Chapter 6 part 1 Flashcards
Factors of Innate Immunity (5)
- Epithelial barriers
- Phagocytes
- Dendritic Cells
- Complement
- NK Cells
Adaptive Immunity (2)
- B-Lymphocytes => Antibodies
2. T-cells => Effector T-cells
Epithelial barriers (3)
- Produce antibicrobes - Defensins
- Lymphocytes found here
- Mechanical stuff
Phagocytes (2)
- Monocytes/Neutrophils in blood
2. Sense microbe presence and murder invaders
Dendritic Cells (3)
- Found in epithelium and lymphoid organs
- Capture Ags and present to T-cells
- Stim cytokine secretion (inflammation and Antiviral response)
Natural Killer cells (1)
- Early protection (viruses and INTRACELLULAR bacteria)
Mast Cells (1)
- Release inflammation mediators
Plasma Proteins types (3)
- Complement system
- Mannose binding lectin and C-Reactive protein
- Lung Surfactant
- Complement system
- Proteins activated by microbes
- Alternative and lectin pathways
- classic pathway activated via Abs (adaptive immunity)
Coat microbes and promote phagocytosis?
Mannose binding lectin and C-reactive protein
Protection against inhaled microbes?
Lung surfactant
How does Innate Rec Microbes?
Pattern Recognition patterns (infecting and cell damage activities)
Main Receptors? (2)
- TLRs
2. NOD-Like receptors (NLRs)
TLRs activate?
- NF-kB
2. Interferon Regulatory Factors (IRFs)
What does NF-kB do?
- Stimulates cytokine secretion and expression of adhesion molecules
- Results in the attraction of Leukocytes
Interferon Regulatory Factors (IRF
Increase Antiviral Cytokine secretion (type 1 interferons)
NLRs are found where?
in the cytosol
TLRs are found where?
Plasma membranes
How do NLRs signal?
Via the inlfammasome
What does the inlfammasome do?
- Activates Caspase 1
- Caspase 1 activates IL-1
- IL-1 induces fever
Gain of function mutation in NLR causes what?
Autoinflammatory syndrome
How do you treat Autoinflammatory syndrome?
IL-1 antagonist duh
NLR may also play a role in (3)
- Gout
- Type 2 Diabetes
- Atherosclerosis
Other Receptors? (4)
- C-Type Lectin
- RIG-like R
- G-protein coupled R
- Mannose R
This receptor is in the cytosol an activate cytokines when stimulated by the NA of viruses?
RIG-like R
C-type Lectin are found where?
Macrophages and dendritic cells
-In the plasma membrane
Receptor for Neutrophils, Macrophages and Leukocytes?
G Protein-Coupled R
Microbial sugars received by?
Mannose R
How Does Innate Respond? (3)
- Inflammation: Cytokines/complement
- Antiviral: Type 1 interferons
- Stim Adaptive Immunity
Adaptive immunity traits: 2 types
- Humoral Immunity
2. Cell Mediated Immunity
Extracellular and B-lymphocytes are examples of what type of immunity?
Humoral Immunity
T-cells and Intracellular microbes are involved in what type of immunity?
Cell-mediated Immunity
What allows Lymphocytes to respond to a wide array of AGs?
They have a highly diverse pool of receptors.
B and T cells: general facts (3)
- Circulate in blood
- Considered Naive prior to encountering Ag they are specific for
- Once activated they differentiate into Effector and Memory cells
These cells Neutralize Microbes, phagocytose and activate the complement system.
B-Cells!
These cells kill infected cells (2)
- Cytotoxic T Lymphocytes
2. Natural Killer Cells
Regulatory T-cells…
…suppress the immune system
Helper T-lymphocytes are activated by?
APC-Macrophages (they also activate macrophages themselves) and Dendritic cells
-remember multiples of 8. CD8 = class 1 and CD4 = Class 2 MHC
Helper T-lymphocyte functions?
- Activate Macrophages
- Inflammation
- Activate/proliferate T + B lymphocytes
Lymphocyte diversity
- 1 trillion in healthy adult
2. Not many for each Ag
What is clonal selection?
Once a lymphocyte is exposed to a specific Ag, it makes clones that are specific for that Ag.
How is diversity generated?
Somatic recombination of genes that encode R. Proteins
When and where does this somatic recombination occur?
Durring maturation
T-cells = thymus
B-Cells = Bone marrow
These genes mediate somatic recombination
RAG-1 and RAG-2
-Problems result in an inability to generate mature lymphocytes
Recombined T and B cells result in different…
TCRs and Igs
If lymphocyte proliferation is polyclonal…
…it is considered BENIGN and NON-NEOPLASTIC
If lymphocyte proliferation is neoplastic…
it is considered MONOCLONAL and Malignant
3 types of T-lymphocytes
- Helper T-lymphocytes
- Cytotoxic T-cells
- Regulatory T-cells
These cells stim activation of leukocytes
Helper T-cells
-stim B-cells and thus Ab formation/leukocytes
95% of TCRs are…
- Heterodimers w/alpha + Beta polypeptide chains
- A/B Rec Ags presented by MHC assure T-cells only see associated Ags
These T-cells don’t need MHCs for activation and where do they aggregate?
- Gamma-Delta TCR
2. Epithelial surfaces
These cells have TCR receptors for glycolipids presented by MHC-CD1 (MHC-like but not actually) cells
NK-t cells can express this TCR
More CD8 or CD4?
60% CD4 and 30% CD8
Assist macrophages and B-lymphocytes by secreting cytokines
CD4
CD8 cells are?
Cytotoxic T-lymphocytes => destroy host cells
MHC 1 bind __
MHC 2 bind ___
CD8
CD4
Where do you find B-lymphocytes? (3)
- Lymph nodes
- spleen
- mucosa associated lymphoid tissue
B-cell Ag receptor complex consists of?
- IgM and IgD (membrane bound)
- Found on surface of mature Naive cells
- After stim by Ag => plasma cells
- Igalpha/beta also involved
CR2 and CD21 are examples of?
Type 2 complement receptors
What disease uses Type 2 complement receptors to cause its effects?
Epstein-barr virus (EBV)
-Infects and enters B-cells through this mech
What receives Th signals?
CD40
Dendritic cells “coolest looking according to Dr. G”: Functions/facts
- APC for T-Cells
- Express TLRs and lectins
- Recruited by microbes to T-Cell zones
- Express high levels of MHC