The document discusses various aspects of oral immunology including:
1. Innate immunity in the oral cavity which provides a physical barrier through epithelial cells and produces antimicrobial molecules through saliva.
2. Acquired immunity including the induction of salivary IgA antibodies through oral immunization and the mechanisms of action of IgA such as neutralizing pathogens and preventing their adherence.
3. The four types of hypersensitivity reactions: I) mediated by IgE antibodies and including anaphylaxis, urticaria, and angioedema. II) Mediated by IgG/IgM antibodies associated with conditions like recurrent aphthous stomatitis. III) Mediated by immune complexes seen
The presentation includes an overview of hypersensitivity and type 1 hypersensitivity with certain pictures elaborating the mechanism. The presentation also talks about asthma very briefly as an example of type 1 hypersensitivity.
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
The presentation includes an overview of hypersensitivity and type 1 hypersensitivity with certain pictures elaborating the mechanism. The presentation also talks about asthma very briefly as an example of type 1 hypersensitivity.
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
Normally, immune responses eradicate infectious pathogens without serious injury to host tissues.
However, these responses are sometimes
inadequately controlled
inappropriately targeted to host tissues
triggered by commensal microorganisms or environmental antigens that are usually harmless.
In these situations, the normally beneficial immune response is the cause of disease.
Disorders caused by immune responses are called hypersensitivity diseases.
This term , hypersensitivity , arose from the clinical definition of immunity as sensitivity, which is based on the observation that an individual who has been exposed to an antigen exhibits a detectable reaction, or is sensitive, to subsequent encounters with that antigen.
Today, we will describe the pathogenesis of different types of hypersensitivity reactions, with an emphasis on the effector mechanisms that cause tissue injury.
A variety of human diseases are caused by immune responses to non-microbial environmental antigens, and involve the type 2 cytokines interleukin-4 (IL-4), IL-5, and IL-13 produced by Th2 cells and innate lymphoid cells (ILCs), immunoglobulin E (IgE), mast cells, and eosinophils.
The antigens that elicit immediate hypersensitivity are called allergens. Most of them are common environmental proteins, animal products, and chemicals that can modify self proteins.
In the effector phase of these responses, mast cells and eosinophils are activated to rapidly release mediators that cause
increased vascular permeability
Vasodilation
bronchial and visceral smooth muscle contraction
This vascular reaction is called immediate hypersensitivity because it begins rapidly, within minutes of antigen challenge in a previously sensitized individual (immediate), and has major pathologic consequences (hypersensitivity).
Following the immediate response, there is a more slowly developing inflammatory component called the late-phase reaction characterized by the accumulation of neutrophils, eosinophils, and macrophages.
hypersensitivity 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 an antigen. Hypersensitivity reactions can be classified as either immediate or delayed. Obviously immediate reactions appear faster than delayed ones, but the main difference between them is the nature of the immune response to the antigen.
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Normally, immune responses eradicate infectious pathogens without serious injury to host tissues.
However, these responses are sometimes
inadequately controlled
inappropriately targeted to host tissues
triggered by commensal microorganisms or environmental antigens that are usually harmless.
In these situations, the normally beneficial immune response is the cause of disease.
Disorders caused by immune responses are called hypersensitivity diseases.
This term , hypersensitivity , arose from the clinical definition of immunity as sensitivity, which is based on the observation that an individual who has been exposed to an antigen exhibits a detectable reaction, or is sensitive, to subsequent encounters with that antigen.
Today, we will describe the pathogenesis of different types of hypersensitivity reactions, with an emphasis on the effector mechanisms that cause tissue injury.
A variety of human diseases are caused by immune responses to non-microbial environmental antigens, and involve the type 2 cytokines interleukin-4 (IL-4), IL-5, and IL-13 produced by Th2 cells and innate lymphoid cells (ILCs), immunoglobulin E (IgE), mast cells, and eosinophils.
The antigens that elicit immediate hypersensitivity are called allergens. Most of them are common environmental proteins, animal products, and chemicals that can modify self proteins.
In the effector phase of these responses, mast cells and eosinophils are activated to rapidly release mediators that cause
increased vascular permeability
Vasodilation
bronchial and visceral smooth muscle contraction
This vascular reaction is called immediate hypersensitivity because it begins rapidly, within minutes of antigen challenge in a previously sensitized individual (immediate), and has major pathologic consequences (hypersensitivity).
