Type IV Hypersensitivity |T- Cell mediated Hypersensitivity |Mechanism | Examples
Summary
TLDRThis tutorial delves into type four hypersensitivity reactions, focusing on cell-mediated immunity. It explains how CD4+ T cells produce cytokines leading to chronic inflammation. The video outlines the pathogenesis of delayed-type hypersensitivity, highlighting T helper 1 and T helper 17 responses. It also covers clinical examples like tuberculin reactions and contact dermatitis, and discusses T cell-mediated cytotoxicity in diseases like type 1 diabetes and rheumatoid arthritis. The tutorial encourages active learning through practice tests on Visia, an engaging platform for medical knowledge.
Takeaways
- 𧬠Type Four Hypersensitivity, also known as cell-mediated hypersensitivity, is primarily caused by inflammation resulting from cytotoxic T cells.
- π¬ CD4 positive T cells produce cytokines that lead to chronic inflammation, often in response to environmental or self-antigens.
- π Delayed Type Hypersensitivity (DTH) is a prototype of T-cell mediated inflammation, detectable within 24 to 48 hours post-antigen exposure.
- π T helper 1 (Th1) and T helper 17 (Th17) cells are key contributors to DTH, with Th1 promoting macrophage activation and Th17 recruiting neutrophils.
- π‘ The pathogenesis of DTH involves the activation of CD4 positive T cells, differentiation into effector T cells, and resulting inflammation and tissue injury.
- π Upon re-exposure to an antigen, memory T cells, which are long-lived, respond quickly to prevent further inflammation.
- π Clinical examples of CD4 positive T cell-mediated inflammation include tuberculin reactions and contact dermatitis.
- π In persistent antigen scenarios, such as with Mycobacterium tuberculosis, T helper one cells can lead to granuloma formation, a hallmark of granulomatous inflammation.
- π¨ CD8 positive cytotoxic T lymphocytes kill antigen-expressing target cells through apoptosis, a key mechanism in cell-mediated immunity.
- π₯ Diseases mediated by T cell cytotoxicity include type 1 diabetes, graft rejection, and responses against viruses and tumor cells.
- π The script concludes with a summary of type four hypersensitivity, its mechanisms, and examples, encouraging active learning through practice tests and feedback on the Visia platform.
Q & A
What is type four hypersensitivity?
-Type four hypersensitivity, also known as cell-mediated hypersensitivity, is primarily caused by inflammation resulting from cytotoxic T cells, which are produced by CD4 positive T cells.
What are the main cells involved in type four hypersensitivity reactions?
-The main cells involved in type four hypersensitivity reactions are CD4 positive T cells, which produce cytokines leading to inflammation.
What type of inflammation is typically associated with type four hypersensitivity?
-Type four hypersensitivity is most often associated with chronic inflammation.
Which T helper cells contribute to delayed type hypersensitivity?
-T helper 1 (Th1) and T helper 17 (Th17) cells contribute to delayed type hypersensitivity.
What is the role of interferon gamma in T helper 1 cells?
-Interferon gamma, produced by T helper 1 cells, promotes further helper cell development and activates other immune cells, such as macrophages.
How do T helper 17 cells respond to extracellular pathogens?
-T helper 17 cells produce interleukin-17 and other cytokines and chemokines, which recruit more neutrophils and monocytes to promote inflammation against extracellular pathogens.
What happens to effector T cells after the inflammation is cleared?
-After the inflammation is cleared, effector T cells transform into memory T cells, which are long-lived and respond quickly to the same antigen if encountered again.
What are the clinical examples of CD4 positive T cell-mediated inflammatory reactions?
-Clinical examples of CD4 positive T cell-mediated inflammatory reactions include tuberculin reaction and contact dermatitis.
What is the difference between T helper 1 and T helper 17 in terms of the pathogens they target?
-T helper 1 cells target intracellular pathogens, such as some bacteria and viruses, while T helper 17 cells handle extracellular bacteria and fungi.
How do activated CD8 positive cytotoxic T lymphocytes kill target cells?
-Activated CD8 positive cytotoxic T lymphocytes kill target cells by inducing apoptosis, either through the Fas ligand and Fas receptor interaction or by forming a perforin and granzyme complex.
What are some diseases associated with T cell-mediated cytotoxicity?
-Diseases associated with T cell-mediated cytotoxicity include type 1 diabetes, graft rejection, reactions against various viruses, and destruction of some tumor cells.
