The immune system has both innate (non-specific) defenses and adaptive (specific) defenses. The innate system uses physical and chemical barriers like skin and mucus as well as cells that attack foreign substances. If pathogens breach these defenses, the adaptive system mounts an antigen-specific response using B cells, T cells, and antibodies. Vaccines help active immunity develop by exposing the body to antigens without causing disease. The immune system defends the body but can also cause issues like allergies and asthma when improperly activated.
White blood cells & Immunity (The Guyton and Hall Physiology)Maryam Fida
Leukocytes or WBCs are the mobile units of the body’s immune defense system.
Immunity is the body’s ability to resist or eliminate potentially harmful foreign materials or abnormal cells.
WBC count: 5000 to 11000/ul of blood
GRANULOCYTES
Polymorphonuclear neutrophils 60-70%
Polymorphonuclear eosinophils 2-3%
Polymorphonuclear basophils 0.4%
NON-GRANULOCYTES
Monocytes 5.3%
Lymphocytes 30%
Granulocytes and monocytes are formed and stored only in bone marrow
Lymphocytes and plasma cells are formed and stored mainly in various lymphoid tissue such as lymph node, spleen, thymus and tonsils as well as in bone marrow.
GRANULOCYTES
4 to 8 hours in blood and 4 to 5 days in tissues
MONOCYTES
Monocytes also have a short transit time:
10 to 20 hours in blood and In tissue they swell to much larger size to become tissue macrophages.
LYMPHOCYTES
weeks to months
neutrophil
. 60-70% of leukocytes
nucleus: 2-5 lobes
Counting the number of lobes and grouping them is called Arneth count.
Shift to left means (increase no of young and predominant WBCs) e.g During acute infection.
Shift to right means, old cells are predominant. e.g During recovery phase
NEUTROPENIA
Decrease in neutrophils count
Typhoid
AIDS and viral hepatitis
Kalazar fever
Bone marrow depression by drugs and radiations
NEUTROPHILIA
Increase in neutrophils count
Appendicitis , Tonsillitis, Pneumonia
Burns, Hemorrhage, MI, Pain
Hypoxia, Pregnancy
BASOPHIL
Their cytoplasmic granules take up basic dyes and appear deep blue
MAST CELLS are derived from basophils under the influence of interleukins 3 and 4
Under many allergic conditions basophils and mast cells bursts and releases
Histamine
Bradykinin
Serotonin
Slow reacting substance of anaphylaxis
Heparin
Lysosomal enzymes
It is the capacity of the human body to resist and destroy the invading organisms or toxins.
IMMUNITY:
INTRODUCTION:
Our immune system is essential for our survival.
Without an immune system, our bodies would be open to attack from bacteria, viruses, parasites, and more.
It is our immune system that keeps us healthy as we drift through a sea of pathogens.
Introduction:
RNA interference (RNAi) or Post-Transcriptional Gene Silencing (PTGS) is an important biological process for modulating eukaryotic gene expression.
It is highly conserved process of posttranscriptional gene silencing by which double stranded RNA (dsRNA) causes sequence-specific degradation of mRNA sequences.
dsRNA-induced gene silencing (RNAi) is reported in a wide range of eukaryotes ranging from worms, insects, mammals and plants.
This process mediates resistance to both endogenous parasitic and exogenous pathogenic nucleic acids, and regulates the expression of protein-coding genes.
What are small ncRNAs?
micro RNA (miRNA)
short interfering RNA (siRNA)
Properties of small non-coding RNA:
Involved in silencing mRNA transcripts.
Called “small” because they are usually only about 21-24 nucleotides long.
Synthesized by first cutting up longer precursor sequences (like the 61nt one that Lee discovered).
Silence an mRNA by base pairing with some sequence on the mRNA.
Discovery of siRNA?
The first small RNA:
In 1993 Rosalind Lee (Victor Ambros lab) was studying a non- coding gene in C. elegans, lin-4, that was involved in silencing of another gene, lin-14, at the appropriate time in the
development of the worm C. elegans.
Two small transcripts of lin-4 (22nt and 61nt) were found to be complementary to a sequence in the 3' UTR of lin-14.
