The document provides an introduction to the immune system, covering both innate and adaptive immunity. It discusses the key components of the innate immune system, including anatomical barriers, white blood cells like neutrophils and macrophages, cytokines, complement proteins, and pattern recognition receptors. It also describes inflammation and how it helps initiate immune responses against pathogens. The adaptive immune system generates immunological memory through antibodies and T-cells that recognize specific antigens or epitopes. The document defines important immunological terms and concepts.
An undergraduate lecture on immunologic tolerance, it's various types and how a breakdown of tolerance contributes to the pathogenesis of autoimmune diseases. Additionally a small quiz at the end to gauge the students' learning.
ELISA Vs ELISPOT - Principle, Procedure, Advantagesajithnandanam
The Enzyme Linked Immunospot (ELISPOT) technique was developed by Cecil Czerkinskdy in 1983. ELISPOT is used for the detection of secreted proteins, such as cytokines and growth factors. ELISPOT is primarily used in immunology research in the following areas:
An undergraduate lecture on immunologic tolerance, it's various types and how a breakdown of tolerance contributes to the pathogenesis of autoimmune diseases. Additionally a small quiz at the end to gauge the students' learning.
ELISA Vs ELISPOT - Principle, Procedure, Advantagesajithnandanam
The Enzyme Linked Immunospot (ELISPOT) technique was developed by Cecil Czerkinskdy in 1983. ELISPOT is used for the detection of secreted proteins, such as cytokines and growth factors. ELISPOT is primarily used in immunology research in the following areas:
Curso realizado por Javier Godino, César Vallejo de los Servicios Científicos Técnicos del IACS y Desirée Perebom del Servicio General de Apoyo a la Investigación - SAI de la Universidad de Zaragoza.
Resumen de Contenidos:
- Que es la citometría de flujo.
- Componentes de un citómetro de flujo.
- Dispersión de la luz.
- Fluorescencia. Fluorocromos, Compensación de
fluorescencias.
- Ventajas e inconvenientes de la citometría de flujo
La inmunidad humoral es el mecanismo principal de defensa contra los microorganismos extracelulares y sus toxinas, en el cual, los componentes del sistema inmune que atacan a los antígenos no son las células directamente sino los anticuerpos secretados por activación antigénica
Immune response during bacterial, parasitic and viral infection.pptxVanshikaVarshney5
when a pathogen attacks on our body how's our body react to it?
this presentation is all about that.
How the immune respone to the parasite, virus or bacteria and save our body.
Curso realizado por Javier Godino, César Vallejo de los Servicios Científicos Técnicos del IACS y Desirée Perebom del Servicio General de Apoyo a la Investigación - SAI de la Universidad de Zaragoza.
Resumen de Contenidos:
- Que es la citometría de flujo.
- Componentes de un citómetro de flujo.
- Dispersión de la luz.
- Fluorescencia. Fluorocromos, Compensación de
fluorescencias.
- Ventajas e inconvenientes de la citometría de flujo
La inmunidad humoral es el mecanismo principal de defensa contra los microorganismos extracelulares y sus toxinas, en el cual, los componentes del sistema inmune que atacan a los antígenos no son las células directamente sino los anticuerpos secretados por activación antigénica
Immune response during bacterial, parasitic and viral infection.pptxVanshikaVarshney5
when a pathogen attacks on our body how's our body react to it?
this presentation is all about that.
How the immune respone to the parasite, virus or bacteria and save our body.
immunity, types,Innate immunity and Adaptive Immunity, primary and secondary immune response, structure and functions of antibodies, immunoglobulins, hypergammaglobulinemia, multiple myeloma, bence jones protein, electrophoretic pattern of multiple myeloma.
