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Immunopathology > Lecture 12 > Flashcards

Lecture 12 Flashcards

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1
Q

What is immunisation?

A

The process by which a person becomes protected against a disease

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2
Q

How does immunisation occur?

A

Naturally (infection) or artificially (vaccination)

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3
Q

What are the types of immunisation?

A

Active and passive

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4
Q

What is passive immunisation?

A
  • Preformed antibodies are given to individual to confer immediate, short-terms protection against a specific pathogen.
  • Does not involve the immune system producing its own antibodies or memory cells.
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5
Q

What are the types of passive immunisation?

A

Natural and artificial

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6
Q

Natural Passive Immunisation

A

Occurs when antibodies are transferred from mother to baby through placenta or milk.

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7
Q

Artificial Passive Immunisation

A

Achieved by injecting pre-formed antibodies to provide immediate protection.

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8
Q

What is an example of natural passive immunisation?

A

Newborns receiving maternal antibodies for temporary protection against infection.

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9
Q

What is an example of artificial passive immunisation?

A

Receiving rabies immunoglobulin after exposure to rabies virus

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10
Q

What are the characteristics of Passive Immunisation?

A
  • Direct Antibody Transfer
  • Immediate Protection
  • No Memory Cell Formation
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11
Q

Advantages of Passive Immunisation

A
  • Provides immediate protection
  • Useful for individuals with weakened immune systems or those exposed to deadly pathogens
  • Effective in post-exposure scenarios
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12
Q

Limitations of Passive Immunisation

A
  • Short-term immunity
  • No memory cell formation
  • Risk of allergic reactions
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13
Q

What are the types of active immunisation?

A
  • Natural active immunisation
  • Artificial active immunisation
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14
Q

Natural Active Immunisation

A
  • Occur when a person gets infected with a disease and the immune system responds by producing antibodies and memory cells
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15
Q

Artificial active immunisation

A

Achieved through vaccination, where an antigen is introduced to trigger an immune response without causing disease.

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16
Q

Natural active immunisation example

A

Immunity developed after recovering from measles

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17
Q

Artificial active immunisation examples

A

Receiving the MMR vaccine to prevent measles, mumps and rubella

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18
Q

Characteristics of Active Immunisation

A
  • Exposure to Antigen
  • Immune response activation
  • Antibody production
  • Memory cell formation
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19
Q

Advantages of Active Immunisation

A
  • Long-term or lifelong immunity
  • Safer than acquiring immunity through natural infection
  • Can lead to herd immunity, protecting those who cannot be vaccinated
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20
Q

Limitations of Active Immunisation

A
  • May require booster doses for prolonged immunity
  • Takes time to develop immunity
  • SOme individuals may have reduced immune responses
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21
Q

What is a vaccine?

A

A biological preparation that stimulates the immune system to develop protection against a specific disease

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22
Q

What does a vaccine contain?

A

Typically contains an antigen (weakened, inactivated, or synthetic components of a pathogen) that triggers an immune response, enabling the body to recognise and fight the disease in future

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23
Q

What do vaccines prevent?

A

Infections, reduce disease severity, and contribute to herd immunity, protecting both individuals and communities

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24
Q

What are the methods to create vaccines?

