defenses against disease ch. 43
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Defenses Against Disease Ch. 43. From the Tiniest Things…. Everyday we are invaded by bacteria, viruses, and non-self molecules Immune system natural protection against non-self substances 3 parts: Physical barriers skin, tight junctions, mucus layers, acidic environments - PowerPoint PPT PresentationTRANSCRIPT
Defenses Against DiseaseCh. 43
From the Tiniest Things…• Everyday we are invaded by
bacteria, viruses, and non-self molecules
• Immune system natural protection against non-self substances
• 3 parts:1) Physical barriers skin, tight
junctions, mucus layers, acidic environments
2) Innate Immune system non-specific reaction to all non-self molecules
3) Adaptive Immune system specific reaction to reoccurring non-self molecules
The White Army• Leukocytes “white blood cells”, soldiers
protecting your body; patrol the blood and lymph
• 6 main types:1) Macrophage phagocyte (cell eater)
that consume infected cells, pathogens, and non-self molecules
2) Monocyte become macrophages during 2nd wave of protection
3) Neutrophil consumes pathogens and tissue debris
4) Eosinophil secret enzymes to kill parasites (too big for phagocytosis)
5) Basophil respond to allergens, secrete histamine and cause inflammation
The White Army: Lymphocytes• Lymphocytes Groups of
cells in innate and adaptive immunity– NK cells natural killer cells;
kill cells infected by viruses or cancerous cells
– B-Cells capture and present antigens from bacteria
– Plasma cells secrete antibodies
– Helper T-cells help activate other B-cells
– Cytotoxic T-cells kill infected cells
Innate Immunity: Nonspecific!• Recovery time: 7-10 days• Various steps that are
generally effective• Steps made to build adaptive
immunity for faster response time
• Reactions:1) Antimicrobial peptides
simplest response; pathogens interacting with inner lining of body trigger release of defenins (enzymes that destroy membranes)
Innate Immunity: Inflammation• Inflammation heat, pain,
and swelling in infected area– Local only at infection site;
caused by histamine– Systemic throughout the
body (fever); caused by pryrogens which cause the hypothalamus to turn up the heat
• Heat and swelling allow better macrophage attack at infection site and help phagocytosis
Innate Immunity: Inflammation• Steps:1) Infection occurs; macrophages
at site detect pathogens2) Cytokines and histamine are
released; inflammation starts and blood vessels dilate
3) Neutrophils and monocytes drawn towards site (chemokines) and pass through permeable blood vessels
4) Neutrophils consume bacteria and die in the process (pus)
5) Monocytes change to macrophages as 2nd wave attack
6) Infection clears up; inflammation stops
Innate Immunity: Complement Systemand Interferons
• Complement system 30 proteins that recognize and attach to pathogens
• Membrane attack complex after proteins attach; attack complexes bind to them and attack pathogen membranes– Enzymes will produce holes in plasma
membrane– Cell cannot maintain homeostasis with
ions freely flowing; Pathogen swells and lyses
• Interferons released by cells infected with a virus; help block viruses from attaching to new hosts– Activated RNA degrading enzymes to
stop all protein synthesis
Innate Immunity: Natural Killer Cells• NK cells target cells infected by
viruses/cancer• Identify infected cells by the
number of MHC (major histocompatibility complex) proteins on their surface– Normal cell high number– Infected/Cancer protein synthesis
inhibited so low number• Releases perforin to degrade holes
in cell’s membrane; cell swells and lyses
• Also secretes proteases (degrades proteins) into the cell which causes apoptosis
Adaptive Immunity: Specific Defense!• All methods in innate immunity
are generalized; but each attack on our system allows us to build a strong adaptive immunity
• Antigen non-self molecule that generates antibodies; can be any organic molecule but mostly large proteins
• Antigens are recognized by:1) B-cells come from bone
marrow; produce antibodies2) T-cells mainly in Thymus; can
help spread antigen info (helper T-cells) and kill infected cells (cytotoxic T-cells)
Adaptive Immunity: Two Ways to Play• Antibody-mediated (humoral)
B-cells change into plasma cells to release large amounts of antibodies
• Cell-mediated T-cells become active and kill infected cells
• Both methods follow the same pattern:
1) Antigen is recognized2) Lymphocytes are activated3) Antigen is removed from the
