Lecture 7 Flashcards
1
Q
Autoimmunity
A
- Is a form of immunopathology
- The body’s own immune system targets cells and tissues, a specific organ, or may be far more widespread of the body
2
Q
Autoimmune disease
A
- Is the disease which results from this process.
- Generally occurs in a person who is genetically susceptible.
- Females > Males
3
Q
What is immune tolerance?
A
It’s the immune system’s ability to recognize the body’s own tissues and not attack them.
4
Q
When does tolerance begin?
A
It starts in the embryo, in the primary lymphoid organs—this is called central tolerance
5
Q
What is peripheral tolerance?
A
It’s tolerance that continues after birth in the secondary lymphoid organs.
6
Q
What happens to self-reactive immune cells?
A
They are usually destroyed or controlled by regulatory T cells.
7
Q
What is autoimmunity?
A
t’s when self-tolerance fails, and the immune system attacks the body’s own tissues.
8
Q
What shows up in the blood during autoimmunity?
A
Anti-tissue antibodies, like anti-thyroid antibodies.
9
Q
What does autoimmune disease usually mean?
A
It means the body’s tolerance system has failed.
10
Q
Genetic factors and familial component to autoimmune disorders:
A
- MHC (Major Histocompatability complex) set of alleles, or to non-MHC alleles.
- HLA (human leukocyte antigens) is synonymous with
MHC
11
Q
Breakdown of tolerance theories
A
- Cross reacting antigens
- Altered ratio of T helper to regulatory T cell populations
- Modified self-antigens
- Sequestered antigens
- Re-emergence of a ‘forbidden clone of lymphocytes
12
Q
Breakdown of tolerance theories: Cross reacting antigens
A
A foreign antigen may closely
resemble a self-Ag, so the immune response react with the self-Ag, resulting in an autoimmune
disease.
13
Q
Breakdown of tolerance theories: Altered ratio of T helper to regulatory T cell
populations
A
Interferes with the functions of the regulatory cells, which
are to dampen the immune response –> the immune
system becomes more active.
14
Q
Breakdown of tolerance theories: Modified self-antigens
A
Injured tissue (eg by some infective agents) may result in an alteration of the self-Ag, and hence viewed as ‘foreign’ –>
initiated immune response.
15
Q
Breakdown of tolerance theories: Sequestered antigens
A
- Some tissues are ‘hidden’ from the immune system
- Self-antigens are thus never exposed to the immune system and do not go through the normal process of selftolerance.
- If that barrier fails –> the previously sequestered cells are
exposed to the immune system and can now be damaged.
16
Q
Breakdown of tolerance theories: Re-emergence of a ‘forbidden clone of
lymphocytes
A
- In the process of developing self-tolerance, lymphocytes which could react with the person’s tissues are normally destroyed.
- Occasionally, one of these may survive, and years later re-emerge and start to damage tissue
17
Q
What is the difference between
autoimmunity and alloimmunity?
A
Alloimmunity refers to the reaction of the immune system to cells or tissues of another individual from the same species.
Examples:
* Transfusion reactions, incompatibility between the donor and recipient blood
* Transplant rejections, incompatibility between the HLAs of donor and recipient.
18
Q
Rheumatoid Arthritis
A
A common progressive, systemic
disease involving chronic inflammation of synovial membranes and other connective tissues.
Aetiology
* Unknown
* In susceptible individuals, an external trigger leads to autoimmune reaction that affects both articular and extra-articular tissues.
19
Q
Rheumatoid Arthritis Pathophysiology
A
- The synovial membrane becomes thick due to chronic inflammation.
- Joint cartilage is gradually damaged and worn away.
- Bone under the cartilage (subchondral bone) may erode, especially at the edges.
- Tendon sheaths in hands and feet become inflamed and thickened.
- These sheaths may weaken and rupture, worsening deformities.
- Inflammatory nodules can form in soft tissues.
- Other connective tissues may also be affected.
