells to stop doing that.
We can do that if I want to suppress the immune system. do you know the
hyposensitization which is used to treatment of allergies and hypersensitivities ??
what do we do in order to treat allergy if we are allergic to olive pollens ?. the idea is
not to be expose to the pollens of olives , but we cant do that if the patient live in
the area with a lot of pollens in the air. So, how Im going to get rid that permanently
once and for all; I will be exposed to the antigen of the olives pollen continuously so,
here patients body will realize that this is not needed so, start to produce
mechanism will tell u more that At the end, every time he will be exposed to olive
pollens, the suppression of the immune response is going to take place. This is the
idea why you should not give continuously booster doses.
This was studied how many booster doses I should be given in order to
have ultimate immune response that is going to protect me forever.
Cell meditated immunity: T cells which eliminate intracellular pathogens!
Humoral response: B cells (antibodies) which eliminate extracellular pathogens.
14
7/31/2019 Immunology Lecture #2 (1)
17/19
Cells of the Immune System
1. Innate :-Neutrophils 66%:-
They have granulocytes which have granules,
and these granules have enzymes like:
myloperoxidasis, I will tell you more about
those and how they get activated and how
they produce cytocidal, molecules. And
how they kill the bacteria and phagocyte.
Eosinophils 4% :-
We will see where eosinophils will be
produced, and which type of infections in
which we see eosinophils. Parasitic type
of infection and in allergies .
You know the percentage of eosinophils is 4%,
so if I see eosinophils go up to around 40%
then I know that I could be infected withparasite, or I could have allergy. The
granules that are produced by eosinophils are so important for neutralization of
vaso-active amines that are produced in allergies.
Macrophages:-
They are considered as Phagocyticcells and antigen presentingcells.
and Macrophages differ from neutrophils,
i. They dont get expired by Act.ii. They can phagocytose once , twice , third, in fact we see those sometimes when we
have immune complexes, if I have antigen antibody reactions, those immune
complexes could develop and precipitate in tissues , if this happened the
macrophages come and try to phagocytose immune complexes .If they are free in
serum, macrophages could phagocytose immune complexes and clear our bodies
from them, but if immune complexes bind into the tissues like basement membrane
of the kidney, so the macrophages come and try to phagocytose those and they
couldnt, bcz they are so adherent to the basement membrane of the kidney, what
the macrophages will do is to release vaso-active amines over the basement
15
7/31/2019 Immunology Lecture #2 (1)
18/19
membrane, and they cause damage to the basement membrane, we called those
frustrated macrophages.
And this is the damage that occurs to the
basement membrane, the joints and the
others; this is bcz of the phagocytes .for
example ; one smoker who have chronic
bronchitis why ?. bcz the carbon molecules
stimulate macrophages ,these
macrophages release their enzymes into
the cells , they damage the cilia , and
stimulate the mucus cells to produce
mucus and coughing and end up chronic
obstructive lung disease.
Mast cells:-
They are involved also in hypersensitivity types of reaction.
Natural killer (NK) cell:-
It is looks like a lymphocyte but they are large,
and have larger granular than lymphocytes,
and the NK cells involved in virally infected
cells tumor cells as well.
2. Adaptive :-T- helper cell or T cytotoxic all of them look the
same, and there are plasma cells that are
differentiated from B-cells but if u look at the
fig. down at these type of cells and what is
the outcome of their activation; if you have B-
cell and T-cell, morphologically they look the
same, so how we differentiate between B-celland T-cell if they are looking the same?? Based
on the antigenic marker that presents on
their surfaces:
16
7/31/2019 Immunology Lecture #2 (1)
19/19
B-cell: - have immunoglobulin on their surface IgM.
T-cell: - have CD4+ and CD8+ .
B-cell can be activated to change into plasma cell and then immunoglobulin will develop
.while T-cell if it is T-helper as you can see T-helper has CD4+ when gets activated
produces cytokines, thats why it is orchestrator cell .and if you look into the surfaceof the T-helper, there is one type of a receptor one shape wedont see 2 shapes in
one cell, this is the clonal selection theory.
And the T- cytotoxic cells has the same thing they have CD8+ as surface marker and I will
stop here.
17