Definitions:
1. Immune system- cells, tissues, and molecules that mediate resistance to infections.
2. Immunology- Study of structure and fcn of immune system.
3. [TQ] Immunity- Resistance of a host to pathogens and their toxic effects. A state of protection from a
particular infectious disease.
4. Immune response- collective and coordinated response to introduction of foreign substances in an
individual mediated by cells and molecules of immune system.
5. Thymus- Where all immature T-cell go to mature. A primary lymphoid organ, in thoracic cavity, where
T-cell maturation takes place.
6. Bone Marrow- All cells of entire immune system come from till about 1 yr old. Living tissue found
w/I hard exterior of bone.
7. Spleen- Filters blood and contains cells of immune system. Secondary lymphoid organ where old erythrocytes are
destroyed and blood-borne antigens are trapped and presented to lymphocytes in the
PALS and .marginal zone
8. Lymph nodes- All T, B-cells in immune system. Where foreign bodies are taken. Small secondary lymphoid
organ that contains lymphocytes, macrophages, and dendritic cells and serves as a site for filtration of foreign
antigen and for activation and proliferation of lymphocytes.
9. [TQ] Vaccines- induced strong immunity. Most humans are vaccinated. There is a vaccine for Polio, but
polio cases are still reported. A preparation of immunogenic material used to induce immunity against
pathogenic organisms.
10. Humoral immunity- combats pathogens via antibodies. Antibodies are produced by B cells. Antibodies
can be transferred b/w individuals to provide passive immunity.
11. Cell-mediated- immunity involves primarily T lymphocytes. These can eradicate pathogens,
clear infected self-cells, or aid other cells in inducing immunity.
12. Gene segments- Germ-line gene sequences that are combined w/ others to make a complete coding
sequence; Ig and TCR genes are products of V, D, J segments. Germ-line theory suggest that all
antibodies are encoded in the host chromosomes.
13. Immunoglobulin (Ig)- Protein consisting of 2 identical light chains, that recognizes a particular
epitope on an antigen and facilitates clearance of that antigen. There are 5 types: IgA, IgD, IgE, IgG,
IgM. Also called antibody.
14. T-cell receptor (TCR)- Antigen binding molecule expressed on surface of T cells and associated w/ CD3
molecule. TCRs are heterodimeric, consisting of either an α and β chain or a γ and δ chain.
15. Clonal selection- antigen-mediated activation and proliferation of members of a clone of B cells that
have receptors for antigen (or for complexes of MHC and peptides derived from antigen, in case of
T cells.
16. Tolerance- State of immunologic unresponsiveness to particular antigens or set of antigens. Typically, an
organism is unresponsive or tolerant of self-antigens.
1. Innate immunity-Non-antigen specific host defenses that exist prior to exposure to an antigen and involve
anatomic, physiologic, endocytic and phagocytic, anti-microbial, and inflammatory mechanisms,
and which exhibit no adaptations or memory characteristics. everything you are born with. Doesn’t get better
or smarter. ex)PAMPs. If you have 12 PRR, then you will have 12 for the rest of your life.
17. Adaptive immunity- Host defenses that are mediated by B cells and T cells following exposure to antigen and that
exhibit specificity, diversity, memory and self -nonself discrimination. Can live w/o this for a while. All antibodies,
T-cels. Can adapt and is the target of vaccines. .Memory is the hallmark
18. Memory immunologic- memory cells attribute of immune system mediated by whereby a 2 encounter
nd
w/ an antigen induces a heightened state of immune reactivity.
1
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19. Primary response- Immune response following exposure to antigen; this response is characterized
by short duration and low magnitude compared to response following subsequent exposures to same
antigen (2ndary response).
20. Secondary immune response- immune response to antigen that has been previously introduced and recognized by
adaptive immune cells. It is mediated primarily by memory T and B lymphocytes that have differentiated to respond
more quickly and robustly to antigenic stimulation that the primary response.
21. Immunodeficiency- Any deficiency in immune response, whether inherited or acquired. It can result
from defects in phagocytosis, humoral immunity, cell-mediated responses, or some combination of
these.
22. [TQ] Hematopoietic stem cells (HSCs)-have ability to differentiate into many types of blood cells. All
red and white blood cells develop from HSC during hematopoiesis.pluripotent
23. Hematopoiesis- Highly regulated process that occurs in the bone marrow for adult vertebrates. The
formation and differentiation of blood cells.