Overview of the Immune System: Innate vs. Adaptive Defenses
Innate-Nonspecific Defenses
First Line of defense: Physical barriers
Second Line of defense:
- Major cellular components
Phagocytes
Basophils
Eosinophils
NK cells
- Chemical signals
Interferons
Complement Proteins
Inflammation
Fever (pyrogens)
Introduction
History
Types of immunity
Tissues of immunity
Cells of immunity
Basic aspects of immunology
Major histocompatibility complex
Cytokines
Disorders of immune system
Immune responses in periodontal pathogenesis
Periodontal vaccine
Host modulation
Conclusion
References
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
1. Introduction to the immune
system
Vivekanandan Perumal
vperumal@bioschool.iitd.ac.in
011-26597532
Office hours Wednesday and Friday 5-6pm
2. Immunity
• Immunity is body's ability to resist or eliminate
potentially harmful foreign materials or abnormal
cells
3. History: what imparts Immunity?
• Emil von Behring and Kitasato (1890)
– Serum from vaccinated animals was protective
(diptheria)
• Metchinkoff (1880)
– Cell based Immunity
• Merrill Chase (1940)- Transfer of WBC (immunity to
tuberculosis)
Both serum and cells contribute to immunity
5. The immune system
A functional system – NOT an organ system:
Complex system – includes
• Skin – physical barrier
• Lining of mucus membranes – physical barrier
• Secretions – tears, mucus etc - antimicrobial
• Blood cells and vasculature – WBCs
• Bone marrow
• Liver – makes complement proteins
• Lymphatic system and lymphoid organs
• Most tissues – have resident immune cells
6. Immunity
• Immunity (immunis- Latin-exempt, state of protection
from infectious diseases)
• Immunity is body's ability to resist or eliminate
potentially harmful foreign materials or abnormal cells
• consists of following activities:
– Defense against invading pathogens (viruses & bacteria)
– Removal of 'worn-out' cells (e.g., old RBCs) & tissue debris
(e.g., from injury or disease)
– Identification & destruction of abnormal or mutant cells
(primary defense against cancer)
– Rejection of 'foreign' cells (e.g., organ transplant)
– Inappropriate responses:
• Allergies - response to normally harmless substances
• Autoimmune diseases
8. Overview of the Immune System
Immune System
Innate
(Nonspecific)
1o line of defense
Adaptive
(Specific)
2o line of defense
Interactions between the two systems
9. A typical immune response
INNATE IMMUNITY
Rapid responses to a
broad range of microbes
ACQUIRED IMMUNITY
Slower responses to
specific microbes
External defenses Internal defenses
Skin
Mucous membranes
Secretions
Phagocytic cells
Antimicrobial proteins
Inflammatory response
Natural killer cells
Humoral response
(antibodies)
Cell-mediated response
(cytotoxic
lymphocytes)
Invading
microbes
(pathogens)
Complement
10. Innate immunity vs Adaptive Immunity
No memory
• No time lag
• Not antigen specific
• A lag period
• Antigen specific
• Development
of memory
Innate Immunity
(first line of defense)
Adaptive Immunity
(second line of defense)
11. The innate immune System
Innate Immune
System
External
defenses
Internal
defenses
Interactions between the two systems
14. Anatomical Barriers – Chemical factors
Antimicrobial
Peptides in sweat
Lysozyme in tears /saliva
HCl in stomach
15. Anatomical Barriers – Biological factors
Normal flora – microbes in many parts of the body
Normal flora – competes with pathogens
for nutrients and space
Normal flora – > 1000 species of bacteria
25. Monocytes
• Monocytes (~5% of WBCs)
• Migrate into the tissues and
become Macrophages
Lung Bone
Liver Brain intestine
26. Macrophages
• “Big eaters”
• Phagocytosis of microbes in tissue
(neutrophils are present only in blood)
• Antigen presentation
27. Natural killer cells
• Not B-lymphocytes / T-
lymphocytes
• Important part of the innate
immune system
• Kill virus /bacteria infected
cells (Intracellular
pathogens)
