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Dr. Muhammad Muqeem Mangi
Associate Professor, Physiology
Suleman Roshan Medical Medical College, Tando Adam, Sindh,
Pakistan
ALLERGY
HYPERSENSITIVITY
DELAYED REACTION
THE DELAYED REACTION ALLERGY APPEARED BY ACTIVATED T
– CELL
IN TOXIN OF POISON IVY IT ITSELF IS NOT POISON , DOEST NOT
GIVE ANY HARM .
BUT ON REPEATED EXPOSER IT DOES CAUSE THE ACTIVATION
OF HELPER AND CYTOTOXIC T CELLS
WITH CONTINUE EXPOSURE WTHIN A DAY THE ACTIVATED T
CELL ATTRACT AND DIFFUSE FROM CIRCULATION TO SKIN IN
HUGE NUMBER.
SUCH ACTIVATION CAUSES TO PRODUCE VERY LETHAL TOXIC
SUBSTANCES FROM T CELL AND ACTIVATED MACROPHAGES
DAMAGE OCCUR IN THE TISSUES
WHERE THE CAUSITIVE INSTIGATING
ANTIGEN IS PRESENT .
THE TISSUES THE SKIN OR LUNGS
CAUSES EDEMA AND ASTHMA
CONT DELAYED
REACTION
ATOPIC ALLERGIES
ASSOCIATED WITH
EXCESS IGE ANTIBODIES
THE PEOPLE WHO HAVE ALLERGIC TEDENCY
ARE CALLED ATOPIC ALERGY.
BCZ ITS NONORDINARY RESPONSE PASSING
GENETICALLY
FROM PARENTS TO CHILDRENS,
CHARACTERISED BY PRODUCING LARGE
QUANTITIES OF IgE ANTIBODIES IN THE
BLOOD.
THE ANTIBODIES ARE CALLED REAGINS OR
SENSITIZING ANTIBODIES
THESE REAGINS MEANS IgE ARE
DISTINGUISH THEM FROM THE
MORE COMMON IgG
WHEN AN ALLEGEN ENTER IN THE
BODY AN ALLERGEN- REAGIN
REACTION OCCUR
ANTIGEN REACT ALWAYS WITH
SPECIFIC TYPE OF IgE
CONT: ATOPIC ALLERGIES
ASSOCIATED WITH EXCESS IGE
ANTIBODIES
THESE IgE HAVE HABBIT TO ATTACH TO MAST
CELLS AND BASOPHIL.
A SINGLE MAST CELL AND BASOPHIL
ATTACHED OR BIND HALF A MILLION
MOLECULES OF IgE.
THIS CAUSES IMMEDIATE CHANGE IN THE
MEMBRANE OF CELLS DUE TO PHYSICAL
EFFECT OF ANTIBODIES TO DEFORM THE CELL
MEMBRANE .
MANY MAST AND BASOPHIL RUPTURE, AND
OTHER RELEASES SPECIAL AGENTS
CONT: ATOPIC ALLERGIES ASSOCIATED
WITH EXCESS IGE ANTIBODIES
THE SUBSTANCES RELEASES SOON
AFTER RUPTURING THE CELLS
HISTAMIN
PROTEASE
SLOW REACTING SUBSTANCES OF
ANAPHYLAXIS ( MIXTURE OF TOXIC
LEUKOTRIENES).
EOSINOPHIL AND NEUTROPHIL
CHEMOTACTIC SUBSTANCES
HEPARIN .
AND PALTELETS ACTIVATING FACTORS,
THESE CAUSES EFFECTS AS FOLLOW
CONT: ATOPIC ALLERGIES ASSOCIATED WITH
EXCESS IgE ANTIBODIES
THESE SUBSTANCES EFFECT TO CAUSE
DILATATION OF LOCAL BLOOD VESSELS.
ATTRACTION OF EOSINOPHIL AND NEUTROPHIL TO
REACTIVE SITE.
INCREASE PERMEABILITY OF THE CAPILLARIES
WITH LOSS OF FLUID INTO THE TISSUES:
AND CONTRACTION OF LOCAL SMMOTH MUSCLE
CELLS APPEAR.
SO THE SEVERAL DIFFERENT TISSUE RESPONSES
APPEAR .