24. Progenitor cells- cell that has lost the capacity for self-renewal and is committed to generation of
particular cell lineage.
25. [TQ] Common myeloid-erythroid progenitor- immature blood cell that develops from hematopoietic stem cell
and gives rise to all red blood cells and myeloid cells, including monocytes, macrophages, and granulocytes.
RMGM: Red blood cells, Monocytes- differentiate into migrate into tissues and macrophage-fcn to
repair/remodel., destroy pathogens, present antigens. Can also differentiate into dendritic cells-High degree of fcn
as “ingesters” of antigens, followed by to naïve T lymphocytes for initial activationpresentation ,
Granulocytes( Neutrophils- Basophils (histamine and cytokines)/mast direct harm to pathogens (histamine),
cells-inflammation/allergies, Eosinophils-antiviral activity, antiparasitic activity (cytokines and chemokines),
Megakaryocytes.
26. [TQ] Common lymphoid progenitor- immature blood cell that develops from hematopoietic stem
cell and gives rise to lymphocytes, including B and T cells and NK cells.
27. [TQ] Cluster of differentiation (CD)-collection of monoclonal antibodies that all recognize an antigen
found on a particular differentiated cell type or types. Each of antigens recognized by such a collection of
antibodies is called a CD marker and is assigned a unique protein identifying #.
28. [TQ] B cell receptor (BCR)-Complex comprising a membrane-bound immunoglobulin molecule
and 2 associated signal-transducing Igα/Igβ molecules. Contains and antibody of defined specificity.
Binds anything (nucleic acids, proteins, bonds). Has catalytic uses.
29. [TQ] T cell receptor (TCR)-Antigen-binding molecules expressed on the surface of T cells and
associated w/ CD3 molecule. TCRs are heterodimeric, consisting of either an α and β chain or a γ and δ
chain. Can only bind proteins.
30. Stromal cells-A nonhematopoietic cell that supports growth and differentiation of hematopoietic cells.
31. Thymic cortex and medulla- Directs stepwise changes in thymocytes.
32. Medulla- innermost central region of lymph node.
33. Fibroblastic reticular cell conduit (FRCC)
34. Follicles-Microenvironments that specifically support development of B lymphocyte response in
lymph node, spleen, and other 2ndary lymphoid tissue. They also become site of development of
germinal center when a B cell is successfully activated.
35. Red Pulp-where Red Blood Cells are compartmentalized.
36. White pulp-Portion of spleen that surrounds arteries, forming a periarteriolar lymphoid sheath
(PALS) populated mainly by T cells.
37. Mucosa-associated lymphoid tissue (MALT)-Lymphoid tissue situated along mucous membranes
that line digestive, respiratory, and urogenital tracts. Lymphoid cells and tissues organized below
epithelial layer of body’s mucosal surfaces.
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38. Gut-associated lymphoid tissue (GALT)-2ndary lymphoid microenvironments in intestinal (gut)
system that support development of T and B lymphocytes response to antigens that enter gut mucosa.
Part of MALT.
Notes:
1. Many pathogens can expand rapidly in nutrient-rich environment of host.
2. There are 2 major systems: (1) Circulatory System. (2) Lymphatic system- Drain all fluids and filters
back thru lymph nodes.
3. [TQ] Steps of Inflammatory Response- Inflammatory response is a body’s 2 line of defense against
nd
invasion by pathogens. Inflammation helps to know where the problem is and can attract cells. Also, fluid
comes out and drains out of lymphatic system (hurts lil, redness). (1) Damaged tissues release histamines,
increasing blood flow to area. (2) Histamines cause capillaries to leak, releasing phagocytes and clotting
factors into wound. (3) Phagocytes engulf bacteria, dead cells, and cellular debris. (4) Platelets move out of
capillary to seal the wounded area.
4. Immune system recognizes self or not self, rather than foreign objects. Ex) tissue transplantation
5. A portion of immunity involves both humoral and cellular components.
6. Humoral and cell-mediated immunity relies on surface receptors (B and T-cell receptors). These are
randomly generated by gene segment rearrangements in B and T-cells. B cells that encounter antigen
produce the antibody specificity of their cell membrane . immunoglobulin T-cell receptors bind
specific peptides presented by MHC molecules.