Outlines
𧬠Immune System Diseases: Type Four Hypersensitivity
This paragraph introduces the seventh part of a pathology tutorial series focusing on the immune system, specifically type four hypersensitivity reactions. It explains that type four hypersensitivity, also known as cell-mediated hypersensitivity, is primarily caused by inflammation due to cytotoxic T cells, which are produced by CD4 positive T cells. The paragraph outlines the process of T cell activation, differentiation into T helper 1 and T helper 17 cells, and their roles in combating intracellular and extracellular pathogens, respectively. It also describes the pathogenesis of delayed type hypersensitivity, the transformation of effector T cells into memory T cells, and the quick response upon re-exposure to the same antigen.
π‘οΈ Clinical Manifestations of Type Four Hypersensitivity
The second paragraph delves into the clinical examples of CD4 positive T cell-mediated inflammatory reactions, such as tuberculin reaction and contact dermatitis. It describes the process of a tuberculin reaction, including the time frame of the reaction and the histopathological features observed. The paragraph also explains granuloma formation in response to persistent or non-degradable antigens, such as Mycobacterium tuberculosis. Contact dermatitis is highlighted as a tissue injury resulting from delayed hypersensitivity, with examples like poison ivy exposure leading to rash and blister formation. Other conditions related to CD4 positive T cell-mediated inflammation, such as rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, and psoriasis, are briefly mentioned.
π‘οΈ CD8 Positive T Cell-Mediated Cytotoxicity
The final paragraph discusses CD8 positive cytotoxic T lymphocytes and their role in killing antigen-expressing target cells through apoptosis. It outlines the mechanisms of cell death, including Fas ligand and Fas receptor interaction, as well as the perforin and granzyme complex. The paragraph provides examples of diseases where CD8 positive T cell-mediated cytotoxicity is observed, such as type 1 diabetes, graft rejection, reactions against various viruses, and destruction of tumor cells. It also revisits rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, and psoriasis, but from the perspective of cytotoxic T cell activity. The paragraph concludes with a call to action for viewers to engage with the content through multiple choice questions on the Visia platform and encourages feedback and subscription for further educational content.
Mindmap
Keywords
π‘Hypersensitivity Reactions
π‘Type Four Hypersensitivity
π‘Cytokines
π‘CD4 Positive T Cells
π‘Delayed Type Hypersensitivity
π‘T Helper 1 and T Helper 17 Cells
π‘Inflammation
π‘Antigen Presentation
π‘Memory T Cells
π‘Cytotoxic T Cells
π‘Autoimmune Diseases
Highlights
Introduction to the seventh part of the 'Diseases of the Immune System' series, focusing on type four hypersensitivity reactions.
Type four hypersensitivity, also known as cell-mediated hypersensitivity, is mainly caused by inflammation from cytotoxic T cells.
CD4 positive T cells produce cytokines leading to chronic inflammation in type four hypersensitivity.
Delayed type hypersensitivity is the prototype of T-cell mediated inflammation, detectable within 24 to 48 hours.
T helper 1 and T helper 17 cells contribute to delayed type hypersensitivity with distinct immune responses.
Pathogenesis of type four hypersensitivity involves activation of CD4 positive T cells and their differentiation into effector T cells.
Memory T cells, resulting from inflammation clearance, are long-lived and respond quickly to repeated antigen exposure.
Tuberculin reaction is a clinical example of type four hypersensitivity, characterized by induration and inflammation at the injection site.
Persistent non-degradable antigens like Mycobacterium tuberculosis can lead to granuloma formation in type four hypersensitivity.
Contact dermatitis is an example of tissue injury from delayed type hypersensitivity, often resulting in itchy rashes and blisters.
Examples of CD4 positive T cell mediated inflammation include rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, and psoriasis.
CD8 positive cytotoxic T lymphocytes kill antigen-expressing target cells through apoptosis in type one hypersensitivity.
Type 1 diabetes, graft rejection, and reactions against viruses are examples of diseases involving CD8 positive T cell-mediated cytotoxicity.
Rheumatoid arthritis involves antigens like collagen and results in chronic inflammation and joint deformity.
Multiple sclerosis is characterized by demyelination in the CNS and inflammation, leading to paralysis and optic neuritis.
Inflammatory bowel disease is an aggressive immune response to normal gut bacteria, resulting in chronic intestinal inflammation.
Psoriasis is a skin condition with unknown antigens that manifest as raised plaques.
The video concludes with a summary of type four hypersensitivity reactions, mechanisms, and examples.
Invitation to engage with the content through liking, commenting, subscribing, and sharing the video.