Because lin-4 encoded no protein, she deduced that it must be these transcripts that are causing the silencing by RNA-RNA interactions.
Types of RNAi ( non coding RNA)
MiRNA
Length (23-25 nt)
Trans acting
Binds with target MRNA in mismatch
Translation inhibition
Si RNA
Length 21 nt.
Cis acting
Bind with target Mrna in perfect complementary sequence
Piwi-RNA
Length ; 25 to 36 nt.
Expressed in Germ Cells
Regulates trnasposomes activity
MECHANISM OF RNAI:
First the double-stranded RNA teams up with a protein complex named Dicer, which cuts the long RNA into short pieces.
Then another protein complex called RISC (RNA-induced silencing complex) discards one of the two RNA strands.
The RISC-docked, single-stranded RNA then pairs with the homologous mRNA and destroys it.
THE RISC COMPLEX:
RISC is large(>500kD) RNA multi- protein Binding complex which triggers MRNA degradation in response to MRNA
Unwinding of double stranded Si RNA by ATP independent Helicase
Active component of RISC is Ago proteins( ENDONUCLEASE) which cleave target MRNA.
DICER: endonuclease (RNase Family III)
Argonaute: Central Component of the RNA-Induced Silencing Complex (RISC)
One strand of the dsRNA produced by Dicer is retained in the RISC complex in association with Argonaute
ARGONAUTE PROTEIN :
1.PAZ(PIWI/Argonaute/ Zwille)- Recognition of target MRNA
2.PIWI (p-element induced wimpy Testis)- breaks Phosphodiester bond of mRNA.)RNAse H activity.
MiRNA:
The Double-stranded RNAs are naturally produced in eukaryotic cells during development, and they have a key role in regulating gene expression .
White blood cells & Immunity (The Guyton and Hall Physiology)Maryam Fida
Leukocytes or WBCs are the mobile units of the body’s immune defense system.
Immunity is the body’s ability to resist or eliminate potentially harmful foreign materials or abnormal cells.
WBC count: 5000 to 11000/ul of blood
GRANULOCYTES
Polymorphonuclear neutrophils 60-70%
Polymorphonuclear eosinophils 2-3%
Polymorphonuclear basophils 0.4%
NON-GRANULOCYTES
Monocytes 5.3%
Lymphocytes 30%
Granulocytes and monocytes are formed and stored only in bone marrow
Lymphocytes and plasma cells are formed and stored mainly in various lymphoid tissue such as lymph node, spleen, thymus and tonsils as well as in bone marrow.
GRANULOCYTES
4 to 8 hours in blood and 4 to 5 days in tissues
MONOCYTES
Monocytes also have a short transit time:
10 to 20 hours in blood and In tissue they swell to much larger size to become tissue macrophages.
LYMPHOCYTES
weeks to months
neutrophil
. 60-70% of leukocytes
nucleus: 2-5 lobes
Counting the number of lobes and grouping them is called Arneth count.
Shift to left means (increase no of young and predominant WBCs) e.g During acute infection.
Shift to right means, old cells are predominant. e.g During recovery phase
NEUTROPENIA
Decrease in neutrophils count
Typhoid
AIDS and viral hepatitis
Kalazar fever
Bone marrow depression by drugs and radiations
NEUTROPHILIA
Increase in neutrophils count
Appendicitis , Tonsillitis, Pneumonia
Burns, Hemorrhage, MI, Pain
Hypoxia, Pregnancy
BASOPHIL
Their cytoplasmic granules take up basic dyes and appear deep blue
MAST CELLS are derived from basophils under the influence of interleukins 3 and 4
Under many allergic conditions basophils and mast cells bursts and releases
Histamine
Bradykinin
Serotonin
Slow reacting substance of anaphylaxis
Heparin
Lysosomal enzymes
It is the capacity of the human body to resist and destroy the invading organisms or toxins.
IMMUNITY:
INTRODUCTION:
Our immune system is essential for our survival.
Without an immune system, our bodies would be open to attack from bacteria, viruses, parasites, and more.
It is our immune system that keeps us healthy as we drift through a sea of pathogens.
