-
Th1 cells make ____ to activate ___
- IL-2 and IFN-gamma
- macrophages and CD8 T cells
-
Th1 cells are inhibited by this
IL-10
-
Th2 cells make hese
IL-4, 5, 10
-
Th2 cells are inhibited by this
IFN-gamma
-
Where is the antigen loaded for MHC I?
In the RER of mostly intracellular peptides
-
Which MHC uses Ag loading involving release of invarient chain, and where does this occur
- MHC II
- In an acidified endosome
-
Structure of MHC II molecules
- alpha and beta chains
- symetrical
- peptide-binding groove between the two
-
Structure of MHC I molecules
- alpha clover leaf
- beta-2 microglobulin
- Peptide-binding groove is in alpha clover
-
-
Psoriasis, IBD, Reiter's syndrome HLA
B27
-
-
MS, hay fever, SLE, Goodpasture's HLA
DR2
-
-
-
Pernicious anemia and Hashimoto's HLA
DR5
-
Steroid-responsive nephrotic syndrome HLA
DR7
-
NK cells use these to kill cells
perforin and granzymes
-
These enhance NK cell activity
IL-12, IFN-B, IFN-a
-
Macrophage-lymphocyte interaction
- Lymphocytes release IFN-gamma
- Macrophages release IL-1 and TNF-a
- They stimulate each other this way
-
Action of superantigens
- Cross-link B-region of TCR to the MHC class II on APCs
- IFN-g released from Th1 cells
- IL-1 IL-6 and TNF-a released from macrophages
-
Effect of endotoxins/LPS
- Directly stimulate macrophages by binding to endotoxin receptor CD14
- Th cells are NOT involved
-
Th activation costimulator signal
Interaction of B7 and CD28
-
CD8 T cell activation following MHC I recognition
IL-2 from Th cell activation CD8 to kill
-
B-cell class switching: 2 steps
- IL-4, 5, or 6 from Th2 cell
- CD40 receptor activation by binding CD40L on Th cell
-
Igs allowing complement binding
IgG and IgM
-
IL-1 secreted by
macrophages
-
IL-1 activity
- Pyrogen, lethargy, anorexia, inflammation
- Induces chemokine production to recruit leukocytes
-
IL-2 secreted by ___ and stimulates ___
- Th cells
- Helper and cytotoxic T cells
-
IL-3 source and function
- Activated T cells
- Like GM-CSF, supports bone marrow growth
-
IL-4 source and function
- Th2 cells
- Class switching to IgE and IgG
-
IL-5 source and function
- Th2 cells
- Class switching to IgA
- Production and activation of eos
-
IL-6 source
Th cells and macrophages
-
IL-6 function
Proudction of acute-phase reactants and Igs
-
-
IL-10 source and fxn
- Tregs
- Inhibits Th1, activates Th2
-
IL-12 source and function
- B cells and macrophages
- Activates NK and Th1 cells
-
IFN-g source and function
- Th1 cells
- Stimulates macrophages
- Activates Th1, inhibits Th2 (opposite IL-10)
-
TNF source and function
- Macrophages
- Mediates septic shock
- Leukocyte recruitment, vascular leak
- Cachexia
-
-
B cell surface proteins
- IgM
- CD 19, 20, 21 (EBV), 40
- MHC II
- B7
-
Macrophage cell surface proteins
- MHC II
- B7
- CD 40, 14
- Fc and C3b receptors
-
-
Anti-inflammatory
- TGF-B (induces apoptosis, inhibits Th2)
- IL-10
-
C1 esterase inhibitor deficiency
Hereditary angioedema
-
C3 deficiency
- Severe recurrent pyogenic sinus and respiratory tract infections
- Type III hypersensitivity susceptibility
-
DAF deficiency
Complement-mediated lysis of RBCs and PNH
-
IFNs induce this
Ribonuclease production for viral protein synthesis inhibition
-
Passive immunization following exposure to these
Tetanus, Botulinum, HBV, Rabies
-
What is anergy?
When self-reactive T cells become nonreactive due to lack of costimulatory molecule
-
Defect in Bruton Tyrosine Kinase
- Bruton's agammaglobulinemia
- Blocks B-cell differentiation
- Recurrent bacterial infections
- Decreased B cells and Igs of all classes
-
Defective CD40L on helper T cells
- Inability to class switch --> Hyper-IgM syndrome
- Severe pyogenic infections early in life
- Lots of IgM, little of the rest
-
IgA deficiency
- Sinus and lung infections
- Milk allergies, etc
- Anaphylaxis on exposure to blood products
-
Normal number of B cells with decreased plasma cells and Ig
- Common variable immunodeficiency
- Defect in B cell maturation
- Can be acquired in 20s-30s
- Risk of autoimmune, lymphoma, sinopulmonary infections
-
Disseminated mycobacterial infections
- IL-12 receptor deficiency
- Low Th1 response, low IFN-g
-
Hyper-IgE syndrome (Job's)
- Failure to produce IFN-gamma --> nonresponsive PMNs
- Coarse facies, cold staph abscesses, retained teeth, derm problems
-
Ataxia-telangiectasia triad
Ataxia, spider angiomas, IgA deficiency
-
Wiskott-Aldrich syndrome
- Deletion of B and T cells, XLR
- Thrombocytopenic purpura, Infections, Eczema
- IgM will be low, high IgE and IgA
-
Recurrent bacterial infections without pus, delayed umbilicus separation
- LAD
- Defect in LFA-1 integrin (CD18) protein on phagocytes
- Labs show neutrophilia
-
Chediak-Higashi syndrome defect and symptoms
- AR defect in microtubules
- Staph and strep pyogenic infections, partial albinism, peripheral neuropathy
-
Negative nitroblue tetrazolium dye reduction test
- CGD
- Lack of NADPH oxidase causing decreased ROS and absent PMN respiratory burst
-
Susceptibility in CGD
- Catalase-positive organisms:
- s. aureus
- e.coli
- pseudomonas capecia
- serratia
- nocardia
- aspergillus
|
|