DEPENDING THE TYPE OF TISSUE IN WHICH THE
CONT: ATOPIC ALLERGIES ASSOCIATED WITH
EXCESS IgE ANTIBODIES
Anaphylaxis
WHEN A SPECIFIC ALLERGEN INJECTED DIRECTLY
IN THE CIRCULATION
IT WILL REACT WITH MAST CELLS AND BASOPHIL
CELL IMMEDIATELY OUTSIDE BLOOD VESSELS
WIDESPREAD REACTION OCCUR THROUGH OUT
THE VASCULAR SYSTEM
THIS REACTION IS CALLED ANAPHYLAXIS
SOME TIME CAUSES DEATH DUE TO SUFFOCATION
, APPEAR DUE TO LEUKOTIENS SUBSTANCES AND
SLOW REACTING SUBSTANCES OF ANAPHYLAXIS
CAUSES SPASM OF SMOOTH MUSLES OF
BRONCHIOLES,
UTRICARIA
ITS REACTION OF ANTIGEN IN THE SKIN
MEANS LOCALIZE REACTION OCCUR
BY RELEASING HISTAMIN
IT CAUSES VASODILATION THAT INDUCE AN
IMMEDIATE RED FLARE AND,
INCREASE LOCAL PERMEABILITY OF THE
CAPILLARIES THAT LEADS TO SWELLING OF
THE AREAS OF THE SKIN WITHIN A MINUTE
THE SWELLING ARE CALLED HIVES
HAY FEVER
THIS FEVER APPEAR DUE TO REACTION OF
ALLEGEN –REAGIN IN THE NOSE
IN RESPONSE OF REACTION HISTAMINE RELEASED
CAUSES
LOCAL INTRNASAL VASCULAR DILATION WITH
INCREASE CAPILLARY PRESSURE AND INCREASE
PEMEABILITY
BOTH EFFECTS CAUSE RAPID FLUIED LEAKAGE, IN
NOSE AND DEEPER TISSUES OF NOSE .
OTHER ALLERGEN – REAGIN REACTION
SECRETION ALSO CAUSES IRRITATION OF NOSE ,
ASTHMA
ITS ALSO MENIFEST IN ALLERGIC PERSON
THE ALLEGEN-REAGIN REACTION OCCURS
IN BRONCHIOLES OF THE LUNGS
HERE AN IMPORTANT PRODUCT RELEASE
FROM MAST CELLS THAT MAY BELIEVE TO
BE SLOW REACTING SUBSTANCE OF
ANAPHYLAXIS
WHICH CAUSES SPASM OF BRONCHIOLAR
SMOOTH MUSCLE
UNTIL EFFECTS REMAIN OF REACTIVE
PRODUCT
The term allergy was originally defined by Clemens Von Pirquet as “an
altered capacity of the body to react to a foreign substance,” which was
an extremely broad definition that included all immunological
reactions.
Allergy is now defined in a much more restricted manner as “disease
following a response by the immune system to an otherwise harmless
antigen.” Allergy is one of a class of immune system responses that are
termed hypersensitivity reactions. These are harmful immune responses
that produce tissue injury and may cause serious disease.
Hypersensitivity reactions were classified into four types by Coombs
and Gell
Allergy is often equated with type I hypersensitivity (immediate-type
hypersensitivity reactions mediated by IgE),
and will be used in this sense here.
Allergy
Undesirable reactions produced by the
normal immune system.
Hypersensitivity is an exaggerated immune
response that results in tissue damage and is
manifested in the individual on a second or
subsequent contact with anantigen.
Hypersensitivity reactions can be classified as either
immediate or delayed. Clearly immediate reactions
appear faster than delayed ones, but the main
difference between them is the nature of the immune
response to the antigen.
Allergy
Allergies, also known as allergic diseases, are a
number of conditions caused by hypersensitivity
of the immune system to something in the
environment that usual y causes little or no
problem in most people.
These diseases include hay fever, food all ergies,
atopic dermatitis, allergic asthma, and anaphylaxis
.
Symptoms may include red eyes, an itchy
rash, runny nose, shortness of breath, or
swelling.
General Features
1.Hypersensitivity reactions can be elicited by
exogenous environmental antigens or
endogenous self antigens.