Introduction:
RNA interference (RNAi) or Post-Transcriptional Gene Silencing (PTGS) is an important biological process for modulating eukaryotic gene expression.
It is highly conserved process of posttranscriptional gene silencing by which double stranded RNA (dsRNA) causes sequence-specific degradation of mRNA sequences.
dsRNA-induced gene silencing (RNAi) is reported in a wide range of eukaryotes ranging from worms, insects, mammals and plants.
This process mediates resistance to both endogenous parasitic and exogenous pathogenic nucleic acids, and regulates the expression of protein-coding genes.
What are small ncRNAs?
micro RNA (miRNA)
short interfering RNA (siRNA)
Properties of small non-coding RNA:
Involved in silencing mRNA transcripts.
Called “small” because they are usually only about 21-24 nucleotides long.
Synthesized by first cutting up longer precursor sequences (like the 61nt one that Lee discovered).
Silence an mRNA by base pairing with some sequence on the mRNA.
Discovery of siRNA?
The first small RNA:
In 1993 Rosalind Lee (Victor Ambros lab) was studying a non- coding gene in C. elegans, lin-4, that was involved in silencing of another gene, lin-14, at the appropriate time in the
development of the worm C. elegans.
Two small transcripts of lin-4 (22nt and 61nt) were found to be complementary to a sequence in the 3' UTR of lin-14.
Because lin-4 encoded no protein, she deduced that it must be these transcripts that are causing the silencing by RNA-RNA interactions.
Types of RNAi ( non coding RNA)
MiRNA
Length (23-25 nt)
Trans acting
Binds with target MRNA in mismatch
Translation inhibition
Si RNA
Length 21 nt.
Cis acting
Bind with target Mrna in perfect complementary sequence
Piwi-RNA
Length ; 25 to 36 nt.
Expressed in Germ Cells
Regulates trnasposomes activity
MECHANISM OF RNAI:
First the double-stranded RNA teams up with a protein complex named Dicer, which cuts the long RNA into short pieces.
Then another protein complex called RISC (RNA-induced silencing complex) discards one of the two RNA strands.
The RISC-docked, single-stranded RNA then pairs with the homologous mRNA and destroys it.
THE RISC COMPLEX:
RISC is large(>500kD) RNA multi- protein Binding complex which triggers MRNA degradation in response to MRNA
Unwinding of double stranded Si RNA by ATP independent Helicase
Active component of RISC is Ago proteins( ENDONUCLEASE) which cleave target MRNA.
DICER: endonuclease (RNase Family III)
Argonaute: Central Component of the RNA-Induced Silencing Complex (RISC)
One strand of the dsRNA produced by Dicer is retained in the RISC complex in association with Argonaute
ARGONAUTE PROTEIN :
1.PAZ(PIWI/Argonaute/ Zwille)- Recognition of target MRNA
2.PIWI (p-element induced wimpy Testis)- breaks Phosphodiester bond of mRNA.)RNAse H activity.
MiRNA:
The Double-stranded RNAs are naturally produced in eukaryotic cells during development, and they have a key role in regulating gene expression .
Richard's entangled aventures in wonderlandRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
The increased availability of biomedical data, particularly in the public domain, offers the opportunity to better understand human health and to develop effective therapeutics for a wide range of unmet medical needs. However, data scientists remain stymied by the fact that data remain hard to find and to productively reuse because data and their metadata i) are wholly inaccessible, ii) are in non-standard or incompatible representations, iii) do not conform to community standards, and iv) have unclear or highly restricted terms and conditions that preclude legitimate reuse. These limitations require a rethink on data can be made machine and AI-ready - the key motivation behind the FAIR Guiding Principles. Concurrently, while recent efforts have explored the use of deep learning to fuse disparate data into predictive models for a wide range of biomedical applications, these models often fail even when the correct answer is already known, and fail to explain individual predictions in terms that data scientists can appreciate. These limitations suggest that new methods to produce practical artificial intelligence are still needed.