20
Q
Rheumatoid Arthritis Epidemiology
A
- Women are affect approx 3x more
- First degree relatives have higher risk
- Peak onset 35-50 years
21
Q
Rheumatoid Arthritis Clinical Features
A
- May begin with arthralgia (joint pain) or myalgia (muscle pain)
- Fingers and toes often first affected
- Affected joints are painful, swollen and warmer
- Muscle stiffness, atrophy and deformities occur later
- Restricted joint movements
22
Q
Non- Articular symptoms of Rheumatoid Arthritis
A
o Appearance of ‘rheumatoid nodules’ (sub-cutaneous, hard swellings):
common sites include
- Olecranon process
- Proximal ulna
- Heels
- Occiput
- Ischial tuberosity
o Leg ulcers
o Fever
o Tachycardia
23
Q
Systemic Lupus Erythematosus
A
- SLE is a multisystem chronic disease, involving a disturbance of immune function.
- It involves the connective tissue in many parts of the body
24
Q
Systemic Lupus Erythematosus Aetiology
A
The aetiology of SLE is unknown, but it appears to be
multifactorial, including a generic predisposition and
environmental factors.
25
Systemic Lupus Erythematosus Epidemiology
* Females : Males (9:1)
* A peak incidence occurs between the ages of 12 and 40.
* Most commonly presents in the 20-30 year age group
26
Systemic Lupus Erythematosus Pathology
- Predominant lesion is a vasculitis of arterioles, capillaries and venules, associated with fibrinoid necrosisand inflammatory cellular infiltrate.
* Deposition of immune complexes and fibrinoid material in tissues.
27
Systemic Lupus Erythematosus Clinical features
Presentation may ‘classically’ be fever, rash and joint pain
o Malar rash (across the cheeks) or a discoid rash
o Ulcers in oral cavity or nasopharynx
o Non-erosive arthritis with tenderness and swelling
o Pleural or pericardial inflammation
o Seizures
o Psychosis
28
Systemic Lupus Erythematosus Lab Findings
o Haematological changes
o Antinuclear antibodies
o Proteinuria or cellular casts in urine which reflect renal involvement
29
Examples of autoimmune
disorders
Rheumatoid arthritis
Systemic lupus erythematosus
Scleroderma
Graves disease
Diabetes Mellitus Type 1
30
Examples of alloimmune
disorders
Transfusion Reactions
Haemolytic disease of newborn
31
Transfusion reactions RBCs
Giving and receiving red blood cells
- So, if a person with Type A blood is given RBCs from a type B donor, the anti-B antibodies in the recipient’s plasma will destroy the donors RBCs.
- A person with AB blood has no anti-A or anti-B antibodies in their plasma, so could receive RBCs from anyone of the other blood types.
- A person with blood type O has no antigens on their red blood cells, so can give them to anyone as they will not be destroyed in the recipient’s blood.
32
Transfusion Reactions Plasma or whole blood
- Opposite to RBCS
- Plasma from a donor with blood type A will contain anti-B
antibodies, which would destroy the RBCs of a person with either
Type B or type AB blood.
- So it is important when giving whole blood transfusions to give the same blood type
33
Haemolytic disease of the newborn
34
Hypersensitivity reactions
Exaggerated/unwanted immune responses that can cause serious cell/tissue injury.
35
What is hypersensitivity?
Is unfavourable consequences of Antigen-Antibody (Ag-Ab), or Ag-lymphocyte interactions.
- An allergic reaction is any hypersensitivity reaction that occurs to an environmental antigen, referred to as an allergen
36
Types of hypersensitivity reactions
Type 1: Anaphylactic reactions
Type 2: Tissue specific reactions
Type 3: Immune complex reactions
Type 4: Delayed Hypersensitivity reactions
37
Anaphylactic reactions
When people talk about having an ‘allergy’, they are usually (but certainly not always) talking about Type 1 reactions.
* Anaphylactic reactions may be local or systemic.
38
Type I: Local reactions
- Generally occur on the skin or mucosal surfaces
- e.g Hay fever and many asthma
- Susceptibility to localised type I reactions appears to be genetically controlled
39
Type I: Systemic reactions (systemic anaphylaxis)
- Associated with parenteral administration of protein antigens
* e.g bee venom, drugs (e.g penicillin) and some foods.