2.Results from failure of normal regulation of
immune response.
3.Development of hypersensitivity diseases is
often associated with the inheritance of
particular susceptibility genes.
Types Of Hypersensitivity: reactions are
divided according to mechanism of action
into four groups:
1-Type I (Immediate hypersensitivity).
2-Type II (Cytotoxic hypersensitivity).
3 Type III (Immune complexhypersensitivity).
4Type IV (Cell -mediated or Delayed hypersensitivity).
5-Type V(Stimulatory Type) Jones-Mote Reaction (or)
Cutaneous Basophil Hypersensitivity
A type I hypersensitive reaction is induced by
certain types of antigens referred to as allergens,
and has all the hall marks of a normal humoral
response. Allergic reactions occur when an
individual who has produced IgE antibody in
response to an innocuous antigen (allergen)
subsequently encounters the same allergen. Type
I, or anaphylactic, reactions often occur within 2
to 30 minutes after a person sensitized to an
antigen is re-exposed to that antigen.
Type I Hypersensitivity (IgE DEPENDENT)
Type II Hypersensitivity
(Cytolysis And Cytotoxic).
These reactions involve a combination of IgG (or IgM)
antibodies with an antigenic determinants on the surface of
cells.
Antibody can activate the complement system, creating
pores in the membrane of a foreign cell, or it can mediate
cell destruction by antibody dependent cell - mediated
cytotoxicity (ADCC).
Type II hypersensitivity is general y, called cytolytic or
cytotoxic reactions because it results in the destruction of
host cells,
either by lysis or toxic mediators. Type II hypersensitive
reactions involve antibody-mediated destruction of cells
Type II hypersensitivity
Type III Hypersensitivity—Immune
Complex- Mediated
Type III reactions involve antibodies against
soluble antigens circulating in the serum.
The antigen-antibody complexes are
deposited in organs and cause inflammatory
damage. The tissue damage that results
from the deposition of immune complexes
is caused by the activation of complement,
platelets and phagocytes; in essence, an
acute inflammatoryresponse
Immune complex-mediated hypersensitivity. (1) Immune complexes on the basement
membrane of the wall of a blood vessel, where they; (2) activate complement and
attract inflammatory cells such as neutrophils to the site. (3) The neutrophilis discharge
enzymes as they react with the immune complexes, resulting in damage to tissue cells
Type IV Hypersensitivity—Delayed
Hypersensitivity Type IV hypersensitivity reactions
(delayed hypersensitivity) constitute one aspect of
cell-mediated immune response and are caused
mainly by T cells. These are typically provoked by
intracellular microbial infections or haptens like
simple chemicals applied on the skin, evolve slowly
and consist of a mixed cellular reaction involving
lymphocytes and macrophages in particular. It is
named delayed hypersensitivity because it appears in
24 to 48 hours after the presensitized host
encounters the antigen, while immediate
hypersensitivity reactions develop in 1/2 to 12
hours..
A major factor in the delay is the time required for the
participating T cells and macrophages to migrate to and
accumulate near the foreign antigens. The T cells
involved in delayed type hypersensitivity reactions are
primarily TD cells. In some types of hypersensitivities
resulting in tissue damage, Tc cells may also participate
CONT: Type IV Hypersensitivity—
Delayed Hypersensitivity Type IV
hypersensitivity reactions (delayed
hypersensitivity)
Type IV (delayed or cell -mediated) hypersensitivity
This is anantibody-mediated hypersensitivity and is a
modification of type I hypersensitivity reaction.
Antibodies interact with antigens on cell surface which leads to
cell proliferation and differentiation instead of inhibition
or killing. Antigen-antibody reaction enhances the activity of
affected cell.
Example of Grave’s disease: Thyroid hormones are produced in excess
quantity in grave’s disease. Long acting thyroid stimulating (LATS)
antibody is an autoantibody to thyroid membrane antigen. It is
presumed that LATS combines with a TSHreceptor on thyroid cell
surface and brings about the the same effect as TSH resulting in
excessive secretion of thyroidhormone.