7. Pathogens fall in to 4 categories: (1)Viruses(2)Bacteria(3)Fungi(4)Parasites
8. Immune responses rely on recognition molecules. Germ-line encoded (pattern recognition receptors, PRRs)-
These bind to pathogen-associated molecular patterns (PAMPs)-generic molecules found on many diff types of
pathogens (peptidoglycan). Randomly generated (B and T-cell receptors)- These bind to very specific antigens,
rather than generic molecules found on many pathogens.
9. Macrophages have tremendous surface area.
10. Pathogens fall in to 4 categories: (1) Viruses- (2) Bacteria- Stay inside cells. Stay extracellular.
Antibodies are efficient. See large lymph nodes. Eukaryotic. Can be extracellular and (3) Fungi-
intracellular. Proteins are similar to us. Recycles everything, tissues. Secretes enzymes-> liquifies->sucks
in. ex) tapeworm. Cells that commit suicide can bind to pathogens and oxidize them or (4) Parasites-
create holes. Ex) eosinophils.
11. Recognition is key: Has to see self, but has to see foreign. Protein-protein interaction.
12. [TQ] Tolerance ensures that the immune system avoids destroying host tissue ( do not activate cytotoxic
T-cell to self)
13. [TQ] Slide on innate vs adaptive.
14. [TQ] Macrophages can also present antigens to T cells via MHC molecules-key molecule(20% diff) why do
not respond to certain pathogens, and determines what you can see or can see.
15. [TQ] Primary lymphoid organs-where immune cells develop = Bone marrow, Thymus.
16. [TQ] Secondary lymphoid organs- where immune response is initiates/ encounters antigen = Lymph nodes, Spleen,
Mucosa-associated lymphoid tissue (MALT), other diffuse and loosely organized areas.
17. Antigens enter via afferent vessel.
18. [TQ] Diff b/w B-cell and plasma cell? Plasma cells secrete antibodies and exclusively make IgA. B-
cells can switch Ig molecules.
19. [TQ] Dendritic cells w/ receptors and MHC molecules and proteins have incredible surface area.
20. The is the 1 line of defense against RBC are in WBC are spleen st bloodborne pathogens. red pulp.
in white pulp.
21. M-cells are void of cilia. Poral of entry for foreign pathogen that have PAMPs or specific sites on surface.
22. [TQ] There is no vaccine that prevents infection. Vaccine can prevent disease.
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Questions:
1. Why is important that clotting factors from the circulatory system have access to injured area?
2. Do vaccines work? To date, have eliminated only 1 disease = small pox.
3. What is immunity? State of protection against foreign pathogens or substances (antigens).
4. Can we generate immunity w/o inducing disease? Yes, through vaccination. Vaccination- prepares
immune system to eradicate an infectious agent before it causes disease. Vaccine have only eradicated
one disease = smallpox thus far.
5. [TQ] B-cells do not make antibodies. They have to become plasma cells first in lymphoid nodes
which end up swelling.
Quiz questions
6. [TQ] Which of the following diseases is NOT currently have an effective vaccine between Chicken
pox, Polio, HIV, smallpox, Diptheria? Answer = HIV
7. [TQ] True or False? Overall, the human immune system views microbes as pathogens? False, they
view self or nonself.
8. [TQ] What are primary lymphoid tissues? Bone marrow, Thymus
9. [TQ] What are secondary lymphoid tissues? Spleen, lymph nodes, Mucosa-associated lymphoid tissue,
Peyer’s patches, other diffuse and loosely organized areas.
10. [TQ] In mammals, T-cell development occurs in the thymus, whereas B-cell development
occurs predominantly in the bone marrow.
Summaries:
Ch1:
Immunity is a complex subject, broken down into many different layers and
areas. Understanding how immunity works allows us to:
a. Exploit it to prevent infections (vaccination).
b. Exploit it to treat illness (shutting down autoimmune disease or ramping up anticancer responses).
c. Provide safer organ and tissue
transplants. Ch2:
Blood cell development is only 1 step
st
Multiple other organs and tissues of body must receive those blood cells and interface them w/
each other to achieve proper immune responses. These interfaces and tissues are complex and
multifaceted.
