MONOALONEL ANTIBODY PRODUCTION
 Monoclonal antibodies (mAbs) are produced from a single clone of
immune cells.
 Typically generated using hybridoma technology or recombinant
DNA technology.
 Hybridoma technology involves fusion of B-cells with myeloma cells
to create immortalized hybridomas.
 Hybridomas produce specific mAbs against a target antigen.
 Recombinant DNA technology involves insertion of genes encoding
mAbs into host cells (e.g., bacteria, yeast, mammalian cells).
 Host cells engineered to express and secrete mAbs.
 Purification of mAbs from cell culture supernatants.
 Widely used in medicine for diagnostics, therapy, and research.
 Examples include cancer treatment (e.g., rituximab), autoimmune
diseases (e.g., adalimumab), and infectious diseases (e.g.,
palivizumab).
TYPES OF INHIBITION
Competitive inhibition:
 Inhibitor competes with substrate for binding to the active site of
enzyme.
 Reversible inhibition that can be overcome by increasing substrate
concentration.
 Increases apparent Km, but Vmax remains unchanged.
Uncompetitive inhibition:
 Inhibitor binds only to the enzyme-substrate complex (ES).
 Inhibitor cannot bind to free enzyme.
 Reduces both Vmax and Km proportionally, maintaining the same
ratio (Vmax/Km).
Non-competitive inhibition:
 Inhibitor binds to enzyme at a site distinct from the active site
(allosteric site).
 Inhibitor can bind to both enzyme and enzyme-substrate complex
(ES).
 Reduces Vmax by decreasing the concentration of active enzyme,
while Km remains constant.
 All forms of inhibition affect enzyme activity, but they differ in their
mechanisms and effects on enzyme kinetics.
HUMORAL IMMUNITY:
 Mediated by antibodies produced by B cells.
 Antibodies circulate in blood and lymph, targeting pathogens and
toxins.
 Effective against extracellular pathogens like bacteria and viruses
outside of host cells.
 Functions include neutralization, opsonization, and complement
activation.
 Memory B cells provide long-term immunity upon subsequent
exposure to the same pathogen.
CELL-MEDIATED IMMUNITY:
 Mediated by T cells (e.g., cytotoxic T cells, helper T cells).
 Targets intracellular pathogens, virus-infected cells, and abnormal
cells (e.g., cancer cells).
 Involves direct killing of infected or abnormal cells by cytotoxic T
cells.
 Helper T cells coordinate immune responses by activating other
immune cells and cytokine secretion.
 Important for defense against viruses, intracellular bacteria, fungi,
and cancer cells.
 Memory T cells provide long-lasting immunity upon re-exposure to
antigens.
DIFFERENT GENERATION OF VACCINES
FIRST-GENERATION VACCINES:
 Traditional vaccines made from weakened or inactivated pathogens.
 Examples include live attenuated vaccines (e.g., measles, mumps,
rubella) and inactivated vaccines (e.g., polio, influenza).
SECOND-GENERATION VACCINES:
 Subunit vaccines containing purified antigens from pathogens.
 May include protein subunits, polysaccharides, or conjugate
vaccines.
 Examples include hepatitis B vaccine (protein subunit) and
Haemophilus influenzae type b (Hib) vaccine (conjugate).
THIRD-GENERATION VACCINES:
 Recombinant vector vaccines using genetically engineered viruses or
bacteria as vectors to deliver antigen genes.
 Stimulate strong immune responses without causing disease.
 Examples include adenovirus-based COVID-19 vaccines and
recombinant vesicular stomatitis virus (rVSV)-based Ebola vaccine.
FOURTH-GENERATION VACCINES:
 Nucleic acid vaccines utilizing DNA or mRNA to encode pathogen
antigens.
 Deliver genetic material directly into cells to induce immune
responses.
 Rapidly developed and scalable, offering potential for personalized
vaccines.
 Examples include mRNA COVID-19 vaccines (Pfizer-BioNTech,
Moderna) and DNA vaccines under development for various
diseases.
INFLAMATORY BARRIERS
PHYSICAL BARRIERS:
 Skin: Forms a physical barrier to prevent pathogen entry.
 Mucous membranes: Line respiratory, gastrointestinal, and
genitourinary tracts, trapping pathogens and preventing their entry.
CHEMICAL BARRIERS:
 Antimicrobial peptides: Small proteins with antimicrobial properties
found in skin, saliva, and mucous membranes.
 Enzymes: Lysozyme in tears and saliva breaks down bacterial cell
walls.
 Gastric acid: Kills ingested pathogens in the stomach.
CELLULAR BARRIERS:
 Phagocytes: White blood cells (e.g., neutrophils, macrophages) engulf
and destroy pathogens.
 Natural killer (NK) cells: Recognize and kill virus-infected cells and
tumor cells.
 Mast cells: Release histamine and other inflammatory mediators in
response to pathogens or tissue damage.
ANTIGENOCITY
 Antigenicity refers to the ability of a substance (antigen) to induce an
immune response.
 Determined by the molecular structure and complexity of the
antigen.
 Antigenicity is influenced by factors such as size, shape, and surface
features.
 Antigens typically contain epitopes, specific regions recognized by
immune cells or antibodies.
 Foreign antigens often elicit stronger immune responses than self-
antigens.
 Antigenicity is crucial for vaccine development and immune system
recognition of pathogens.
IMMUNOGENECITY
 Immunogenicity refers to the ability of an antigen to induce an
immune response in the body.
 Depends on factors like antigenicity, molecular size, complexity, and
foreignness.
 Immunogenic antigens trigger activation of immune cells, leading to
antibody production or cell-mediated responses.
 Adjuvants may enhance immunogenicity by stimulating immune
system components.