• Kills cancer cells
28. NK cells differentiate choose cells to kill ?
Uninfected cell / Normal cell
Microbe infected cell / cancer cell
Some cell surface proteins are missing
29. How does the killer kill ?
Kills both host cells and microbes
Release of granules with perforins and proteases
30. Toll-like receptors (TLRs)
• Transmembrane proteins
• Present on macrophages / few other cells
• Conserved across vertebrates
• Important part of innate immune system
31. TLRs – What do they do ?
They look out for microbes (or their components)
They bind to the microbes (or their components)
They trigger a cascade of events to kill or protect
against pathogens
THEY ARE INNATE IMMUNE SENSORS
35. What happens when a TLR bind to a microbe ?
TLR binding
to microbe
Inflammation
Secretion of
Cytokines /
Interferon
Phagocytosis
of infected
cell
Apoptosis of
infected cell
36. Summary: innate response – internal
defenses – Cellular (WBCs)
Come into play when the external defenses are breached
• Neutrophils
• Monocytes /macrophages
• NK cells
• TLRs
38. Cytokines
• Small proteins – secreted by
cells of the immune system
• Affect the behaviour of other
cells
• signalling molecules
• Key players in innate and
acquired immunity
39. Which cells release cytokines ?
Cells of the immune system:
• Neutrophils – when they encounter a pathogen
• Macrophages – when they encounter a pathogen
• TLRs – bind to microbe / components of a microbe
• NK cells – on encountering a microbe infected cell /tumour cell
• Lymphocytes – when they are activated
41. Interferons (IFN)
• Signalling proteins produced by by virus infected monocytes
and lymphocytes
• Secreted proteins – Key anti-viral proteins
• “Interfere” with virus replication
• Warn the neighbouring cells that a virus is around...
• If we did not have IFNs – most of us may die of influenza virus
infection
43. 43
The infected cells release IFN
antiviral state
antiviral state
antiviral state
antiviral state
44. 44
Virus infects the neighbouring cells
antiviral state
antiviral state
antiviral state
antiviral state
45. 45
Prewarned cells are able to quickly
inhibit the virus
antiviral state
antiviral state
antiviral state
antiviral state
46. How do interferons inhibit viruses ?
Host protein
Induction
Cascade of events
Virus ds-RNA
Activation
Inactive host protein
Active host protein
Inhibition of
host protein
synthesis
Virus cannot replicate
47. Interleukins
• Interleukins – 1-37
• Not stored inside cells
• Quickly synthesized and secreted in response to infection
• Key modulators of behaviour of immune cells
• Mostly secreted by T-lymphocytes & macrophages
48. What to interleukins do ?
Interleukins
Proliferation of immune cells
Activation of immune cells
Increase antibody production
Inflammation
50. Complement (C`)
• a large number of distinct plasma proteins that react with
one another (C1 thro’ C9)
• Complement can bind to microbes and coat the microbes
• Essential part of innate immune response
• Enhances adaptive immune resposne (taught later)
51. Complement proteins: role in innate
immune system
C`proteins
Inflammation
Facilitates phagocytosis Direct lysis of pathogens
52. How do C` proteins facilitate phagocystosis ?
Bacteria coated with C` Neutrophils have C` receptors
Initiation of phagocytosis
53. How do C` proteins lyse pathogens?
Membrane attack complex formed by c` proteins
54. Coagulation proteins
• Coagulation: mechanism to stop bleeding after injury to blood
vessels
Complex pathway involves
• Platelets
• Coagulation factors
• Vitamin K
56. Coagulation: Delicate balance
Coagulation proteins Anticoagulants
Blood clotting
Inflammation
Apoptosis (prog. Cell death)