- Itching hives and skin erythema within minutes
- Dyspnea
- Laryngeal oedema
- Shock
40
Primary Mediators
- Rapidly released from mast cells and thus act early in the course of type 1 hypersensitivity
- Histamine
41
Secondary mediators
- Lipid mediators
- Cytokines
- Prostaglandins
42
What is the first step in Type I hypersensitivity?
Initial exposure to an allergen.
43
What happens after allergen exposure?
CD4 T-helper cells activate B cells to produce IgE antibodies.
44
What do the IgE antibodies do?
They bind to receptors on mast cells and basophils.
45
Where are mast cells found?
In mucosal tissues, skin, and around blood vessels.
46
What does IgE binding to mast cells cause?
It "primes" the person for an allergic (Type I) reaction.
47
What happens on re-exposure to the allergen?
The allergen binds to the cell-bound IgE, cross-linking two IgE molecules on mast cells.
48
What does cross-linking of IgE on mast cells trigger?
A signal that starts two processes:
Release of primary mediators (degranulation)
Production of secondary mediators
49
What are primary mediators?
Pre-stored substances released quickly from mast cells (e.g., histamine).
50
What does histamine do?
Causes vasodilation, increased permeability, bronchospasm, mucus secretion, and GI movement.
51
What are chemotactic factors?
Substances that attract immune cells like neutrophils and eosinophils.
52
What is the role of eosinophils in allergic reactions?
They help remove allergens and are important in phagocytosis.
53
What are secondary mediators?
Newly made substances like cytokines, prostaglandins, and arachidonic acid metabolites.
53
What are antibodies targeting in Type II hypersensitivity?
Antigens on cell membranes—either normal or altered.
54
How many antibody-dependent mechanisms are involved in Type II hypersensitivity?
Five different mechanisms.
55
Why are only certain cells affected in Type II hypersensitivity?
Because cells have tissue-specific antigens, not just MHC antigens.
56
What happens in Mechanism 1 Type II hypersensitivity?
Antibody binds to an antigen on the cell → complement enzymes destroy the cell (cell lysis).
57
Give examples of Mechanism 1 Type II hypersensitivity?
Transfusion reactions, autoimmune haemolytic anaemia.
58
What happens in Mechanism 2 Type II hypersensitivity?
Antibody binds → complement C3b attaches → phagocytosis of the cell.
59
What happens in Mechanism 3 Type II hypersensitivity?
Neutrophils try to phagocytose but can't (cell/tissue too large), so they release enzymes and ROS → causes tissue damage.
60
What happens in Mechanism 4 Type II hypersensitivity?
Antibody binds → NK cells recognize it → release toxic substances → tissue damage.
61
What happens in Mechanism 5 Type II hypersensitivity?
Antibody binds to a receptor and changes cell function without destroying the cell.
62
Give an example of Mechanism 5 Type II hypersensitivity?
Graves’ disease – an antibody (LATS) overstimulates the thyroid gland.
63
What does LATS do in Graves' disease?
Binds to TSH receptors on thyroid cells and keeps stimulating thyroxine production, ignoring feedback signals.
64
What forms in Type III hypersensitivity?
An antigen-antibody complex.
65
What happens to the antigen-antibody complex Type III hypersensitivity?
It deposits on healthy tissue and causes inflammation.
66
What does the complex trigger Type III hypersensitivity?
Activation of complement enzymes, neutrophil attraction, and tissue damage.
67
What are common sites of immune complex deposition Type III hypersensitivity?
Kidneys, joints, skin, heart, and small blood vessels.
68
Can immune complex disease be localized or systemic Type III hypersensitivity?
It can be either localized or systemic.
69
Type III hypersensitivity?
70
What causes extrinsic allergic alveolitis Type III hypersensitivity?
Repeated inhalation of antigens from moulds, plants, or animals.
71
What are two examples of Extrinsic Allergic Alveolitis Type III hypersensitivity?