Type V: Hypersensitivity (Stimulatory Type) Jones-Mote
Reaction(or) Cutaneous Basophil Hypersensitivity
Thank
You
Histamin
e
Thank
You
Histamin
e
Thank
You
Histamin
e

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Hypersensitivty & allergy

  • 1.
  • 2. Dr. Muhammad Muqeem Mangi Associate Professor, Physiology Suleman Roshan Medical Medical College, Tando Adam, Sindh, Pakistan ALLERGY HYPERSENSITIVITY
  • 3. DELAYED REACTION THE DELAYED REACTION ALLERGY APPEARED BY ACTIVATED T – CELL IN TOXIN OF POISON IVY IT ITSELF IS NOT POISON , DOEST NOT GIVE ANY HARM . BUT ON REPEATED EXPOSER IT DOES CAUSE THE ACTIVATION OF HELPER AND CYTOTOXIC T CELLS WITH CONTINUE EXPOSURE WTHIN A DAY THE ACTIVATED T CELL ATTRACT AND DIFFUSE FROM CIRCULATION TO SKIN IN HUGE NUMBER. SUCH ACTIVATION CAUSES TO PRODUCE VERY LETHAL TOXIC SUBSTANCES FROM T CELL AND ACTIVATED MACROPHAGES
  • 4. DAMAGE OCCUR IN THE TISSUES WHERE THE CAUSITIVE INSTIGATING ANTIGEN IS PRESENT . THE TISSUES THE SKIN OR LUNGS CAUSES EDEMA AND ASTHMA CONT DELAYED REACTION
  • 5. ATOPIC ALLERGIES ASSOCIATED WITH EXCESS IGE ANTIBODIES THE PEOPLE WHO HAVE ALLERGIC TEDENCY ARE CALLED ATOPIC ALERGY. BCZ ITS NONORDINARY RESPONSE PASSING GENETICALLY FROM PARENTS TO CHILDRENS, CHARACTERISED BY PRODUCING LARGE QUANTITIES OF IgE ANTIBODIES IN THE BLOOD. THE ANTIBODIES ARE CALLED REAGINS OR SENSITIZING ANTIBODIES
  • 6. THESE REAGINS MEANS IgE ARE DISTINGUISH THEM FROM THE MORE COMMON IgG WHEN AN ALLEGEN ENTER IN THE BODY AN ALLERGEN- REAGIN REACTION OCCUR ANTIGEN REACT ALWAYS WITH SPECIFIC TYPE OF IgE CONT: ATOPIC ALLERGIES ASSOCIATED WITH EXCESS IGE ANTIBODIES
  • 7. THESE IgE HAVE HABBIT TO ATTACH TO MAST CELLS AND BASOPHIL. A SINGLE MAST CELL AND BASOPHIL ATTACHED OR BIND HALF A MILLION MOLECULES OF IgE. THIS CAUSES IMMEDIATE CHANGE IN THE MEMBRANE OF CELLS DUE TO PHYSICAL EFFECT OF ANTIBODIES TO DEFORM THE CELL MEMBRANE . MANY MAST AND BASOPHIL RUPTURE, AND OTHER RELEASES SPECIAL AGENTS CONT: ATOPIC ALLERGIES ASSOCIATED WITH EXCESS IGE ANTIBODIES
  • 8. THE SUBSTANCES RELEASES SOON AFTER RUPTURING THE CELLS HISTAMIN PROTEASE SLOW REACTING SUBSTANCES OF ANAPHYLAXIS ( MIXTURE OF TOXIC LEUKOTRIENES). EOSINOPHIL AND NEUTROPHIL CHEMOTACTIC SUBSTANCES HEPARIN . AND PALTELETS ACTIVATING FACTORS, THESE CAUSES EFFECTS AS FOLLOW CONT: ATOPIC ALLERGIES ASSOCIATED WITH EXCESS IgE ANTIBODIES
  • 9. THESE SUBSTANCES EFFECT TO CAUSE DILATATION OF LOCAL BLOOD VESSELS. ATTRACTION OF EOSINOPHIL AND NEUTROPHIL TO REACTIVE SITE. INCREASE PERMEABILITY OF THE CAPILLARIES WITH LOSS OF FLUID INTO THE TISSUES: AND CONTRACTION OF LOCAL SMMOTH MUSCLE CELLS APPEAR. SO THE SEVERAL DIFFERENT TISSUE RESPONSES APPEAR . DEPENDING THE TYPE OF TISSUE IN WHICH THE CONT: ATOPIC ALLERGIES ASSOCIATED WITH EXCESS IgE ANTIBODIES
  • 10. Anaphylaxis WHEN A SPECIFIC ALLERGEN INJECTED DIRECTLY IN THE CIRCULATION IT WILL REACT WITH MAST CELLS AND BASOPHIL CELL IMMEDIATELY OUTSIDE BLOOD VESSELS WIDESPREAD REACTION OCCUR THROUGH OUT THE VASCULAR SYSTEM THIS REACTION IS CALLED ANAPHYLAXIS SOME TIME CAUSES DEATH DUE TO SUFFOCATION , APPEAR DUE TO LEUKOTIENS SUBSTANCES AND SLOW REACTING SUBSTANCES OF ANAPHYLAXIS CAUSES SPASM OF SMOOTH MUSLES OF BRONCHIOLES,
  • 11.