Prevent blood clotting
Inhibit inflammation
Inhibit apoptosis
Too much of clotting – Problem
Too little clotting - Problem
Maintenance of a balance
57. Coagulation and innate immunity
Coagulation proteins
Anticoagulants
Pathogens and cytokines
Increased inflammation and increased apoptosis of infected cells
58. Summary: what happens when external defenses fail ?
INNATE IMMUNITY
Rapid responses to a
broad range of microbes
ACQUIRED IMMUNITY
Slower responses to
specific microbes
External defenses Internal defenses
Skin
Mucous membranes
Secretions
Phagocytic cells
Antimicrobial proteins
Inflammatory response
Natural killer cells
Humoral response
(antibodies)
Cell-mediated response
(cytotoxic
lymphocytes)
Invading
microbes
(pathogens)
Complement
62. Inflammation
• Complex biological process by which body responds
to pathogens and irritants
• Associated with swelling of tissue
• Key player in innate immune repsone
63. All roads lead to inflammation
Inflammation
Neutrophils
Monocytes /macrophages
NK cells
TLRs
Cytokines /IFN
C` proteins
Coagulation proteins
Cellular Extracellular
64. Inflammation and vascular changes
• Vasodilatation • Increased capillary permeability
Normal blood vessel Dilated blood vessel
Normal blood vessel
Leaky blood vessel
67. Inflammation and innate immunity
Mast cells – similar to basophils in blood;
mast cells are present in tissues and release histamines in response to wound / infection /irritant
Histamine
Pathogen
removal
Adaptive immune
response
+ + +
68. Summary: role of Inflammation in
innate immunity
• Initiation of phagocytosis – killing of pathogen
• Limiting the spread of infection
• Stimulate adaptive immune response
• Initiate tissue repair
70. The good and bad about inflammation
Acute /short-term -Good chronic /long-term - Bad
71. Chronic inflammation = tissue damage
• Chronic inflammation -
macrophages in the injured
tissue.
• Macrophages release toxins
(including reactive oxygen
species or ROS) that injure
tissues
• chronic inflammation is
almost always accompanied
by tissue destruction.
Normal tissue
Tissue : chronic inflammation
72. Chronic inflammation and tissue
damage
Reduced
tissue
function
Tissue
damage
Chronic
inflammation
Activation of
immune cells
Killing of host cells
75. Immunogens and antigens
• Immunogen / antigen: a substance that elicits
an immune response [i.e. a humoral (antibody
response) or cell-mediated immune response]
Immune response generator
Though the two terms are used interchangeably – there are differences between the two
76. Epitope
• Epitope: the portion of an antigen that is recognized
and bound by an antibody (Ab) or a T-cell receptor
(TCR)
• epitope = antigenic determinant
77. Epitopes
•Epitope: the portion of an antigen that is recognized and bound by an Ab or a T Cell receptor
One protein may have multiple antigenic determinant
79. Immunogenicity
• Immunogencity: is the ability to induce a humoral
(antibody) and/or cell-mediated immune response.
• Weak immunogens
• Strong immunogens
80. What determines immunogenicity ?
• Foreignness: essential for immunogenicity (self-responsive
immune cells are eliminated during lymphocyte development)
• Size: Bigger>Smaller
• Chemical composition: Proteins > nucleic acids /
polysaccharides / lipids
• Structure: Primary /secondary /tertiary structures play a role
• Physical form: Particulate> Soluble
81. Host factors affecting immunogencity
• Difference across species (interspecies)
• Differences within a species (intraspecies)
- Responders / non-responders to vaccine
- differences in disease severity in epidemics
Genetics
Age
82. Isoantigens
• Isoantigens: Antigens present in some but not all
members of a species
• Blood group antigens – basis of blood grouping
• MHC (major histocompatibility complex)- cell surface
glycoproteins
83. Autoantigens
• Autoantigens are substances capable of immunizing
the host from which they are obtained.
• Self antigens are ordinarily non-antigenic
• Modifications of self-antigens are capable of eliciting
an immune response
84. Haptens
• Haptens are small molecules which are non-
immunogenic, thus could never induce an
immune response by themselves.
87. What is an antibody?
• Produced by Plasma cell (B-lymphocytes producing Ab)
• Essential part of adaptive immunity
• Specifically bind a unique antigenic epitope (also called an
antigenic determinant)
• Possesses antigen binding sites
• Members of the class of proteins called immunoglobulins
88. What does an antibody look like ?
• 2 identical heavy chains
• 2 identical light chains
• Each heavy chain – has a
constant and a variable
region
• Each light chain has a
constant and a variable
region
H H
L L
Constant
region
Variable
region
90. Antibody: Fab
Fab region
• Variable region of the
antibody
• Tip of the antibody
• Binds the antigen
• Specificity of antigen
binding determined by
VH and VL
91. Antibody: Fc
Fc region
• Constant region
• Base of the antibody
• Can bind cell receptors
and complement
proteins
92. • Antibodies occur in 2 forms
– Soluble Ag: secreted in blood and tissue
– Membrane-bound Ag: found on surface of B-cell, also
known as a B-cell receptor (BCR)
Antibodies exist in two forms
