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61 Cards in this Set

  • Front
  • Back
Profile of immune Response of Intracellular bacterial infection
Ex) Mycobacterium, Listeria, Legionella

Bacteria can survive intracellularly, including in macrophages/neutrophils

Generalized Response: CD4 Th1 cell-mediated immunity is best response
Innate Immune Mechanism yo Intracellular Bacteria
Neutrophils/Macrophages cannot kill resistant bacteria.
Infected phagocytes express IL-12 and NK cell-activating molecules.
Activated NK cells, produce IFN-γ (less specific than Th1) to activate macrophages
CD4 Th1 T-Cell Response to Intracellular Bacteria
CD4 activated by Antigen-MHC II complex presentation, costimulatory w/ IL-12 from dendritic cell.

At site of infection , CD4 Th1 cell recognizes antigen-MHC complex and CD40L(Th1)-CD40(APC) interactions and secretes IFN-γ (More Specific than NK)
Macrophages activated by IFN-γ to heightened ROS/RNS species, also secrete TNF-α, IL-1, chemokines for inflammation and IL-12 to activate T Cells
CD8 T Cell (CTL) Response to Intracellular Bacteria
Activated by antigen-MHC I complex to activate CTL
CD8 recognized peptide-MHC I complex on infected macrophage and responds by killing macrophage (Perforins, Granzymes Fas-FasL)
Antibody (B-Cell) Response to Intracellular Bacteria
IFN-γ from Th1 cell induced class switching to IgG.
IgG activates classical complement, C3b/IgG opsonize bacteria to help macrophage effector function

Antibody INEFFECTIVE when bacteria is in host cell.
Mechanisms of Evasion by Intracellular Bacteria
Inhibit lysosome fusion to phagosomes
Escape from phagolysosome into cytoplasm
Inactivate oxidative and lysosomal products
Mechanisms of Injury by Intracellular Bacteria
Granulomas - persistance of bacteria causes chronic stimulation of T Cell/ Macrophages
Differences in individual resistance determine dominate type of immune response generate
Profile of Immune Response to Viral Infection
Viruses: Obligate Intracellular microbes. Use host cell surface molecules to enter cell. Use host cellular machinery to replicate. Located in CYTOPLASM

Antibody contain spread of virus, CTL eliminate virus
Innate Immune Response to Viral Infection
Virally Infected Cells produce Type I Interferons (IFN-α/IFN-β)
Type I Interferons: Inhibit viral replication, increase expression of MHC I, and activate NK

NK Cells: recognize infected cells: They lack MHC I but may have NK activating receptors, both of which activated NK Cells

Nk Cells kill virally-infected cell by release cytotoxic molecules (granzymes/perforins_ and cytokines (IFN-γ)
CD8 T-Cell Response to Viral Infection
CD8 cells activate by cross presentation of antigen-MHC I on dendrtitic cells ( CD4 Costimulus by IL-12)
CD8 Effector T cell (CTL) recognize antigen-MHC I complex and release perforins and granzymes to induce apoptosis
Interaction of FAS(Target)-FAS ligand(CTL) also causes apoptosis
CTL can move to the next cell
Antibody Response to Viral Infection
Only effective against Extracellular stage of infections: Early in infection before entry to host cells, or when released from infected cells.
Functions: Neutralizing antibodys (Mostly IgA). Binds to virus, and prevents viral entry into cells. Can be IgG or IgA
Immune Evasion by Virus Infection
Continually change of surface antigens
Interfere with antigen presentation, processing or expression of MHC I
Produce immunosuppressive cytokines
Injury due to Virus Infection
Viral-antibody immune complexes can be deposited in blood vessels to systemic vasculitis
Viral proteins have AA sequences present in self-antigens. Can cause Cross-reaction immune response directed to self-antigens
Profile of Immune Response to Extracellular Bacteria Infection
Sites: Circulation, Epithelial Surfaces, Connective Tissue, Tissue Spaces.
Bacteria cause induction of inflammation, and production of toxins
Immunity Principally mediated by antibody
Innate Immune Response to Extracellular Bacteria
Phagocytosis/Killing by macrophages, monocytes, and neutrophils
Activation of complement by alternative and lectin pathway resulting in Opsonization (C3b), Cell Lysis (MAC), Recruitment of phagocytosis (C5a/C3a) by anaphylatoxins.
Production of cytokines for local inflammation and ehnance adaptive immuen response
Antibody Immune Response to Extracellular Bacteria
B-Cells activated by antigen-MHC II complex w/ costimulation by CD4 Th2(prduced by IL-4) cells. Affinity Maturation + Isotype Switching. Plasma Cells Secreate Antibodies