Farmer’s lung (from mouldy hay)
Bird breeder’s lung (from bird droppings)
72
Acute Poststreptococcal Glomerulonephritis: What triggers this kidney disease? Type III hypersensitivity?
Antibodies formed against streptococcal antigens.
73
Acute Poststreptococcal Glomerulonephritis: What does the immune complex do in the kidneys Type III hypersensitivity?
Causes inflammation and damage to the kidney tissue.
74
Acute Poststreptococcal Glomerulonephritis: What happens after the immune complex forms? Type III hypersensitivity
It travels to the kidneys and deposits on glomeruli basement membranes.
75
What mediates Type IV hypersensitivity?
Sensitized T lymphocytes, not antibodies.
76
Type IV hypersensitivity: What types of T cells are involved?
Tc cells (Cytotoxic T cells)
Th1 and Th17 cells (Cytokine-producing)
77
Type IV hypersensitivity: How do Tc cells cause damage?
By releasing toxins (e.g., perforin) that kill target cells.
78
Type IV hypersensitivity: How do Th1/Th17 cells cause damage?
They attract macrophages → release enzymes & ROS → tissue damage.
79
Type IV hypersensitivity: What is the Mantoux test used for?
Detects prior exposure to Mycobacterium tuberculosis.
80
Type IV hypersensitivity: What causes the swelling in a Mantoux test?
A delayed immune response to injected tuberculosis proteins.
81
Type IV hypersensitivity: Mantoux test, Does the test diagnose active TB?
No — it shows exposure or vaccination, not current infection.
82
Type IV hypersensitivity: What does a negative Mantoux test mean?
Likely no active TB or prior exposure.
83
Type IV hypersensitivity: What causes allergic contact dermatitis?
Small environmental antigens that bind to proteins in the skin.
84
Type IV hypersensitivity: What are some examples of triggers Allergic Contact Dermatitis?
Poison ivy, metals, rubber, detergents, clothing dyes, industrial chemicals.
85
Type IV hypersensitivity: Can foods trigger Type IV reactions?
Yes — milk proteins and gluten can cause milk intolerance and coeliac disease.
86
What molecules trigger transplant rejection?
MHC antigens (also called HLA – Human Leukocyte Antigens).
87
Why must donor and recipient have matched HLA?
To reduce the chance of graft rejection.
88
What causes graft rejection?
The recipient's immune system sees the graft as foreign.
89
What immune reactions are involved in graft rejection?
Type II and Type IV hypersensitivity.
90
What is hyperacute rejection?
Rejection that happens within minutes or hours after transplant.
91
What causes hyperacute rejection?
Antigen-antibody reaction at the blood vessels (Type II reaction).
92
What is acute rejection?
Rejection that occurs within days to months, especially after stopping immunosuppressants.
93
What types of immunity are involved in acute rejection?
Both Type II and Type IV — involving antibodies and T cells.
94
What happens to the graft during acute rejection?
Cellular rejection, vasculitis, and tissue necrosis.
95
What is chronic rejection?
Slow rejection over time, with blood vessel changes, fibrosis, and tissue loss
96
What type of hypersensitivity is chronic rejection mostly due to?
Type IV hypersensitivity.
97
What is autoimmunity?
Autoimmunity is a form of immunopathology where the body’s immune system targets its own cells and tissues.
## Footnote
Autoimmune disease results from this process and is more common in females.
98
What is the term for the disease resulting from autoimmunity?
Autoimmune disease
## Footnote
It typically arises in genetically susceptible individuals reacting abnormally to stressors.
99
What is self-tolerance in the immune system?
Self-tolerance is the immune system's ability to recognize and not react against the body's own tissues.
## Footnote
This process begins in the embryo and continues after birth.
100
What are the two types of tolerance in the immune system?
* Central tolerance
* Peripheral tolerance
## Footnote
Central tolerance occurs in primary lymphoid organs, while peripheral tolerance occurs in secondary lymphoid organs.
101
What happens when self-tolerance breaks down?