Ch3:
Signal transduction is a complex subject
Look for similarities and diff- Both B and T lymphocytes use similar strategies once processes are
underway. Diff lie at level of antigen receptors and early membrane-linked events.
By understanding antigen receptor and early membrane even diff, we can better understand
how signaling (and activation) works in each lymphocyte cell type.
Ch4:
Basic barrier mechanisms and simple biochem defenses are frontline of immunity. Innate
immune response depends on recognition of “general” pathogen molecules.
Responses are varied, but include: Phagocytosis, Triggering of inflammatory responses, Direct
destruction by natural killer cells, Initiation of adaptive immune responses.
Slide Outlines:
A historical perspective of immunology
1. Humoral- combats pathogens via antibodies. Antibodies are produced by B cells. Antibodies can be
transferred b/w individuals to provide passive immunity.
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2. Cell-mediated- immunity involves primarily T lymphocytes. These can eradicate pathogens,
clear infected self-cells, or aid other cells in inducing immunity.
3. Clonal selection- antigen-mediated activation and proliferation of members of a clone of B cells that
have receptors for antigen (or for complexes of MHC and peptides derived from antigen, in case of
T cells.
A historical perspective of immunology
1. Clonal selection and generation of diversity- antigen-mediated activation and proliferation of members
of a clone of B cells that have receptors for antigen (or for complexes of MHC and peptides derived
from antigen, in case of T cells.
Important concepts for understanding mammalian immune response
1. Surface receptors (B and T-cell receptors) are randomly generated by Gene segment rearrangements in B and T
cells. B cells that encounter antigen produce antibody specificity of their cell membrane . Immunoglobulin T-cell
Receptors bind specific peptides by MHC molecules.
2. Pathogens: (1) Viruses- (2) Bacteria- Stay inside cells. Stay extracellular. Antibodies are efficient. See large
lymph nodes. Eukaryotic. Can be extracellular and intracellular. Proteins are similar to us. Recycles (3) Fungi-
everything, tissues. Secretes enzymes-> liquifies->sucks in. ex) tapeworm. Cells that commit (4) Parasites-
suicide can bind to pathogens and oxidize them or create holes. Ex) eosinophils.
3. Immune responses rely on recognition molecules. Germ-line encoded (pattern recognition receptors, PRRs)-
These bind to pathogen-associated molecular patterns (PAMPs)-generic molecules found on many diff types of
pathogens (peptidoglycan). Randomly generated (B and T-cell receptors)- These bind to very specific antigens,
rather than generic molecules found on many pathogens.
4. Tolerance- State of immunologic unresponsiveness to particular antigens or set of antigens. Typically, an
organism is unresponsive or tolerant of self-antigens.
5. Innate immunity- Everything your born with, doesn’t get any better or smarter. Ex) PAMPs, IL for rest of life. Non-
antigen specific host defenses that exist prior to exposure to an antigen and involve anatomic, physiologic, endocytic and
phagocytic, anti-microbial, and inflammatory mechanisms, and which exhibit no adaptations or memory characteristics.
everything you are born with. Doesn’t get better or smarter. ex)PAMPs. If you have 12 PRR, then you will have 12 for the
rest of your life. 1 line of defense, and uses recognition molecules, and . Activation
st Germ-line-encoded phagocytic cells
of innate immune responses produces (often cytokines)- stimulate and direct adaptive immune response.Signal molecules
6. Adaptive immunity- You can live w/o for a while. All antibodies. Host defenses that are mediated by B cells and T
cells following exposure to antigen and that exhibit specificity, diversity, memory and self -nonself discrimination.
Can live w/o this for a while. All antibodies, T-cels. Can adapt and is the target of vaccines. Memory is the
hallmark specific Primary response-. Highly to individual antigen molecules. Immune response following
exposure to antigen; this response is characterized by short duration and low magnitude compared to response
following subsequent exposures to same antigen (2ndary response). Secondary immune response- immune
response to antigen that has been previously introduced and recognized by adaptive immune cells. It is mediated
primarily by memory T and B lymphocytes that have differentiated to respond more quickly and robustly to
antigenic stimulation that
the primary response.