Transcripts
hello everyone welcome back to this
short tutorial from pathology M simple
at IOP pathology.com and supported by
visia an active learning platform this
is the part seven of diseases of immune
system in this section we will be
completing the hyper sensitivity
Reactions where I'll be discussing type
four hyper sensitivity in the earlier
sections we have completed type one type
two and type three so let's move on to
understand type four hyper sensitivity
reactions so type four hyper sensitivity
is also referred to as Hil mediated
hypers sensitivity which is caused
mainly by inflammation resulting from
cyto mines and these cyto are produced
by CD4 positive T cells and that's why
it's referred to as C T cell mediated
hyper sensitivity okay so it is these
CD4 positive T cells which produces cyto
kindes and that results in inflammation
most often the inflammation is chronic
and dist and the antigens uh implicated
in type four hypersensitivity can be
environmental antigens as well as self
antigens to understand more about C cell
mediated hypers sensitivity let's see
this delayed type hypers sensitivity
which is the Prototype of t- cell
mediated inflammation here what happens
you know there is a tissue reaction to
antigens when it is given to an immune
individual right and this tissue
reaction is detectable within 24 to 48
hours the cells which contribute to
delayed type of hypers sensitivity are T
helper 1 and T helper 17 cells T helper
one is a one which is dominated by
activated macres whereas T helper 17
response is dominated by neutrophils
unlike macrophases from tper one cells
so what is a pathogenesis as I told the
first step is the activation of CD4
positive t- cells remember t- cells will
be in Nave State they have to be
activated so activation of CD4 positive
t- cells and then these become effect
our T cells and then the second step is
the responses of these effector
differentiated effector t- cells and
finally resulting in inflammation and
tissue injury so let's understand this
in detail let us assume that this is a
Nave t- cell and you have an antigen
which to which these Nave T cells are
exposed the antigen presenting cells
that is the dritic cells presents
antigenic component you know to the
peptide from this antigen to the Nave T
Cell which produces inin 2 which is an
autocrine growth factor resulting in
more and more of these t- cells and now
these t- cells are antigen responsive t-
cells right so these antigen responsive
t cells further differentiate upon
reexposure to antigen one and these
antigen responsive te cells as I told
you they differentiate into T helper one
cells with the help of cyto interlukin
12 and these t- helper cells as I told
you they are the ones which act against
intracellular pathogens like some
bacteria viruses promoting inflammation
and also activating other immune cells
further these antigen responsive te
cells differentiate into tper 17 cells
with the help of cyto inin 1 6 and inin
23 produced by these antigen presenting
cells and these T helper 17 produces
interin 17 inin 22 and various other
chemokines and cytokines which recruit
more and more neutrophils and monocytes
which promote inflammation and this kind
of response is important while defending
extracellular bacteria and fungi right
so the T helper one tackles the
intracellular pathogens whereas T helper
17 handles these extracellular bacteria
T helper 1 also secretes lots and lots
of interferon GMA which promotes further
the helper cell development so this is
the basic pathogenesis of delayed type
hyper sensitivity once the inflammation
is cleared what happens the effect our T
cells they get transformed into memory T
cells and these memory t- cells are long
lived and they respond very quickly if
the same antigen is encountered again
and that's the role of these memory t-
cells let's see what happens when there
is repeat exposure to antigen so then
the T one secretes lots and lots of
interferon gamma you know which further
activates macrofagos and these
macrofagos are referred to as interferon
gamma activated macrophages are so what
special characteristics these macres
have and these are the ones which have
increased ability to phagocytose and
kill various pathogens they also Express
more and more class to Hy molecules on
the surface and that results in increase
in antigen presentation they secrete
tubon necrosis Factor interlukin one and
chemokines which further promote
inflammation and lastly they also
produce more incin 12 and we know inin
12 is responsible for amplification of e
one response okay more and more tper one
cells are recruited so what are the
clinical examples of CD4 positive t-
cell mediated inflammatory reactions two
most common examples are tucine reaction
and contact dermatitis let's see what
tubine reaction is after intracutaneous
injection of purified protein derivative
within 8 to 12 hours in the injected
site there is rening and in duration
which Peaks at around 24 to 72 hours
this is what happens that's the
enduration at the injection site of
purified protein derivative which is
speaking at around 24 to 72 hours it
finally subsides so if you take a biopsy
from this site what do you see the
histopathological features include
perivascular accumulation of mononuclear
inflammatory cells these are the
intradermal blood vessels and you find
lots of these mononuclear cells
lymphocytes and macro right that's
called as perivascular cuffing of