The immune system destroys body tissues and anti-tissue antibodies appear in the blood.
## Footnote
An example of such antibodies is anti-thyroid antibodies.
102
What role do genetic factors play in autoimmunity?
Genetic factors contribute to the predisposition for autoimmune disorders, often linked to MHC alleles.
## Footnote
There is a familial component to many autoimmune diseases.
103
What is the common term used synonymously with Major Histocompatibility Complex (MHC)?
HLA (human leukocyte antigens)
## Footnote
HLA is the human version of MHC found in all animal species.
104
Which HLA allele is closely associated with Ankylosing spondylitis?
HLA allele B27
## Footnote
Individuals with this allele are predisposed to an abnormal immune reaction.
105
List some autoimmune disorders linked to specific HLA alleles.
* Ankylosing spondylitis - B27
* Diabetes Mellitus Type 1 - DR3, DR4
* Rheumatoid arthritis - DR4
* Systemic lupus erythematosus - DR3
* Reactive arthritis - B27
* Coeliac disease - DR3
* Graves disease - DR3
## Footnote
These associations indicate a genetic predisposition to these disorders.
106
What is one theory explaining the breakdown of tolerance?
Cross reacting antigens: A foreign antigen may resemble a self-antigen, triggering an autoimmune response.
## Footnote
An example is rheumatic fever due to shared antigens between streptococcal cell walls and heart muscle.
107
What effect does an altered ratio of T helper to regulatory T cells have?
It can lead to increased immune activity by interfering with regulatory cell functions.
## Footnote
This disruption may enhance autoimmune responses.
108
What are modified self-antigens?
Injured tissue may alter self-antigens, making them appear foreign to the immune system.
## Footnote
This can initiate an immune response against the body's own tissues.
109
What are sequestered antigens?
Antigens hidden from the immune system by barriers, such as the blood-brain and blood-eye barriers.
## Footnote
If these barriers fail, previously sequestered antigens can trigger an immune response.
110
What is a forbidden clone of lymphocytes?
Lymphocytes that could react with the body’s tissues but are normally destroyed during self-tolerance development.
## Footnote
Occasionally, one may survive and later cause tissue damage.
111
What is the difference between autoimmunity and alloimmunity?
Autoimmunity is the immune reaction against self, while alloimmunity is the reaction against cells or tissues from another individual of the same species.
## Footnote
Examples of alloimmunity include transfusion reactions and transplant rejections.
112
What are examples of autoimmune diseases?
* Rheumatoid arthritis
* Systemic lupus erythematosus
* Scleroderma
* Myasthenia gravis
* Graves disease
* Hashimoto’s thyroiditis
* Diabetes Mellitus Type 1
* Inflammatory bowel disease (Crohn’s disease and Ulcerative colitis)
* Guillain Barre syndrome
* Chronic inflammatory demyelinating polyneuropathy
* Psoriasis
* Psoriatic arthropathy
* Ankylosing Spondylitis
* Sjögren’s syndrome
* Coeliac disease
* Multiple sclerosis
* Polymyalgia Rheumatica
* Temporal arteritis
* Many more
## Footnote
This list includes both common and uncommon disorders.
113
Define rheumatoid arthritis
A common progressive, systemic disease involving chronic inflammation of synovial membranes and other connective tissues.
## Footnote
It is characterized by a range of clinical features and affects both articular and extra-articular tissues.
114
What is the aetiology of rheumatoid arthritis?
Unknown; however, an external trigger (e.g., infection, trauma) sets in motion an autoimmune reaction in susceptible individuals.
## Footnote
This autoimmune reaction affects both articular and extra-articular tissues.
115
What are the key features of the pathophysiology of rheumatoid arthritis?
* Thickening of synovial membrane due to chronic inflammation
* Erosion of articular cartilage and subchondral bone
* Inflammation of tendon sheaths
* Formation of inflammatory nodules
* Permanent joint damage after prolonged disease
* Other connective tissues can also be affected.
## Footnote
These changes can lead to significant joint deformities and complications.