Effector Functions:
Neutralization or microbes/toxins by IgG or IgA (mucosal) by prevention of attachment of microbe, preventing spread of microbes, inhibiting binding and/or effects of toxins
Opsonization: IgG coats microbes: Fcγ Binds phagocytes
Complement: Activation of classic complement by IgG and IgA
ADCC: Cytotoxicity, IgG coating causes release of mediators from Innate Immune Cells by attachment of Fcγ
CD4 Th1 t Cell Response to Extracellular Bacteria
Contribute to response by releasing cytokines
IFN-Extracellular Bacteria causes class switching to IgG and enhancement of macrophage activation
TNF: Inflammation w/ recruitment
Mechanism of Evasion by Extracellular Bacteria
Genetic Variation of Surface Antigens
Bacterial Capsules prevent phagocytosis and complement activation
Secrete molecules to degrade complement components or antibodies
Interfere with complement activation sequence
Impaired host integrity of epithelial or mucosal surfaces by toxins
Mechanism of Injury due to Extracellular Bacteria
LPS: causes Inflammation and septic Shock
Toxic Shock: toxins act as superantigens to activate large amount of CD4 T Cells.
Generation of Disease-producing Antibodies: Rheumatic Fever M-protein of β-strep cross react with myocardial proteins and myosin
Glomerulonephritis: antigen-antibody complexes deposit in kidneys
Profile of Immune Response to parasitic infections
Hoest defense dependant on location of parasite
Most parasites cause chronic infections because of weak innate immunity and ability to evade adaptive immunity
Protozoa: CD8 cell lysis & CD4 Th1 Activaiton of Macrophages
Helminth: Activated Eosinophils produce Major Basic Protein (MBP)
Innate Immune Response to Parasitic Infection
NK cells through ADCC
T Cell Immune Response to Protozoa Infections
Protozoa can survive within Macrophages. CD4 Th1 cells secrete IFN-γ to cause Macrophage activation.
Immunity to other host cells mediated by CD8 CTL.
Antibody Immune Response to Protozoa Infections
Protozoa found in extracellular sites eliminated by antibody by complement-mediated lysis, neutralization or opsonization.
T Cell Immune Response to Helminth Infections
Major: Th2 cell activation causing production of IgE and activation of eosinophils and mast cells. IL-4 causes class switching to IgE, IL-5 activated Eosinophils, IL-13 induces epithelial cell turnover and mucus production from goblet cell to expel worms
IgE: arm mast cells and eosinophils to degranulate. Eosinophils produce Major Basic Protein to kill parasites.

Th1: IFN-γ isotype switching to IgG to activate complement and ADCC
Evasion mechanisms to Immune Destruction by Parasties
Masking, shedding, or varying surface antigens.
Disguising surface with host antigens
Interfering with host's immune response
Sequester within host
Injury due to Parasitic Infection
Enlargment og liver/spleen due to increase in macrophages
Formation of Immunocomplexes and deposition in kidney
Autoantibodies against RBC, lymphocytes, DNA or crossreaction
Non-Specific Immunosupression
Immune Response to Fungi
Fungi live either intra or extracellularly so immune response similar to extra or intracellular bacteria
Innate: Mostly phagocytosis by neutrophils/macrophages
Adaptive: mechanisms involving both CD4 and CD8 T Cells, mainly ADCC
Evasion mechanisms of Immune Destruction by Fungi
Formation of a capsule to inhibit phagocytosis: Crytococcus