  • 12.
  • 13. UTRICARIA ITS REACTION OF ANTIGEN IN THE SKIN MEANS LOCALIZE REACTION OCCUR BY RELEASING HISTAMIN IT CAUSES VASODILATION THAT INDUCE AN IMMEDIATE RED FLARE AND, INCREASE LOCAL PERMEABILITY OF THE CAPILLARIES THAT LEADS TO SWELLING OF THE AREAS OF THE SKIN WITHIN A MINUTE THE SWELLING ARE CALLED HIVES
  • 14.
  • 15. HAY FEVER THIS FEVER APPEAR DUE TO REACTION OF ALLEGEN –REAGIN IN THE NOSE IN RESPONSE OF REACTION HISTAMINE RELEASED CAUSES LOCAL INTRNASAL VASCULAR DILATION WITH INCREASE CAPILLARY PRESSURE AND INCREASE PEMEABILITY BOTH EFFECTS CAUSE RAPID FLUIED LEAKAGE, IN NOSE AND DEEPER TISSUES OF NOSE . OTHER ALLERGEN – REAGIN REACTION SECRETION ALSO CAUSES IRRITATION OF NOSE ,
  • 16.
  • 17. ASTHMA ITS ALSO MENIFEST IN ALLERGIC PERSON THE ALLEGEN-REAGIN REACTION OCCURS IN BRONCHIOLES OF THE LUNGS HERE AN IMPORTANT PRODUCT RELEASE FROM MAST CELLS THAT MAY BELIEVE TO BE SLOW REACTING SUBSTANCE OF ANAPHYLAXIS WHICH CAUSES SPASM OF BRONCHIOLAR SMOOTH MUSCLE UNTIL EFFECTS REMAIN OF REACTIVE PRODUCT
  • 18.
  • 19. The term allergy was originally defined by Clemens Von Pirquet as “an altered capacity of the body to react to a foreign substance,” which was an extremely broad definition that included all immunological reactions. Allergy is now defined in a much more restricted manner as “disease following a response by the immune system to an otherwise harmless antigen.” Allergy is one of a class of immune system responses that are termed hypersensitivity reactions. These are harmful immune responses that produce tissue injury and may cause serious disease. Hypersensitivity reactions were classified into four types by Coombs and Gell Allergy is often equated with type I hypersensitivity (immediate-type hypersensitivity reactions mediated by IgE), and will be used in this sense here. Allergy
  • 20. Undesirable reactions produced by the normal immune system. Hypersensitivity is an exaggerated immune response that results in tissue damage and is manifested in the individual on a second or subsequent contact with anantigen. Hypersensitivity reactions can be classified as either immediate or delayed. Clearly immediate reactions appear faster than delayed ones, but the main difference between them is the nature of the immune response to the antigen.
  • 21. Allergy Allergies, also known as allergic diseases, are a number of conditions caused by hypersensitivity of the immune system to something in the environment that usual y causes little or no problem in most people. These diseases include hay fever, food all ergies, atopic dermatitis, allergic asthma, and anaphylaxis . Symptoms may include red eyes, an itchy rash, runny nose, shortness of breath, or swelling.