116
What demographic factors influence the epidemiology of rheumatoid arthritis?
* Women are affected approximately 3 times as often as men
* First degree relatives have a 2-3 times higher risk
* Peak age of onset: 35-50 years
* May occur in children.
## Footnote
Understanding these factors can aid in early diagnosis and management.
117
What are common clinical features of rheumatoid arthritis?
* Insidious or acute onset
* Transient arthralgia or myalgia
* Swellings of metacarpophalangeal and proximal interphalangeal joints
* Affected joints are painful and swollen
* Muscle stiffness, atrophy, and deformities in later stages
* Non-articular symptoms like rheumatoid nodules, leg ulcers, fever, tachycardia.
## Footnote
The disease can lead to significant functional impairment if not managed properly.
118
What is Systemic Lupus Erythematosus (SLE)?
A multisystem chronic disease involving a disturbance of immune function, affecting connective tissue in many parts of the body.
## Footnote
SLE can be triggered or exacerbated by factors like sunlight, infection, and emotional stress.
119
What is the aetiology of SLE?
Unknown; appears to be multifactorial, including genetic predisposition and environmental factors.
## Footnote
This complexity makes SLE challenging to manage.
120
What are the demographic factors influencing the epidemiology of SLE?
* Females to males ratio: 9:1
* Peak incidence between ages 12 and 40
* Most commonly presents in the 20-30 year age group.
## Footnote
Awareness of these factors is crucial for healthcare providers.
121
What are the predominant pathological features of SLE?
Vasculitis of arterioles, capillaries, and venules, associated with fibrinoid necrosis and an inflammatory cellular infiltrate.
## Footnote
This pathology leads to systemic complications involving multiple organ systems.
122
What are common clinical features of SLE?
* Fever
* Rash (malar or discoid)
* Joint pain
* Symptoms from various body systems (musculoskeletal, integumentary, renal, neuropsychiatric, respiratory, digestive, cardiovascular, haematological)
* Laboratory findings: anaemia, leukopenia, thrombocytopenia, antinuclear antibodies.
## Footnote
SLE can manifest in many ways, complicating diagnosis.
123
What are examples of alloimmune diseases?
* Transfusion reactions
* Haemolytic Disease of the Newborn.
## Footnote
These conditions arise from immune responses against foreign antigens.
124
What occurs during transfusion reactions?
Destruction (haemolysis) of red blood cells from an incompatible donor, caused by recipient antibodies against blood ABO group antigens.
## Footnote
Understanding blood compatibility is critical for safe transfusions.
125
What are the ABO blood types?
* Type A: Antigen A, anti-B antibodies
* Type B: Antigen B, anti-A antibodies
* Type AB: Antigens A & B, no antibodies
* Type O: No antigens, anti-A and anti-B antibodies.
## Footnote
Blood type compatibility is essential for transfusions and organ transplants.
126
What is the significance of RhD antigen in transfusions?
85% of the population is Rh positive; incompatibility can lead to serious complications in transfusions and pregnancy.
## Footnote
Rh compatibility is especially important for Rh-negative mothers with Rh-positive fetuses.
127
What is Haemolytic Disease of the Newborn?
Occurs when an Rh positive fetus is carried by an Rh negative mother, leading to potential immune reactions.
## Footnote
Administration of anti-D immunoglobulin can prevent complications.
128
What are Hypersensitivity reactions?
Exaggerated/unwanted immune responses that can cause serious cell and tissue injury.
129
How are hypersensitivity diseases classified?
Based on the immunologic mechanism mediating the disease.
130
What are the four types of hypersensitivity reactions?
* Type 1: Anaphylactic reactions
* Type 2: Tissue specific reactions
* Type 3: Immune complex reactions
* Type 4: Delayed Hypersensitivity reactions
131
What is an allergic reaction?
Any hypersensitivity reaction that occurs to an environmental antigen (allergen).
132
Which type of hypersensitivity reactions are commonly 'allergic' in nature?
Type 1 reactions.
133
What are the characteristics of Type 1 Anaphylactic reactions?