Evasion of Macrophage killing: Histoplasma

Formation of granulomas cause injury
Overveiw of the Gut- associated Lymphoid Tissue (GALT)
Immune Cells - Found in Sruface Epithelium and Lamina Propria
Also contains Mesenteric Lymph Nodes along lining of cavity which are organized similar to other 2ndary lymphoid tissues.
The presence of these lymph nodes also allows for adaptive immune responses to mucosal infection to develop locally
Immune Components of the Gut- associated Lymphoid Tissue (GALT)
- Goblet Cells
- Paneth Cells
- Intraepithelial Lymphocytes
- Lamina Propria
- Peyer's Patches : M Cells, Dome Area, Efferent Lymphatics
- Isolated Lymphoid Follicles
Role of Goblet cells in Mucosal Immunity
Secrete mucus which contains components such as lysozyme, lactoferrin, peroxidase and secretory IgA.
Functions to protect against attachement and colonization of pathogenic microbes
Role of Paneth Cells in Mucosal Immunity
Specialized cells found at thebase of the crypts.
Produce antimicrobial proteins
Role of Lamina Propria in Mucosal Immunity
Contain CD4 & CD8 T cells, Plasma Cells, Mast Cells, Dendritic Cells, and Macrophages

Also contain lymphatics that drains to the mesenteric lymph nodes
Role of Peyer's Patches in Mucosal Immunity
Integrated in Epithelium and contain B & T Cell Areas
Lumen separated from Peyer's Patches by M-Cells which lack microvilli
"Dome" Area immediately under epithelium w/ B cells similar to Marginal zone of B-1 B cells.
Antigens enter through M-Cells
NO Afferent but Efferent lymphs which drain to mesenteric lymph nodes
Role of Isolated Lymphoid Follicles in Mucosal Immunity
Single follicles consisting of Mostly B Cells overlayed by M-Cells
Role of M Cells in Mucosal Immunity
Specialized for Uptake of Antigens and transport to basal side
Have Deep invaginations on basolateral side forming pockets which contain lymphocytes, dendritic cells and macrophages.
Dendritic cells take up antigen fro T Cell presentation
Role of Dendritic Cells in Mucosal Immunity
Besides M Cells found in Lamina Propria and can take up antigen independently by extension through epithelial cells.
Migrate to T Cell areas of Peyer's patches or draining lymphatics to T Cell Area of Mesenteric Lymph Nodes for presentation
Migration of B/T Effector Cells in GALT
Naive B/T Cells enter Peyer's Patches or Mesenteric Lymph Nodes through HEVs.
B/T Cells are activated, proliferate, and differentiate into effector/memory cells.
Effector Cells from Peyer's Patches leave through efferent lymphatics, through mesenteric lymph nodes to the blood, migrate back to musocal tissue.
Effector cells from Mesenteric Lymph Nodes leave and travel to mucosal tissue of provoking antigen
Effector B & T Cell "Homing"
Controlled by adhesion molecules and chemokines
Dendritic Cells induce correct homing molecules for type of mucosa in which cells were activated
Homing Molecules for Intestinal Mucosa
Effector Lymphocytes:Express Integrin α4:β7 which binds MAdCAM-1
Homing Molecules for Lamina Propria
Effector Lymphocytes: Express CCR9 which binds CCL25
Homing Molecules for Intraepithelial Lymphocytes (IEL)
IEL: Express Integrin αE:β7 which binds to E-cadherins expressed by epithelial cells and allows movement within epithelium
Effector Functions of B & T Cells in Mucosal Immunity
Effector T Cells: produce cytokines or killing infected host cells

Effector B Cells: differentiate into plasma cells produce dimeric IgA induced by TGF-β
Lattice Theory
Basis for Immunoprecipitation with soluble antigen.
At optimal concentrations of antigen (ag) and antibody(Ab) extensve cross linking occurs.
Precipitation occurs of growing Ag-Ab aggregate crosslinking into 3D lattice
3 Zones of Precipitation Activity
Excess Antibody: No cross linking, little precipitate

Equivalence: Optimal precipitation, Crosslinking occurs

Excess Antigen: No Cross-linking, very little precipitate. Precipitate dissociation
Formation of immune complexes measured in photoelectic cell as an optical density.