Good, bad, ugly of immune system- (rejection)
1. Overly active or misdirected immune responses = Allergies, asthma, autoimmunediseases.
2. Immunodeficiency- Primary (genetic) loss of immune fcn. 2ndary (aquired) loss of immune fcn. Any
deficiency in immune response, whether inherited or acquired. It can result from defects in
phagocytosis, humoral immunity, cell-mediated responses, or some combination of these.
The Microbiome
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1. Commensal: organisms that live in and on us that cause no harm. Function in metabolic and immune
balance called Imbalance or leads to immune overstimulation resulting in homeostasis. Dysbiosis
inflammation.
Cells of immune system
1. Hematopoiteic stem cells (HSCs) have ability to differentiate into many types of blood cells. All red
and white blood cells develop from HSC during hematopoiesis.pluripotent
2. Hematopoiesis- Highly regulated process that occurs in the bone marrow for adult vertebrates. The
formation and differentiation of blood cells.
1. W/I bone marrow, HSCs are constantly renewed and directed to differentiate in 2 major types of
progenitor cells Common myeloid progenitors Common lymphoid progenitor cells: (1) (2)
2. Common myeloid progenitors- immature blood cell that develops from hematopoietic stem cell and gives rise to all
red blood cells and myeloid cells, including monocytes, macrophages, and granulocytes.
RMGM: Red blood cells, Monocytes- differentiate into macrophage migrate into tissues and -fcn to
repair/remodel., destroy pathogens, present antigens. Can also differentiate into dendritic cells-High degree of fcn
as “ingesters” of antigens, followed by to naïve T lymphocytes for initial activationpresentation ,
Granulocytes( Neutrophils- histamine), Basophils (histamine and cytokines)/mast direct harm to pathogens (
cells-inflammation/allergies, Eosinophils-antiviral activity, antiparasitic activity (cytokines and chemokines),
Megakaryocytes.
3. Common lymphoid progenitor- immature blood cell that develops from hematopoietic stem cell
and gives rise to lymphocytes, including B and T cells and NK cells.
4. Macrophages and neutrophils are specialized for . phagocytosis [TQ] Macrophages can also present
antigens to T cells via MHC molecules.
39. Cluster of differentiation- collection of monoclonal antibodies that all recognize an antigen found on a
particular differentiated cell type or types. Each of antigens recognized by such a collection of antibodies
is called a CD marker and is assigned a unique protein identifying #.
5. B-cell receptor (BCR)-Contains an antibody of defined specificity. Binds anything.
6. T-cell receptor (TCR)- Antigen binding molecule expressed on surface of T cells and associated w/ CD3
molecule. TCRs are heterodimeric, consisting of either an α and β chain or a γ and δ chain. Can only
bind protein.
Primary lymphoid organs-where immune cells develop:
1. bone marrow- All cells of entire immune system come from till about 1 yr old. Living tissue found
w/I hard exterior of bone.
2. stromal cells of bone marrow. A nonhematopoietic cell that supports growth and differentiation of
hematopoietic cells.
3. Thymus- Where all immature T-cell go to mature. A primary lymphoid organ, in thoracic cavity, where
T-cell maturation takes place.
4. Thymic cortex and medulla- microenvironments direct stepwise changes in thymocytes.
5. [TQ] Affinity of binding: TCR to MHC-peptide drives positive and negative selection.
Secondary lymphoid organs-where immune response is initiated
1. Encounter antigen, undergo clonal expansion, differentiate into effector cells
2. Medulla- Macrophages and dendritic cells are found here in the innermost lymph node.
3. Antigens enter via afferent vessel. Naïve lymphocytes enter by High Endothelial Venule (HEV),
Lymphocytes exit via efferent vessel
4. Lymphoid Fibroblastic reticular cell conduit (FRCC)- guides T cells and APCs toward activation
interactions. Differentiation into effector cells takes place in of 2ndary lymph organsfollicles
5. Red pulp , white pulp-where Red Blood Cells are compartmentalized -Where white blood cells are.
6. MALT-important layer of defense against infection. Organizes responses to antigens that enter mucosal tissue ,
includes network of follicles and lymphoid microenvironments associated w/ intestines = GALT
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Common features of Receptor-Ligand interactions
1. Receptor-ligand interactions may be the strength of an individual bondMultivalent: affinity- .
Avidity-combined strength of binding of multiple interactions.