* Local or systemic reactions
* Local reactions occur on skin/mucosal surfaces
* Systemic reactions can result from protein antigens or drugs
134
What is atopy?
Familial predisposition to localized Type 1 hypersensitivity reactions.
135
What are the primary mediators released during Type 1 hypersensitivity reactions?
* Histamine
* Chemotactic factors
136
What is the basic sequence of events in Type 1 hypersensitivity reactions?
* Initial exposure to allergens
* Immune system activation and IgE production
* IgE binds to mast cells
* Re-exposure leads to cross-linking of IgE and subsequent mediator release
137
What is the role of IgE in Type 1 hypersensitivity?
IgE binds to mast cells and primes the individual for a hypersensitivity reaction.
138
What is the pathogenesis of systemic anaphylaxis?
Rapid onset of symptoms like itching, hives, dyspnoea, and potential shock.
139
What characterizes Type 2 Hypersensitivity reactions?
Antibodies formed against target antigens on cell membranes.
140
What is the first mechanism of Type 2 hypersensitivity?
An antibody attaches to a tissue specific antigen, leading to complement activation and destruction.
141
What is an example of a disorder caused by Type 2 hypersensitivity?
Autoimmune hemolytic anemia.
142
What is the effect of the antibody LATS in Type 2 hypersensitivity?
Stimulates thyroid cells to produce excess thyroxine, leading to Graves disease.
143
What characterizes Type 3 Hypersensitivity reactions?
Formation of immune complexes that deposit on tissues and cause damage.
144
What are favored sites for immune complex deposition?
* Kidneys
* Joints
* Skin
* Heart
* Small blood vessels
145
What is an example of an immune complex reaction?
Acute poststreptococcal glomerulonephritis.
146
What characterizes Type 4 Delayed Hypersensitivity reactions?
Mediated by sensitized T lymphocytes without involvement of antibodies.
147
What types of T cells are involved in Type 4 hypersensitivity?
* Cytotoxic T lymphocytes (Tc cells)
* Cytokine producing T cells (Th1 and Th17)
148
What is a classic example of a delayed hypersensitivity reaction?
Positive Mantoux reaction (tuberculin test).
149
What is the role of macrophages in Type 4 hypersensitivity?
Attracted by cytokines to release enzymes and reactive oxygen species causing tissue damage.
150
What induces allergic contact dermatitis in Type 4 hypersensitivity?
Environmental antigens binding to carrier proteins in the skin.
151
Fill in the blank: Type 1 hypersensitivity reactions are often associated with _______.
[allergic reactions]
152
True or False: All hypersensitivity reactions are allergic reactions.
False.
153
What are the immunogenic molecules that stimulate rejection of transplanted organs?
Major histocompatibility complex (MHC) antigens, also known as human leucocyte antigens (HLA).
154
What is required for optimal survival of a graft?
The recipient and the donor must have as closely matched HLA as possible.
155
What occurs during graft rejection?
The host recognizes the grafted tissue as foreign.
156
What types of immune reactions are involved in graft rejection?
Cell-mediated immune reaction (Type IV) and circulating antibodies (Type II – Antibody Dependent Cellular Cytotoxicity reaction).
157
What are the three types of graft rejection?
* Hyperacute rejection
* Acute rejection
* Chronic rejection
158
When does hyperacute rejection occur?
Within minutes or hours after transplantation or even recognized on the operating table.
159
What causes hyperacute rejection?
An antigen-antibody reaction at the vascular level (Type 2 reaction).
160
When does acute rejection occur?
Within days of transplantation in the untreated recipient or appears suddenly (days to months) after the termination of immunosuppression.
161
What mechanisms are involved in acute rejection?
Both cell-mediated and humoral mechanisms of tissue damage.
162
What are the consequences of acute rejection?
Results in acute cellular rejection and acute vasculitis with extensive necrosis.
163
What characterizes chronic rejection?
Dominated by vascular changes, interstitial fibrosis, and loss of parenchyma.
164
What type of reaction usually results in chronic rejection?
Type 4 reaction.