mononuclear inflammatory cells and you
also see variable amount of dermal edema
and fibrin deposition this is what you
see in a tuberculin reaction now
consider when there is a persistent or
non-degradable antigen for example you
know hubal baselite which is a
microbacterium tuberculosis which
colonizes lungs or other tissues so this
has this basill act as an antigen which
is non-degradable and persistent so
there is a very strong T helper one Cell
Activation right so once there is a t
helper one Cell Activation we know that
it recruits lots and lots of macres in
the initial phases these macras are just
not enough to tackle these tubic
baselite what do they do they get
transformed into epithelioid cells okay
they have more cytoplasm they have
elongated pale nucleus and these are
epithelioid cells and they cluster
together to form a granuloma okay so
this granuloma is surrounded by a cuff
of lymphocytes and this kind of
inflammation is known as granulo matus
inflammation I have discussed this in
detail when I talked about me granul
matus inflammation in my earlier videoos
so you can just go back and then watch
that video as well the second example
which you need to understand is contact
dermatitis which is an example of tissue
injury resulting from delayed type of
hyper sensitivity reaction which is a
CD4 positive T C mediated inflammation
one example you need to be aware is if
an individual is exposed to this poison
IV or poison o when when I say expose it
has to be in terms of contact contact
with poison IV or poison o these leaves
contain you know rool which is an
antigenic component which binds and
modifies the self proteins self proteins
means the proteins in our body and the
peptides which are released from these
modified proteins they are recognized by
CD4 positive T cells right and they
induce inflammatory response which is
clinically manifested by rash and these
rashes are often itchy and also result
in blister formation and that's why it's
referred to as blistering dermatitis or
vesicular dermatitis other examples of
CD4 positive T cell mediated
inflammation include romatoid arthritis
multiple sclerosis inflammatory bubble
disease till now what did we see we saw
CD4 positive T cell mediated
inflammation now there is another entity
which is called a cd8 positive P cell
mediated cytotoxicity now what does that
mean which means cd8 positive cytotoxic
T lymphocytes they kill the antigen
expressing target cells in in the
earlier cases what we studied there was
inflammation whereas in these cases we
see that the antigen expressing target
cells are killed so how are they killed
see after identifying the target cells
the activated cd8 positive cytotoxic T
lymphocytes they kill the target cells
by means of epopt Tois now how does this
happen let us see this see these
activated cd8 positive cells they
express fast liand which activate fast
receptor which is expressed on the
target cells and we know fast receptor
fast legant interaction is the one which
activates the extrinsic pathway of
apoptosis the second mechanism includes
formation of perforin and granzyme
complex so once this complex is formed
this enters into the cytoplasm and
within the cytoplasm of the target cell
the perforin you know they help in
release of the granzymes from the
complex and these granzymes CLE and
activate caspases which further result
in proptosis because we know caspases
are the most important proteases which
result in apoptosis so what are the
examples of CD positive t- cell mediated
cytotoxicity I mean where the cells are
killed the examples include the most
common one being type 1 diabetes it can
be graft Rejection it could be reaction
against various viruses and even
destruction of some tumor cells let us
see more examples of T cell mediated
diseases first one is rheumatoid
arthritis where the antigen involved is
the collagen or citrated self proteins
the manifestations include ch arthritis
and inflammation multiple sclerosis is
another disease where the antigens
involved are the protein antigens in
mine example milin basic protein what
happens here is that there is
demyelination in CNS central nervous
system with inflammation resulting in
paralysis and even optic neuritis type
one diabetes as I told you earlier where
the antigen involved are the antigens of
pancreatic highet beta cells okay and
inflammation of these cells result in
insulitis or chronic inflammation of
eyelets where they result in destruction
of beta cells leading to diabetes
inflammatory disease another condition
where the antigen involved is various
entric bacteria okay you know they
respond very aggressively to normal
entric bacter resulting in chronic
intestinal inflammation and the last but
not the least is psorasis where we do
not know what antigen is implicated but
they manifest with dtive plages in the
Skin So this completes type four hypers
sensitivity if you watch this entire
video I would request you to you know
just click on the link below in the
description as well as in the pin
comment where you can solve various
multiple choice questions from bolia I
have tried visia and this is an amazing
platform where you can learn very
actively because you have various
practice tests given you can even get
feedback ultimately it's fun to learn so
in summary we did learn about typ for
hypers sensitivity reaction the
mechanisms along with some examples
thank you for watching if you like this
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