2. Aggregation-due to ligand binding enhance ligand binding measure strength of ligand bindingKd = .
3. Extended contact facilitates signal transduction and exchange of Cytokine signals.
4. Cytoskeletal reorganization- may occur upon extended binding.
5. Immune receptors bear immunoglobulin and can be domains transmembrane, cytosolic, or secreted.
Immune antigen receptor molecules
1. CD4, CD8- are T-cell coreceptors that define diff subsets of T-cell fcn.
Immune antigen receptor molecules antibody
1. Quaternary protein w/ 2 identical heavy chains and 2 identical light chains. Antigen is byspecificity
interaction b/w light/heavy chain variable regions. Antibody activity, phagocytosis and effector
complement fixation, is a fcn of constant regions of heavy chain.
2. Memorize slide with antibody
3. Hypervariable regions of amino acids = V and V = antibody combining site = H L
complementarity-determining regions = CDR1, CDR2, CDR3
4. Invariant amino acids near CDR form Framework region-responsible for folding CDRs to form
antibody combining site.
5. Isotypes: IgA, IgD,IgE,IgG,IgM
6. Light chain isotypes: kappa or lambda
7. Igα, Igβ transduce signals via ITAMs
8. CD19, CD81, CD21 transmit and relay signals to cell interior.
Immune antigen receptor molecules T-cell receptor
1. Structurally similar to immunoglobulin domain.
2. Peptide sources can be from or processed antigensendogenously exogenously
3. CD3 contains ITAMs that transmit signal to cell
4. CD4, CD8 fcn in increasing avidity of peptide binding by TCR
5. CD28 engages CD80 or CD86 on APC to fully activate a naïve T cell
Immune antigen receptor molecules PAMPs
1. PAMPs equally expressed on same cell types
2. PAMPs receptors integral membrane proteins intracellular proteins. may be or
3. PAMPs motifs represent on bacteria, yeast, parasites
Cytokines and their receptors
1. Cytokine ligand-signals are usually generated by binding of a to a complementarity cell-bound receptor
2. Cytokine-receptor noncovalent binding is , although it may be of generally high affinity.
3. Cytokine-signaling end results often induce change in transcriptional program of target cell.
General properties of cytokines and chemokines
1. Endocrine= distant cells
2. Paracrine = nearby
3. Autocrine-binds receptors of cells that produced them.
4. Pleiotrophic-activity induces diff biological effect dependent on target cell.
5. Redundant-activity mediates similar effects on target cell.
6. Synergy-effect combines 2 cytokine activities to be greater than additive effect.
7. Antagonistic-effect inhibits one cytokine’s effect by another’s action
8. Cascade-effect of one cytokine on one target cell to produce additional cytokines.
Cytokine Classes and their actions
1. Cytokines of the family promote inflammation. Acts on capillary permeability and to pull IL-1 locally
leukocytes to infected tissues. Acts to signal liver to produce acute phase proteins.systemically
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Chemokine classes and their actions
1. Chemokine receptors are an ex) of G-protein coupled receptors. Transduce signals via interactions w/ a
polymeric GTP/GDP-binding G protein leukocyte migration.. Chemokines direct
Receptors and Cell Signaling
1. Cellular signal is any event that instructs a cell to change its metabolic or proliferative state. Signals are
usually generated by t a complementarity cell-bound receptor. Cell can more or less binding of a ligand
susceptible to actions of ligand by increasing or decreasing expression of receptor for that ligand. Cell
signaling often in transcriptional program of target cell. induces a change Multiple signals thru multiple
receptors are required to effect particular outcomes. of all signals received by cell occurs at Integration
molecular level inside recipient cell.
2. [TQ] memorize slide
3. Adapter proteins help to gather members of signaling pathways.
4. Ras is a G proteins. Activated when GTP exchanged for GDP Guanine-nucleotide Exchange
Factors (GEFs) activate Ras by inducing this exchange.
5. GTPase activating proteins (GAPs) inhibit Ras by stimulating its ability to break down GTP into GDP.
6. Phosphoylated ERK ( ) phosphorylates and activates transcription factor leading to production of FospERK Elk-1
protein. Fos is phosphorylated by ERK and binds w/ phosphorylated protein. This combination isJun pJun/pFos
known as transcription factor can facilitate transcription of gene.AP-1- IL-2
7. Phosphokinase C Nuclear factor kappa B (PKC) activates (NF-κB)- inactivates in cytoplasm when
bound to inhibitor (IκB).