In this talk, I will discuss our work in (1) building an integrative knowledge infrastructure to prepare FAIR and "AI-ready" data and services along with (2) neurosymbolic AI methods to improve the quality of predictions and to generate plausible explanations. Attention is given to standards, platforms, and methods to wrangle knowledge into simple, but effective semantic and latent representations, and to make these available into standards-compliant and discoverable interfaces that can be used in model building, validation, and explanation. Our work, and those of others in the field, creates a baseline for building trustworthy and easy to deploy AI models in biomedicine.
Bio
Dr. Michel Dumontier is the Distinguished Professor of Data Science at Maastricht University, founder and executive director of the Institute of Data Science, and co-founder of the FAIR (Findable, Accessible, Interoperable and Reusable) data principles. His research explores socio-technological approaches for responsible discovery science, which includes collaborative multi-modal knowledge graphs, privacy-preserving distributed data mining, and AI methods for drug discovery and personalized medicine. His work is supported through the Dutch National Research Agenda, the Netherlands Organisation for Scientific Research, Horizon Europe, the European Open Science Cloud, the US National Institutes of Health, and a Marie-Curie Innovative Training Network. He is the editor-in-chief for the journal Data Science and is internationally recognized for his contributions in bioinformatics, biomedical informatics, and semantic technologies including ontologies and linked data.
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
Observation of Io’s Resurfacing via Plume Deposition Using Ground-based Adapt...Sérgio Sacani
Since volcanic activity was first discovered on Io from Voyager images in 1979, changes
on Io’s surface have been monitored from both spacecraft and ground-based telescopes.
Here, we present the highest spatial resolution images of Io ever obtained from a groundbased telescope. These images, acquired by the SHARK-VIS instrument on the Large
Binocular Telescope, show evidence of a major resurfacing event on Io’s trailing hemisphere. When compared to the most recent spacecraft images, the SHARK-VIS images
show that a plume deposit from a powerful eruption at Pillan Patera has covered part
of the long-lived Pele plume deposit. Although this type of resurfacing event may be common on Io, few have been detected due to the rarity of spacecraft visits and the previously low spatial resolution available from Earth-based telescopes. The SHARK-VIS instrument ushers in a new era of high resolution imaging of Io’s surface using adaptive
optics at visible wavelengths.
(May 29th, 2024) Advancements in Intravital Microscopy- Insights for Preclini...Scintica Instrumentation
Intravital microscopy (IVM) is a powerful tool utilized to study cellular behavior over time and space in vivo. Much of our understanding of cell biology has been accomplished using various in vitro and ex vivo methods; however, these studies do not necessarily reflect the natural dynamics of biological processes. Unlike traditional cell culture or fixed tissue imaging, IVM allows for the ultra-fast high-resolution imaging of cellular processes over time and space and were studied in its natural environment. Real-time visualization of biological processes in the context of an intact organism helps maintain physiological relevance and provide insights into the progression of disease, response to treatments or developmental processes.
In this webinar we give an overview of advanced applications of the IVM system in preclinical research. IVIM technology is a provider of all-in-one intravital microscopy systems and solutions optimized for in vivo imaging of live animal models at sub-micron resolution. The system’s unique features and user-friendly software enables researchers to probe fast dynamic biological processes such as immune cell tracking, cell-cell interaction as well as vascularization and tumor metastasis with exceptional detail. This webinar will also give an overview of IVM being utilized in drug development, offering a view into the intricate interaction between drugs/nanoparticles and tissues in vivo and allows for the evaluation of therapeutic intervention in a variety of tissues and organs. This interdisciplinary collaboration continues to drive the advancements of novel therapeutic strategies.
This pdf is about the Schizophrenia.
For more details visit on YouTube; @SELF-EXPLANATORY;
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4. • Viruses and bacteria are everywhere.
Some of them want to invade your body.
How does your body defend itself against
viruses and bacteria?
W
O
R
K
T
O
G
E
T
H
E
R
5. Defense Against Disease
If these barriers are penetrated,
the body responds with
If the innate immune response is insufficient,
the body responds with
Adaptive Immune Response
cell-mediated immunity, humoral immunity
Nonspecific External Barriers
skin, mucous membranes
Innate Immune Response
phagocytic and natural killer cells,
inflammation, fever
6. First line of defense
• Non-specific defenses are designed to
prevent infections by viruses and
bacteria. These include:
– Intact skin
– Mucus and Cilia
– Phagocytes
7. Role of skin
• Dead skin cells are
constantly sloughed
off, making it hard for
invading bacteria to
colonize.