Following the immediate response, there is a more slowly developing inflammatory component called the late-phase reaction characterized by the accumulation of neutrophils, eosinophils, and macrophages.
hypersensitivity 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 an antigen. Hypersensitivity reactions can be classified as either immediate or delayed. Obviously immediate reactions appear faster than delayed ones, but the main difference between them is the nature of the immune response to the antigen.
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2. Innate Immunity
• Innate defenses comprise a network of
epithelial cells and molecules derived
from them as well as the salivary
secretions. Innate mucosal immunity
includes the physical barrier provided
by epithelial cells, salivary mucus
production . the various secreted
molecules with antibacterial activity in
saliva. Within the oral epithelium reside
natural killer (NK) cells which also
provide a nonspecific cellular protective
mechanism
3. Acquired Immunity
Induction of Salivary IgA Antibodies
The most effective method of inducing antibodies in
saliva seems to be by stimulation of induction sites of
the mucosal immune system (MALT or mucosa-
associated lymphoid tissue) and thus by
oral/intragastric or intranasal immunization
However, application of antigen directly to the
mucosa can lead to the induction of antibodies in
minor salivary glands
4. Mechanisms of Action of Salivary IgA
1. Virus neutralization (human immunodeficiency
virus (HIV)) either extracellularly or intracellularly
within basal cells of salivary glands
2. Neutralization of toxins (e.g., cholera toxin)
3. Inhibition of adherence (or growth) of
microorganisms on epithelial cells or on teeth
4. Antigen exclusion by preventing the access of
antigen to the systemic immune system
5. Interaction of IgA with nonspecific defense
mechanisms
5. Introduction
• Our immune system plays a crucial role in protecting our body against pathogens, but
sometimes there is an exaggerated response. This exaggerated response is triggered by
the interaction of the immune system with an antigen (allergen) and is referred to as
hypersensitivity. Hypersensitivity reactions are classified into four types by Coombs and
Gell. The first three types are considered immediate hypersensitivity reactions because
they occur within 24 hours. The fourth type is considered a delayed hypersensitivity
reaction because it usually occurs more than 12 hours after exposure to the allergen, with
a maximal reaction time between 48 and 72 hours. The four types of hypersensitivity are:
• Type I: reaction mediated by Ige antibodies
• Type II: cytotoxic reaction mediated by IgG or IgM antibodies
• Type III: reaction mediated by immune complexes
• Type IV: delayed reaction mediated by cellular response
Oral Mucosal Diseases
6. Type I: reaction mediated by Ige antibodies
1. anaphylaxis
2. urticaria
3. angioedema
7. anaphylaxis
• Anaphylaxis is a severe, potentially life-threatening allergic reaction. It can
occur within seconds or minutes of exposure to something you're allergic to,
such as peanuts or bee stings.
• Common triggers include certain foods, some medications, insect venom and
latex.
• Anaphylaxis requires an injection of epinephrine and a follow-up trip to an
emergency room. If you don't have epinephrine, you need to go to an
emergency room immediately. If anaphylaxis isn't treated right away, it can be
fatal.
8.
9.
10. Urticaria
• Urticaria is characterized by very itchy weal's (hives), with or
without surrounding erythematous flares. Urticaria can
be acute or chronic, spontaneous or inducible.
• A weal (or wheal) is a superficial skin-coloured or pale skin
swelling, usually surrounded by erythema that lasts anything
from a few minutes to 24 hours.
• Urticaria can co-exist with angioedema which is a deeper
swelling within the skin or mucous membranes.
11.
12. Angioedema
• Angioedema is an area of swelling (edema) of the lower layer of skin and tissue
just under the skin or mucous membranes. The swelling may occur in the face,
tongue, larynx, abdomen, or arms and legs. Often it is associated with hives,
which are swelling within the upper skin. Onset is typically over minutes to
hours.
• The underlying mechanism typically involves histamine or bradykinin. The
version related to histamine is due to an allergic reaction to agents such as insect
bites, foods, or medications. The version related to bradykinin may occur due to
an inherited problem
• Treatment to protect the airway may include intubation or cricothyroidotomy.
Histamine-related angioedema can be treated with antihistamines,
corticosteroids, and epinephrine.
15. Recurrent Aphthous Stomatitis (RAS)
RAS consists of recurrent bouts of one or more painful, round or oval
shaped ulcers. Most aphthous ulcers last for 10-14 days.The severity
and frequency of RAS tends to decrease with age. The cause is
unknown but there is likely to be an immunological factor involved.