Direct Relationship between complex concentration and optical density.

Quantitative Assay Determined concentration of serum components: Complement, Ig
Radial Immunodiffusion
Either Antigen OR Antibody incorporated into agar.

Other component placed in well cut into agar and diffuses out until equivalence point.

Visible line of precipitate on agar. Determines relative concentrations of Ag or Ab.

Usually compared to STANDARD CURVE of known concentrations

Quantitative Assay: Blood Proteins (Ig)
Primary assay for Blood Group Detection (ABO + Rh(D) +/-)

Blood added to commercially prepared antibody to different blood group antigens.

If Agglutiation (clumping) occurs, Antigen is present.

Person develops antibodies to antigens not present on self blood cells:
IgM for ABO
IgG for Rh(D) Factor
Latex Aggultination
Antigen or Specific Antibody attached to color plastic beads

When added to other component area of color develops (Pregnancy Test has antibodies of hCG)

Replaced by more sensitive methods
Hemagglutianation Inhibition
Special kind of Agglutination.

Involves spontaneous agglutination of non-human RBC by certain virus.

Reaction blocked if if anti-viral antibodies present in serum to binds to virus.

Serial dilutions of serum can be used to determine concentration ( TITER) of anti-viral antibodies present
Antigen/Specific Antibody attached to solid support and immoblized.

Other component added to and will attach if specific

Ligand (usually 2nd antibody) that has enzyme attached added to attached to antibody/antigen from 2nd step.

Enzyme-ligand conjugate added to colorless substrate that will produce colored product which is determined by Spectrophotometer.

Quantitative Assay Used to TITER blood samples.
Titer is usually reciprical of greatest dilution that is able to show positive ELISA reaction with antigen.

Determine acute vs convalescent stage of disease.

Must be 4 fold increase in titer.
Radioimmunoassay (RIA)
Same as ELISA except reagents are labeled with radioisotope.

Quantitative Assay
Western Blotting
Separates proteins in electric field on gel.
Proteins are than transfered to "membrane".
Membrane treated with antibody for specific antigen.
Either ELISA or RIA antibody used to detect antigen-specific antibody.

***Useful in characterizing antibody reactivities in patients with certain pathogens (HIV)***
Protein Electrophoresis
Proteins placed in well on support media and separated based on charge. Support media stained than scanned by densitometry to provide analytical pattern of protein
Combines electrophoretic separation of serum protein followed by immunologic detection using specific antibodies.
Interpretation made by comparing to standard reference.
Qualitative but can be used to determine under production of certain isotypes (immunodeficeny) or overpruction of proteins
qualitatively detects presence of antigens or antibody on cells or tissue
Tissue or cells attached to glass slide. Flourescent or enzyme labeled antibody applied to material.

Used in the Detection of Ag-AB complexes or complement complexes associated with autoimmune diseases
Localizing presence of specific Ags or hormones in tissue
Detecting treponemal-specific antibody from a patient with syphilis
Flow Cytometry
Studies individual cell for reactivity with specific fluorescent markers.
Stream of single cells pass through laser beam(s) which causing light scattering and fluorescence.
Can also sort cells of interest, used in leukemias, and measurement of T Cell subpopulations as prognosis indicator for AIDS
Forward Scatter: Size
Side Scatter: Granularity
Colored Lasers: Detection of fluorescence

Plotted FCS v SSC
Complement Fixation Tests
Step 1: Mix antigen with serum of suspected specific antibody. ** If antigen-antibody complexes for they will fix complement***

Step 2: Add Antibody coated Sheep RBCs as indicator system. If complement depleted in Step 1, RBC will remain intact
Hemolytic Assay
Uses patient serum as source of complement to lyse antibody-coated Sheep RBC.

Measurement of hemolytic activity of serum is taken at the 50% hemolysis level:
Classic: CH50
Alternative: AH50

Determines Activity of complement associated with certain diseases.

*****Assays using specific antibodies for various complement and nephelometry or ELISA determine complement concentrations