  • 22. General Features 1.Hypersensitivity reactions can be elicited by exogenous environmental antigens or endogenous self antigens. 2.Results from failure of normal regulation of immune response. 3.Development of hypersensitivity diseases is often associated with the inheritance of particular susceptibility genes.
  • 23. Types Of Hypersensitivity: reactions are divided according to mechanism of action into four groups: 1-Type I (Immediate hypersensitivity). 2-Type II (Cytotoxic hypersensitivity). 3 Type III (Immune complexhypersensitivity). 4Type IV (Cell -mediated or Delayed hypersensitivity). 5-Type V(Stimulatory Type) Jones-Mote Reaction (or) Cutaneous Basophil Hypersensitivity
  • 24. A type I hypersensitive reaction is induced by certain types of antigens referred to as allergens, and has all the hall marks of a normal humoral response. Allergic reactions occur when an individual who has produced IgE antibody in response to an innocuous antigen (allergen) subsequently encounters the same allergen. Type I, or anaphylactic, reactions often occur within 2 to 30 minutes after a person sensitized to an antigen is re-exposed to that antigen. Type I Hypersensitivity (IgE DEPENDENT)
  • 25.
  • 26. Type II Hypersensitivity (Cytolysis And Cytotoxic). These reactions involve a combination of IgG (or IgM) antibodies with an antigenic determinants on the surface of cells. Antibody can activate the complement system, creating pores in the membrane of a foreign cell, or it can mediate cell destruction by antibody dependent cell - mediated cytotoxicity (ADCC). Type II hypersensitivity is general y, called cytolytic or cytotoxic reactions because it results in the destruction of host cells, either by lysis or toxic mediators. Type II hypersensitive reactions involve antibody-mediated destruction of cells
  • 28. Type III Hypersensitivity—Immune Complex- Mediated Type III reactions involve antibodies against soluble antigens circulating in the serum. The antigen-antibody complexes are deposited in organs and cause inflammatory damage. The tissue damage that results from the deposition of immune complexes is caused by the activation of complement, platelets and phagocytes; in essence, an acute inflammatoryresponse
  • 29. Immune complex-mediated hypersensitivity. (1) Immune complexes on the basement membrane of the wall of a blood vessel, where they; (2) activate complement and attract inflammatory cells such as neutrophils to the site. (3) The neutrophilis discharge enzymes as they react with the immune complexes, resulting in damage to tissue cells
  • 30. Type IV Hypersensitivity—Delayed Hypersensitivity Type IV hypersensitivity reactions (delayed hypersensitivity) constitute one aspect of cell-mediated immune response and are caused mainly by T cells. These are typically provoked by intracellular microbial infections or haptens like simple chemicals applied on the skin, evolve slowly and consist of a mixed cellular reaction involving lymphocytes and macrophages in particular. It is named delayed hypersensitivity because it appears in 24 to 48 hours after the presensitized host encounters the antigen, while immediate hypersensitivity reactions develop in 1/2 to 12 hours..
  • 31. A major factor in the delay is the time required for the participating T cells and macrophages to migrate to and accumulate near the foreign antigens. The T cells involved in delayed type hypersensitivity reactions are primarily TD cells. In some types of hypersensitivities resulting in tissue damage, Tc cells may also participate CONT: Type IV Hypersensitivity— Delayed Hypersensitivity Type IV hypersensitivity reactions (delayed hypersensitivity)
  • 32. Type IV (delayed or cell -mediated) hypersensitivity
  • 33.
  • 34. This is anantibody-mediated hypersensitivity and is a modification of type I hypersensitivity reaction. Antibodies interact with antigens on cell surface which leads to cell proliferation and differentiation instead of inhibition or killing. Antigen-antibody reaction enhances the activity of affected cell. Example of Grave’s disease: Thyroid hormones are produced in excess quantity in grave’s disease. Long acting thyroid stimulating (LATS) antibody is an autoantibody to thyroid membrane antigen. It is presumed that LATS combines with a TSHreceptor on thyroid cell surface and brings about the the same effect as TSH resulting in excessive secretion of thyroidhormone. Type V: Hypersensitivity (Stimulatory Type) Jones-Mote Reaction(or) Cutaneous Basophil Hypersensitivity
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