body4) Memory cells made to prepare
for future infections
Antibody-Mediated Immunity: Receptors• Antigens must be recognized first• B and T cells are covered with
thousands of receptors for antigens• B-cell receptors 2 heavy chains
(transmembrane) and 2 light chains; 2 variable regions on the end react to specific antigen(s)– 10 trillion B-cells with 100 million
different receptors• T-cell receptors 2 short chains
(transmembrane) with 1 variable region
• Variable region only reacts to small part of antigen (epitope), so one antigen can react to multiple receptors
Antibody-Mediated Immunity: Antibodies• Immunoglobulins (Ig) complex
molecules made of 2 heavy chains and 2 light chains; have a constant region and a variable region
• Classes:1) IgM B-cell receptors2) IgG most abundant; used after 2nd
infection3) IgA secreted in specific parts of the
body; block pathogens from binding to cells
4) IgE secreted by plasma cells; bind to basophils and mast cells to release histamine; allergic response
5) IgD works with IgM; still unclear of function
Antibody-Mediated Immunity: Lymphocyte Activation
1) Dendritic cell engulfs pathogen2) Lysosome degrades pathogen;
antigens are isolated3) Dendritic cell presents antigens
on its membrane through class II MHC proteins; now a APC (antigen-presenting cell)
4) Antigen presented to CD4+ T-cell; T-cell activated
5) Interleukins from T-cell promote rapid division; some cells become helper T-cells and activate more lymphocytes (effector T-cells)
Antibody-Mediated Immunity: Lymphocyte Activation
6) B-cells present antigens on their cell surface and link with helper T-cells; when matched the B-cell becomes activated7) B-cells divided rapidly. Some cells become plasma cells and some become memory B-cells8) Plasma cells secrete antibodies which bind to antigens; inhibits pathogens and make them easier to find for phagocytosis9) Memory B-cells stay in body to create a faster response if a second infection occurs
Antibody-Mediated Immunity: Cleaning Up• Antigens removed from
body two ways1) Neutralization antibodies
bind to antigens inhibiting them from infecting cells; filtered from body with time or consumed
2) Agglutination pathogens are stuck together by antibodies; unable to move
• Both methods result in increased phagocytosis by the complement system
Antibody-Mediated Immunity: Memory Cells• Immunological memory
built from memory B-cells and memory helper T-cells after primary immune response (3-14 days)
• Secondary Immune response less antigen is needed to react with immune system so reaction is faster; flood of IgG antibodies
• Related antigens can set off reaction of similar antibodies
Building Immunities• Active immunity you
build your own antibodies– Vaccination dead or weak
form of the pathogen gives your body the antigen needed to make the antibody but not the disease
• Passive immunity antibodies given directly– IgG mother to fetus– IgA breast milk– Weaker form because effect
only last a month
Cell-Mediated Immunity: Cytotoxic T-Cells• System best for viruses1) Pathogen antigens released from
infected cell2) B-cell picks up antigens to become an
APC3) APC and CD+8 T-cell link and
cytokines secreted by helper T-cell trigger response
4) CD+8 T-cell divides to make cytotoxic T-cells and memory cytotoxic T-cells
5) Cytotoxic T-cells find antigen on class I MHC proteins; bind to infected cell
6) Cytotoxic T-cell uses proteases and other enzymes to destroy infected cell
When Immune Systems Break• All systems set up an
immunological tolerance; base level of what is and is not “self”; set up as fetus
• Autoimmune reaction antibodies attack “self” molecules– Type I diabetes body kills own
beta cells; no insulin– Lupus body attacks blood cells,
platelets, mitochondria, etc…– Rheumatoid arthritis body attacks
connective tissue– Multiple sclerosis body attacks
myelin sheaths
Mild to Sever Reactions• Allergic reactions caused by antigens
that cause B-cells to release large amounts of IgE; react with mast and basophil cells which release histamine
• What does this result in?– Inflammation response
• Most effect eyes, nasal and air passage ways; also stimulate smooth muscle contractions and mucus production (allergies)
• Asthma restricted breathing; stopped with antihistamines
• Anaphylactic shock sever reaction that can result in death; stopped with epinephrine
Mild to Sever Reactions• Suggested Homework:– Test Your Knowledge
• Actual Homework:– Discuss the Concepts #1– Interpret the Data