• Sweat and oils
contain anti-microbial
chemicals, including
some antibiotics.
8. Role of mucus and cilia
• Mucus contains lysozymes,
enzymes that destroy
bacterial cell walls.
• The normal flow of mucus
washes bacteria and viruses
off of mucus membranes.
• Cilia in the respiratory tract
move mucus out of the
lungs to keep bacteria and
viruses out.
9. Role of phagocytes
• Phagocytes are several types
of white blood cells (including
macrophages and
neutrophils) that seek and
destroy invaders. Some also
destroy damaged body cells.
• Phagocytes are attracted by
an inflammatory response of
damaged cells.
10. Role of inflammation
• Inflammation is signaled by mast cells,
which release histamine.
• Histamine causes fluids to collect around
an injury to dilute toxins. This causes
swelling.
• The temperature of the tissues may rise,
which can kill temperature-sensitive
microbes.
11. Role of fever
• Fever is a defense mechanism that can
destroy many types of microbes.
• Fever also helps fight viral infections by
increasing interferon production.
• While high fevers can be dangerous,
some doctors recommend letting low
fevers run their course without taking
aspirin or ibuprofen.
12.
13. • Why aren’t non-specific defenses enough?
Why do we also need specific defenses?
W
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14. Specific defenses
• Specific defenses are those that give us
immunity to certain diseases.
• In specific defenses, the immune system
forms a chemical “memory” of the
invading microbe. If the microbe is
encountered again, the body reacts so
quickly that few or no symptoms are felt.
15. Major players
• The major players in the immune system
include:
– Macrophage
– T cells (helper, cytotoxic, memory)
– B cells (plasma, memory)
– Antibodies
16. Cells of the Immune System
White Blood Cells
• Phagocytes - Neutrophils
- Macrophages
• Lymphocytes
19. Neutrophils
• 60% of WBCs
• ‘Patrol tissues’ as they squeeze out of the
capillaries.
• Large numbers are released during
infections
• Short lived – die after digesting bacteria
• Dead neutrophils make up a large
proportion of puss.
20. Macrophages
• Larger than neutrophils.
• Found in the organs, not the blood.
• Made in bone marrow as monocytes,
called macrophages once they reach
organs.
• Long lived
• Initiate immune responses as they display
antigens from the pathogens to the
lymphocytes.
23. Phagocytosis
• If cells are under attack they release histamine.
• Histamine plus chemicals from pathogens mean
neutrophils are attracted to the site of attack.
• Pathogens are attached to antibodies and
neutrophils have antibody receptors.
• Enodcytosis of neutrophil membrane
phagocytic vacuole.
• Lysosomes attach to phagocytic vacuole
pathogen digested by proteases
24. Lymphocytes
• Produce antibodies
• B-cells mature in bone marrow then
concentrate in lymph nodes and spleen
• T-cells mature in thymus
• B and T cells mature then circulate in the
blood and lymph
• Circulation ensures they come into contact
with pathogens and each other
25. B -Lymphocytes
• There are c.10 million different B-
lymphocytes, each of which make a
different antibody.
• The huge variety is caused by genes
coding for abs changing slightly during
development.
• There are a small group of clones of each
type of B-lymphocyte
26. B -Lymphocytes
• At the clone stage antibodies do not leave the B-
cells.
• The abs are embedded in the plasma
membrane of the cell and are
called antibody receptors.
• When the receptors in the membrane recognise
and antigen on the surface of the pathogen the
B-cell divides rapidly.
• The antigens are presented to the B-cells by
macrophages
28. B -Lymphocytes
• Some activated B cells PLASMA
CELLS these produce lots of antibodies, <
1000/sec
• The antibodies travel to the blood, lymph,
lining of gut and lungs.
• The number of plasma cells goes down
after a few weeks
• Antibodies stay in the blood longer but
eventually their numbers go down too.