 Important consideration in vaccine development to ensure effective
immune responses against pathogens.
 Variability in immunogenicity can affect vaccine efficacy and
individual immune responses.
PSYCO-NEURO IMMUNOLOGY
 Psycho-neuroimmunology (PNI) studies interactions between
psychological processes, nervous system, and immune system.
 Investigates how stress, emotions, and behavior influence immune
function and health.
 Emphasizes bidirectional communication pathways between brain,
endocrine system, and immune system.
 Stress hormones (e.g., cortisol) can suppress immune responses,
increasing susceptibility to infections.
 Positive emotions and social support can enhance immune function
and improve health outcomes.
 PNI research informs understanding of conditions like autoimmune
diseases, cancer, and mental health disorders.
ENZYME INHIBITION
 Enzyme inhibition involves the interference with enzyme activity.
 Competitive inhibition occurs when an inhibitor competes with the
substrate for binding to the active site.
 Noncompetitive inhibition involves the inhibitor binding to a site
other than the active site, altering enzyme conformation.
 Uncompetitive inhibition occurs when the inhibitor binds only to the
enzyme-substrate complex, preventing product formation.
 Inhibitors can be reversible or irreversible, depending on their
ability to dissociate from the enzyme.
 Inhibition impacts enzyme kinetics by altering the maximum
reaction rate (Vmax) and/or the substrate concentration at which
the reaction rate is half-maximal (Km).
 Understanding enzyme inhibition is crucial for drug development
and studying enzyme function.
WHY FEMALE ARE DOMINANT TO AUTOIMMUNITY
 Females tend to have a higher prevalence of autoimmune diseases
compared to males, and several factors contribute to this dominance:
 Hormonal influences: Female sex hormones, particularly estrogen,
play a role in modulating immune responses. Estrogen can enhance
immune reactivity, potentially leading to increased susceptibility to
autoimmune diseases.
 Genetic predisposition: Certain autoimmune diseases have a
genetic component, and some genes associated with autoimmunity
are more prevalent or have stronger effects in females.
 X chromosome: Females have two X chromosomes, while males
have one X and one Y chromosome. Genes related to immune
function are located on the X chromosome, and the presence of two X
chromosomes in females may contribute to increased immune
activity.
 Immune system differences: There are intrinsic differences in the
immune systems of males and females, including variations in
immune cell populations, cytokine production, and response to
pathogens. These differences can influence the likelihood of
developing autoimmune diseases.
 Pregnancy: Pregnancy involves complex immunological changes to
tolerate the fetus, which may affect autoimmune diseases. Some
autoimmune diseases improve during pregnancy but worsen
postpartum.
 Environmental factors: Environmental triggers, such as infections,
stress, and dietary factors, can influence the development of
autoimmune diseases and may affect females differently than males.
  Overall, the interplay of genetic, hormonal, immunological, and
environmental factors contributes to the increased susceptibility of
females to autoimmune diseases.
BRONCHIOL ASTHAMA (AUTOIMMUNITY)
 Bronchiolitis asthma is a subtype of asthma characterized by
inflammation and narrowing of the small airways (bronchioles) in
the lungs.
 While asthma is primarily considered an allergic or inflammatory
condition, autoimmune mechanisms may contribute to some cases.
 Autoimmunity in bronchiolitis asthma involves the immune system
mistakenly attacking the body's own lung tissues, leading to
inflammation and airway constriction.
 Autoimmune reactions in bronchiolitis asthma may target specific
lung proteins or structures, triggering an immune response.
 Autoimmune mechanisms can exacerbate asthma symptoms and
contribute to disease severity in some individuals.
 Understanding the autoimmune component of bronchiolitis asthma
can aid in developing targeted therapies to modulate immune
responses and improve treatment outcomes.
MECHENIA GRAVIS DISEASE AUTOIMMUNITY
 Myasthenia gravis (MG) is an autoimmune neuromuscular disease.
 Autoimmune attack targets acetylcholine receptors (AChR) at
neuromuscular junctions, impairing nerve signaling to muscles.
 Antibodies, primarily IgG, bind to AChR, leading to receptor
destruction or blocking neurotransmitter binding.
 Results in muscle weakness and fatigue, especially in facial, ocular,
and limb muscles.
 Thymus gland abnormalities, including thymic hyperplasia or
thymoma, are common in MG patients, suggesting a role in
autoantibody production.
 Treatment involves acetylcholinesterase inhibitors,
immunosuppressive drugs, plasmapheresis, or thymectomy, aimed
at managing symptoms and modulating immune responses.
 Understanding the autoimmune nature of MG informs treatment
strategies and ongoing research for novel therapies.
MHC SELF AND NON SELF
 Major Histocompatibility Complex (MHC) molecules play a crucial
role in the immune system by presenting antigens to T cells.
 MHC class I molecules are found on almost all nucleated cells and
present endogenous antigens (self and non-self) to cytotoxic T cells
(CD8+).
 MHC class II molecules are primarily expressed on antigen-
presenting cells (APCs) and present exogenous antigens to helper T
cells (CD4+).
 MHC molecules bind and present peptide fragments derived from
self and non-self proteins.
 Self-antigens are peptides derived from the body's own proteins and
are recognized as 'self' by the immune system, promoting tolerance
and preventing autoimmune responses.
 Non-self antigens are peptides derived from foreign pathogens (e.g.,
bacteria, viruses) or environmental substances and are recognized
as 'non-self,' triggering immune responses to eliminate the invaders.
 MHC molecules help distinguish between self and non-self antigens,
ensuring that the immune system targets only foreign invaders while
sparing healthy tissues.
 Dysregulation of MHC-mediated antigen presentation can lead to
autoimmune diseases or susceptibility to infections.