8. Diacylglycerol activates PKC-activating IKK complexes and phosphorylates IκB releasing it from NF-κB.
NF-κB to nucleus to enhance transcription.translocates
Anatomical barriers to infection
1. Conserved pathogen-associated molecular patterns (PAMPs) found on microbes. Aging, dead, or damaged self-
structures can also be recognized Damage-associated molecular patterns (DAMPs). Pattern recognition
receptors (PRRs) recognize these structures and target them for clearance.
2. Barriers are just one diff b/w and immune response.innate adaptive
Induced cellular innate responses-
1. Families of PRRs recognize variety of PAMP ligands
a) Toll-like receptors (TLRs)-recognize many types of pathogen molecules. Homologous to fruit fly Toll receptor.
Dimers w/ extracellular leucine-rich (LRR) domains that bind PAMPs and DAMPs. Location helps determine what
each TLR will bind. Of 13 TLRs in mice and humans, some are in lysosomes and some are surface bound. TLR binding
of PAMPs activates signaling pathways. Diff TLRs recruit diff adapter proteins to Toll/IL-1R domain. Pathways
include transcription activation, NF-κB Interferon regulating factor MAP kinase (IRF) pathways, pathway
downstream transcription factors such as .AP-1
b) C-type lectin receptor (CLR)- activate innate and inflammatory responses. Transcription factors
induce expression of cytokines, IL-1β, TNF, and IL-23.proinflammatory
c) AIM2-like receptors (ALRs) are cytosolic receptors that bind bacterial and viral double-stranded DNA.
Binding of multiple ALRs to dsDNA via pyrin domains yields long filaments that together w/ other
cellular proteins form - generates IL-1β, IL-18.inflammasomes
d) RIG-1 like receptor (RLR)- Recognize viral double stranded RNAs. RNA by .RLR helicase domain
Fnc as cytosolic PRRs. Trigger signaling pathways that activate: IRFs to trigger antiviral interferon
responses. NF-κB transcription factor.
e) NOD like receptors (NLRs)
2. PRR signaling pathways activate expression of a large variety of genes. Type 1 interferons (potent
antiviral effect). 4 genes turned on by IFN: Protein kinase R (PKR), 2’,5’-Oligoadenylate synthetase,
mix group proteins, IFIT
Phagocytosis
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1. Defined as and of materials such as microbes for their clearance engulfment internalization
and destruction.
2. Microbes are recognized by receptors on phagocytes. May recognize soluble protein bound to microbes. opsonin
Ingested material are taken in to Phagosomes are fused w/ or granules. Destruction phagosomes. lysosomes
occurs thru enzyme degradation, antimicrobial proteins, and toxic effects of
reactive oxygen reactive nitrogen and species (ROS and RNS).
Regulated cell death (Apoptosis)
Inflammatory responses
1. Proinflammatory and chemokines triggered by innate responses to infection, damage, orcytokines
harmful substances. Early components of inflammation include: Increased vascular permeability,
recruitment of neutrophils and other leukocytes from blood to site of damage/infection.
Natural killer (NK) cells
1. NK cells are lymphocytes w/ innate immune fncs.
2. Activated NK cells perform one of two fncs: Kill altered self-cell by releasing and inducing perforin granzymes
apoptosis. Produce cytokines that induce adaptive responses against altered self-cell.
Innate lymphoid cells (ILC)
1. Derived from cells.common lymphoid progenitor
Regulation and evasion of innate and inflammatory responses
1. Regulation includes both and mechanisms.positive negative feedback
Interactins b/w innate and adaptive immune systems
1. Several innate systems have been co-opted by adaptive immunity to contribute to antibody-mediated
pathogen elimination. Some lymphocytes express TLRs, but Opsonization, Complement activaton.
use them as receptors.costimulatory
2. A constant interplay b/w the two systems exists, are key bridge.dendritic cells
Ubiquity of innate immunity
1. PRRs w/ leucine-rich repeats (LRRs) are found in virtually ALL plants and animals.
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