29. B -Lymphocytes
• Some activated B cells MEMORY
CELLS.
• Memory cells divide rapidly as soon as the
antigen is reintroduced.
• There are many more memory cells than
there were clone cells.
• When the pathogen/infection infects again
it is destroyed before any symptoms show.
30.
31. Antibodies
• Also known as immunoglobulins
• Globular glycoproteins
• The heavy and light chains are polypeptides
• The chains are held together by disulphide
bridges
• Each ab has 2 identical ag binding sites –
variable regions.
• The order of amino acids in the variable
region determines the shape of the binding
site
32. How Abs work
• Some act as labels to identify
antigens for phagocytes
• Some work as antitoxins i.e. they block toxins
for e.g. those causing diphtheria and tetanus
• Some attach to bacterial flagella making
them less active and easier for phagocytes to
engulf
• Some cause agglutination (clumping
together) of bacteria making them less likely
to spread
34. Type Number of
ag binding
sites
Site of action Functions
IgG 2 •Blood
•Tissue fluid
•CAN CROSS
PLACENTA
•Increase
macrophage activity
•Antitoxins
•Agglutination
IgM 10 •Blood
•Tissue fluid
Agglutination
IgA 2 or 4 •Secretions (saliva,
tears, small intestine,
vaginal, prostate,
nasal, breast milk)
•Stop bacteria
adhering to host
cells
•Prevents bacteria
forming colonies on
mucous membranes
IgE 2 Tissues •Activate mast cells
HISTAMINE
•Worm response
35. Some vocabulary:
• Antibody: a protein produced by the
human immune system to tag and destroy
invasive microbes.
• Antibiotic: various chemicals produced by
certain soil microbes that are toxic to many
bacteria. Some we use as medicines.
• Antigen: any protein that our immune
system uses to recognize “self” vs. “not
self.”
36. Antibodies
• Antibodies are
assembled out of
protein chains.
• There are many
different chains
that the immune
system
assembles in
different ways to
make different
37. Antibodies as Receptors
• Antibodies can
attach to B cells,
and serve to
recognize
foreign antigens.
38. Antigens as Effectors
• Free antibodies
can bind to
antigens, which
“tags” the
antigen for the
immune system
to attack and
destroy.
39. Antigen recognition
• Cells of the immune system are “trained”
to recognize “self” proteins vs. “not self”
proteins.
• If an antigen (“not self”) protein is
encountered by a macrophage, it will bring
the protein to a helper T-cell for
identification.
• If the helper T-cell recognizes the protein
as “not self,” it will launch an immune
response.
40. T-Lymphocytes
• Mature T-cells have T cell receptors which
have a very similar structure to antibodies
and are specific to 1 antigen.
• They are activated when the receptor
comes into contact with the Ag with
another host cell (e.g. on a macrophage
membrane or an invaded body cell)
41. T-Lymphocytes
• After activation the cell divides to form:
• T-helper cells – secrete CYTOKINES
help B cells divide
stimulate macrophages
• Cytotoxic T cells (killer T cells)
Kill body cells displaying antigen
• Memory T cells
remain in body
42.
43.
44. Active and Passive Immunity
Active immunity
Lymphocytes are activated by antigens on
the surface of pathogens
Natural active immunity - acquired due to
infection
Artificial active immunity – vaccination
Takes time for enough B and T cells to be
produced to mount an effective response.
45. Active and Passive Immunity
Passive immunity
B and T cells are not activated and plasma
cells have not produced antibodies.
The antigen doesn’t have to be encountered
for the body to make the antibodies.
Antibodies appear immediately in blood but
protection is only temporary.
46. Active and Passive Immunity
Artificial passive immunity
Used when a very rapid immune response
is needed e.g. after infection with tetanus.
Human antibodies are injected. In the
case of tetanus these are antitoxin
antibodies.
Antibodies come from blood donors who
have recently had the tetanus vaccination.
Only provides short term protection as abs
destroyed by phagocytes in spleen and
liver.
47. Active and Passive Immunity
Natural passive immunity
A mother’s antibodies pass across the
placenta to the foetus and remain for
several months.