There are a number of underlying or precipitating factors which
include anaemia, vitamin deficiencies, stress and trauma from sharp
teeth, dental braces/ fillings or a tooth brush.
RAS is classified into three types:
• Minor
• Major
• Herpetiform
16.
17. Erythema Multiforme (EM)
is a hypersensitivity reaction usually triggered by infections, most
commonly herpes simplex virus (HSV). It presents with a skin
eruption characterised by a typical target lesion. There may be
mucous membrane involvement. It is acute and self-limiting, usually
resolving without complications.
18. Pemphigus Vulgaris (PV)
is an autoimmune condition. This means that something goes wrong
with the immune system (the body's defence against infection) and it
starts attacking healthy tissue.
is a rare and serious (potentially life-threatening) condition that
causes painful blisters to develop on the skin and lining of the mouth,
nose, throat and genitals.
The blisters are fragile and can easily burst open, leaving areas of raw
unhealed skin that are very painful and can put you at risk of
infections.
19.
20. Lichen Planus (LP)
is an idiopathic disease. Its pathogenesis is not fully understood, but
it appears to represent a T-cell-mediated autoimmune disease.
is an inflammatory disorder of the skin and mucous membranes with
no known cause. It appears as pruritic, violaceous papules and
plaques most commonly found on the wrists, lower back, and ankles.
A lattice-like network of white lines called Wickham striae overlies
the lesions but is most easily observed on the buccal mucosa where
erosions can also be present
23. Arthus reaction
• noted that daily injections of horse serum into the skin of rabbits
resulted in a localized cutaneous reaction characterized by
erythema, edema, hemorrhage, and necrosis. This reactivity was
found to be transferable with the serum of the immunized rabbit,
and it was associated with the development of antibody to horse
serum proteins. The cutaneous inflammation is caused by a local
vasculitis of the small blood vessels of the skin. Vasculitis follows
the formation of antigen-antibody complexes in the region of the
vessel walls Arthritis
24.
25. Serum sickness
• Serum sickness is an immune-complex-mediated hypersensitivity
reaction that classically presents with fever, rash, polyarthritis or
polyarthralgias.had received heterologous antisera, which was
historically used to treat infectious diseases. The symptoms
typically occur one to two weeks after exposure to an offending
agent and resolve within several weeks of discontinuation. It is a
self-limited disease process with an excellent progn. heterologous
(nonhuman) proteins. Medications containing heterologous
antigens are the most common cause of serum sickness and include
vaccinations (i.e., Rabies), immune modulating agents (i.e.,
rituximab, infliximab) and anti-venoms.osis.
26.
27. Systemic lupus erythematosus
• is an autoimmune disease in which the immune system
attacks its own tissues, causing widespread inflammation
and tissue damage in the affected organs. It can affect the
joints, skin, brain, lungs, kidneys, and blood vessels. There is
no cure for lupus, but medical interventions and lifestyle
changes can help control it.
28.
29. Rheumatoid Arthritis
• is an autoimmune and inflammatory disease, which means
that your immune system attacks healthy cells in your body
by mistake, causing inflammation (painful swelling) in the
affected parts of the body.
• RA mainly attacks the joints, usually many joints at once.
RA commonly affects joints in the hands, wrists, and knees.
In a joint with RA, the lining of the joint becomes inflamed,
causing damage to joint tissue. This tissue damage can
cause long-lasting or chronic pain, unsteadiness (lack of
balance), and deformity (misshapenness).
30.
31. Type IV: delayed reaction mediated by
cellular response
• Contact Hypersensitivity
• Thyroiditis
32. Contact Hypersensitivity
• sometimes called “contact dermatitis,” is a
secondary immune response to a small, chemically
reactive molecule that has bound covalently to self
proteins in the uppermost layers of the skin.
Examples of CHS include the patchy rash and
intense itching that follow a plunge into a patch of
poison oak or poison ivy, and the local skin
irritations experienced by individuals sensitive to
drugs, metals, cosmetics, or industrial or natural
chemicals.
33.
34. Autoimmune Thyroiditis
• is a chronic disease in which the body interprets the
thyroid glands and its hormone products T3, T4 and
TSH as threats, therefore producing special
antibodies that target the thyroid's cells, thereby
destroying it. It may present with hypothyroidism or
hyperthyroidism and with or without a goiter.