A
  • Live attenuated vaccines
  • Inactivated (killed) vaccines
  • Subunit
  • Recombinant vaccines
  • Toxoid vaccines
  • mRNA and Viral Vector Vaccines
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25
Live Attenuated Vaccines
- Pathogens are weakened - Virus of bacteria can still replicate but does not cause severe disease
26
How are pathogens weakened for live attenuated vaccines?
- Genetic modifications - Growing them in non-human cells, making them less virulent but still capable of inducing an immune response
27
Examples of Live Attenuated Vaccines?
- Measles, mumps, and rubella (MMR) vaccine - Bacillus Calmette-Guerin (BCG) vaccine - Yellow fever vaccine
28
Inactivated (killed) vaccine?
- Pathogens are killed using heat, chemicals or radiation, ensuring they cannot replicate but still retain their antigenic properties
29
Examples of inactivated vaccines?
- Inactivated polio vaccine (IPV) - Hepatitis A vaccine - Rabies vaccine
30
Subunit Vaccine
Instead of using the whole pathogen, only specific antigenic parts are used to stimulate an immune response
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What are some important subunit vaccines?
- Polysaccharide vaccines - Conjugate vaccines - Protein-based vaccines
32
Examples of subunit vaccines?
- Pneumococcal and meningococcal vaccines - Haemophilus influenza type B (Hib) vaccine
33
Recombinant vaccines
Genetic engineering used to produce viral or bacterial proteins
34
Recombinant vaccines examples:
- Human papillomavirus (HPV) - Hepatitis B vaccine
35
Toxoid vaccine
Contain chemically inactivated toxins that stimulate an immune response
36
Toxoid vaccines examples?
- Tetanus vaccine - Diphtheria vaccine
37
Messenger RNA (mRNA) vaccines
- Developed using the pathogens genetic code
38
What can cancer cells be viewed as?
Altered self-cells that have escaped normal growth-regulating mechanisms
39
Benign Tumour
- Is not capable of indefinite growth - Does not invade the healthy surrounding tissues extensively
40
Malignant Tumour
- A tumour that continues to grow - Becomes progressively invasive Can inhibit metastasis: - Small clusters of cells dislodge from a tumour - Invade blood or lymph vessels - Carried to other tissues where they can continue to proliferate
41
The hallmarks of cancer
42
Cancer cells resist cell death
- Cells with DNA damage normally undergo apoptosis - Cancer cells disable apoptosis pathways, allowing continued proliferation despite genetic defects
43
Relation to cell cycle and cancer
Cancer arises when cell cycle regulation fails, leading to uncontrolled cell division
44
What can failed cell cycle regulation be due to?
- Mutations in cell cycle regulators (oncogenes and tumour suppressor genes) - Disruption of checkpoints - Overactive cyclin-dependent kinases - Evasion of apoptosis
45
Internal and external signals for cell growth
Internal: - Kinases and cyclins External: - Trigger internal factors, which affect cell cycle
46
Cancer cell growth and metastasis
47
Angiogenesis
The formation of new blood vessels from existing ones, is a crucial process for tumour growth and metastasis
48
Why do tumors need to stimulate the formation of new blood vessels as they grow?
Because as tumors grow beyond a certain size, they require more oxygen and nutrients to survive and proliferate.
49
What is the process called when tumors stimulate the growth of new blood vessels?
Angiogenesis.
50
Which pro-angiogenic factor is commonly secreted by cancer cells?
Vascular Endothelial Growth Factor (VEGF).
51
What is the role of VEGF in tumor growth?
VEGF stimulates blood vessel formation to provide the tumor with nutrients and oxygen and to facilitate the spread of cancer cells.
52
How does angiogenesis benefit cancer cells beyond nutrient supply?
It also facilitates the spread (metastasis) of cancer cells through the newly formed blood vessels.
53
Carcinogens
- The drivers of cancer - A substance, organisms or agent capable of causing cancer
54
What happens to the cells in our body when exposed to carcinogens?
Leads to either direct or indirect DNA damage that can result in transformation of normal cells in neoplastic cells.
55
What are some physical carcinogens?
Radiation UV light
56
What are some chemical carcinogens?
- Alkylating agents - Alfatoxin - Tobacco - Asbestos
57
What are some viral/microbial carcinogens?
- Viruses: HPV, Hepatitis B and C - Bacteria: Helicobacter Pylori
58
The International Agency for Research on Cancer (IARC) classification of substances: Group 1
Carcinogenic to humans
59
The International Agency for Research on Cancer (IARC) classification of substances: Group 2B
Probably carcinogenic to humans
60
The International Agency for Research on Cancer (IARC) classification of substances: Group 2B
Possible carcinogenic to humans
61
The International Agency for Research on Cancer (IARC) classification of substances: Group 3
Carcinogenicity not classifiable
62
The International Agency for Research on Cancer (IARC) classification of substances: Group 4
Probably not carcinogenic
63
Whata re the molecular basis of cancer?
- Genetic mutations (oncogenes, tumour suppressor genes) - Epigenetic changes (DNA methylation, histone modifications) - Chromosomal abnormalities (translocations, amplifications, deletions)
64
Oncogenes
Mutated or overactive versions of normal genes called proto-oncogenes, which regulate cell growth and division - RAS, MYC, HER2
65
When mutated oncogenes drive...?
Excessive and uncontrolled cell proliferation, contributing to tumour formation
66
Tumour Supressor Genes
Regulate cell cycle checkpoints, repair DNA damage and trigger apoptosis if necessary - TP53, RB1, BRAC1, BRCA2
67
What happens to tumour suppressor genes when mutated or lost:
Cells escape normal growth control, allowing cancer prgression
68
What is epigenetic changes role in cancer?
- Alters gene expression without mutating the DNA sequence - Methylation - Histone modifications
69
How do chromosomal abnormalities play a significant role in cancer development?
Disrupting normal gene function lead to the activation of oncogenes, the inactivation of tumor suppressor genes or genomic instability.
70
Types of chromosomal abnormalities
- Numerical abnormality (Aneuploidy) - Structural abnormalities
71
Chromosomal Translocations
A piece of one chromosome breaks off and fuses with another
72
Chromosomal Deletions
Loss of a segment of a chromosome, often leading to tumor suppressor gene loss
73
What are the two major types of tumour antigens?
Tumour specific transplantation Ags (TSTA) - Do not express on normal cells of the body Tumour associated transplantation Ags (TATA) - May be expressed at very low levels on normal cells but expressed much higher levels on tumour cells
74
What are TSTA ((Tumor-Specific Transplantation Antigens)?
Antigens present only on tumor cells.
75
What is TATA (Tumor-Associated Transplantation Antigens) ?
Antigens present on both normal and tumor cells, but expressed at higher levels or in an abnormal context in tumors.
76
What is the expression of TSTA (Tumor-Specific Transplantation Antigens)?
Exclusively found in cancerous cells.
77
What is the expression of TATA (Tumor-Associated Transplantation Antigens)?
Found in both normal and tumor cells, though often re-expressed in cancer.
78
What is the immune cell recognition of TATA (Tumor-Associated Transplantation Antigens) ?
Less immunogenic, as they may be present in normal cells.
79
What are some example antigens of TATA (Tumor-Associated Transplantation Antigens)?
Alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), HER2/neu.
80
What is the use of TATA (Tumor-Associated Transplantation Antigens) in cancer therapy?
Used as biomarkers for cancer diagnosis and prognosis.
81
What is the clinical importance of TATA (Tumor-Associated Transplantation Antigens)?
Used in early cancer detection and monitoring.
82
What is the immune system recognition of TSTA (Tumor-Specific Transplantation Antigens)
Highly immunogenic, as they are foreign to the immune system.
83
What are some example antigens of TSTA (Tumor-Specific Transplantation Antigens)?
Mutated p53, viral oncogene products (e.g., HPV E6/E7).
84
What is the use of TSTA (Tumor-Specific Transplantation Antigens) in cancer therapy?
Ideal targets for immunotherapy since they are not found in normal cells.
85
What is the clinical importance of TSTA (Tumor-Specific Transplantation Antigens)?
More specific for targeted cancer treatment.
86
What are the mechanisms for tumour evasion of the immune system?
- Modulation of tumour specific antigens - Reduction of MHC class I expression on tumour cells - Lack of co-stimulatory signals to stimulate T cell response
87
Immunodeficiency
The immune system's ability to fight infection and disease is weakened or absent
88
What can immunodeficiency result from?
- Genetic defects (primary immunodeficiency) - External factors like infections, malnutrition or medical treatments (secondary immunodeficiency)
89
Primary (congenital) immunodeficiency disorders
Genetic or developmental defects affecting immune function
90
What are the clinical features of Primary (congenital) immunodeficiency disorders?
Recurrent infections, poor response to vaccines, failure to thrive
91
What are the types of primary immunodeficiencies?
- B-cell (antibody) deficiencies - T-cell deficiencies - Combined B-cell and T-cell deficiencies - Phagocytic defects - Complement deficiencies
92
T-Cell deficiencies - DiGeorge Syndrome
- Small jaw - Small upper limb and mouth - May have cleft lip/palate - Eyes slanted - Low set ears
93
Combined B-cell and T-cell deficiencies – e.g., Severe Combined Immunodeficiency (SCID)
Absent or dysfunctional T cells → No adaptive immune response to infections. Absent or very small thymus due to lack of T-cell development.
94
Phagocytic defects Chronic Granulomatous Disease (CGD)
A defect in the ability of phagocytes (neutrophils, monocytes, macrophages) to generate reactive oxygen species (ROS) required for killing certain bacteria and fungi
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96
Clinical features of secondary (acquired) immunodeficiency
Increased susceptibility to opportunistic infections, chronic illness, delayed wound healing
97
What are the common causes of secondary immunodeficiency?
- Infections - Malnutrition - Medical treatments - Metabolic diseases - Cancer
98
Acquired Immunodeficiency Syndrome (AIDS)
- Caused by HIV-1 - Retrovirus with 2 copies of single stranded RNA genome - It uses reverse transcriptase to transform its ss-RNA genome into ds-DNA for integration into host genome
99
AIDS
- HIV-1 and HIV-2 closely related - Long incubation period - Tropism for lymphocytes and nervous system. - Immunosuppression CD4+ T-cells
100
How does AIDS transmit?
- Sexual contact - Parental - Mother-infant
101
Who is at high risk of AIDS?
1. Homosexual males (60%) 2. Intravenous drug abusers (24%) 3. Hemophiliacs (1%) 4. Other blood recipients (2%) 5. Heterosexual partners of other high-risk groups members 6. Children of parents from groups 1-3.
102
Symptoms of AIDS?
- Severe immunosuppression - Secondary tumors - Neurological symptoms
103
Can HIV be vaccinated against?
- HIV thrives in the presence of circulating antibodies directed against it - HIV integrates itself into the host genome and may stay dormant for years

Immunopathology (15 decks)

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