Colostrum (the first breast milk) contains lots
of IgA which remain on surface of the
baby’s gut wall and pass into blood
48.
49. Vaccination
A preparation containing antigenic
material:
• Whole live microorganism
• Dead microorganism
• Attenuated (harmless) microorganism
• Toxoid (harmless form of toxin)
• Preparation of harmless ags
51. Vaccination
Why aren’t they always effective?
• Natural infections persist within the body
for a long time so the immune system has
time to develop an effective response,
vaccinations from dead m-os do not do
this.
• Less effective vaccines need booster
injections to stimulate secondary
responses
52. Vaccination
Why aren’t they always effective?
• Some people don’t respond well/at all to
vaccinations
• Defective immune systems
• Malnutrition particularly protein
53. Vaccination
Why aren’t they always effective?
• Antigenic variation caused by mutation
• Antigenic drift – small changes (still
recognised by memory cells)
• Antigenic shift – large changes (no longer
recognised)
54. Vaccination
Why aren’t they always effective?
• No vaccines against protoctista (malaria
and sleeping sickness)
• Many stages to Plasmodium life cycle with
many antigens so vaccinations would have
to be effective against all stages (or be
effective just against infective stage but
given in very small time period).
55. Vaccination
Why aren’t they always effective?
• Sleeping sickness – Trypanosoma has a
thousand different ags and changes them
every 4-5 days
56. Vaccination
Why aren’t they always effective?
• Antigenic concealment parasites live
inside body cells
• Plasmodium – liver and blood cells
• Parasitic worms – cover themselves in
host proteins
• HIV – live inside T-helper cells
57. Smallpox
Symptoms
• Red spots containing transparent fluid all
over body.
• Spots fill with pus
• Eyelids swell and become glued together
59. Smallpox
Eradication programme
• Started by WHO in 1956
• Aimed to rid world of smallpox by 1977
• Involved vaccination and surveillance
• Over 80% of populations at risk of the
disease were vaccinated
• After any reported case everyone in the
household and 30 surrounding households
vaccinated – RING VACCINATION
61. Smallpox
Eradication programme – why was it successful?
• Variola virus stable -> cheap as everyone used
same vaccine
• Vaccine made from harmless strain of similar
virus (vaccinia)
• Vaccine could be used at high temperatures
• Easy to identify infected people
• Smallpox doesn’t lie dormant in body
63. Measles
• Caused by an airborne virus
• 9th leading cause of death worldwide
• Causes rash and fever
• Can have fatal complications
• Passive immunity from mothers in infants under
8 months
• Now quite a rare disease in developed
countries due to vaccination
64. Measles
• Transmitted easily in overcrowded, insanitary
conditions
• Mainly affects malnourished infants with vitamin
A deficiencies
• Responsible for many cases of childhood
blindness and can cause severe brain damage
• Herd immunity of 93-95% needed to prevent
transmission within a population.
65. Allergies
• When the immune system responds to
harmless substances
• Allergens – antigenic substances which do no
real harm
• Allergens include house dust, animal skin,
pollen, house dust mite and its faeces
66.
67. Allergies
• Histamine causes blood vessels to widen and
become leaky.
• Fluid and white blood cells leave capillaries.
• The area of leakage becomes hot, red and
inflamed
68. Asthma
• Attacks can occur at any time
• Genes play a role in who develops asthma
• Breathing becomes difficult, sufferers
experience wheezing, coughing, a tightness
about the chest and shortage of breath.
• 1/7 children in UK has asthma, number is
increasing.
• >1000 people die each year from asthma every
year in the UK
69. Asthma
• Airways in asthmatics are always inflamed,
during an attack this worsens.
• Fluid leaks from blood into airways and goblet
cells secrete lots of mucus
• Airways can become blocked
• Muscles surrounding trachea and bronchioles
contract which narrows airways further
70. Asthma
• Vaccines are being developed to make allergic
responses less severe
• Designed to desensitise people so they do not
produce antibodies to allergens
• Genetic tests may be used to screen children
and then a vaccine could be given to prevent
them developing asthma
