A. Difference in Immunoglobulins:
Acute Inflammation: IgM = main Ig first, and then IgG
IgM = main Ig; need a lot of complement components in healing process; IgM is the most
potent activator, and have activation of complement pathway (all the way for 1-9); IgM has
10 activating sites (pentamer).
IgG can activate the classical system, but does NOT go passed C3 and stops and does not go
After 10 days, there is isotype switching, and the mu heavy chain is spliced out (mu chain
defies specificity of an Ig); it splices in a gamma heavy chain, and IgG is made via isotype
2. Chronic inflammation: IgG (as main Ig – IgM is coverted to IgG immediately)
Difference in Cell Types:
1. Acute inflammtions = neutrophil
2. Acute allergic reactions= eosinophils (mast cells are in tissues)
3. Viral infections = lymphocytes are the main inflammatory cells
4. Chronic inflammations = monocytes/macrophages are imp. And see a lot of plasma cells and
lymphocytes; do not see pus-exudative (this is in acute inflamm – increased vessel permeability,
and increased emigration of neutrophils into interstitial tissue, a protein rich fluid with >3
grams/dL, with a protein rich fluid = pus). Example: Cholecystis.
Type IV Hypersensitivity Reaction:
Another example: Granuloma = chronic inflammation (never acute); ie caseious necrosis in
someone with TB; roundish, pink, multinucleated giant cells = granulomas; pathogenesis = type
IV hypersentistivity reaction – delayed HPY. The main actors are cytoxic T cells; when they kill
neoplastic, virally infected cells, these are also type IV HPY (no Ab’s involved). Poison ivy = type
IV HPY. Back to TB infection, aleovlar macrophage phagocytoses it, and there is
lymphohemotogenous spread; meanwhile the macrophage is processing the Ag. Then after
weeks, it presents it to helper T cells. Therefore, the key players in Type IV hypersensitivity rxn
are macrophages which process that Ag and presents that Ag via class II MHC sites to the helper
T cells. These helper T-cells release cytokines: gamma IFN and macrophage inhibitory factor.
Gamma IFN will activate the macrophage to kill the TB, Cryptococcus, histoplasmosis, etc.
Therefore the gamma IFN is the trigger to active the macrophage; macrophage cannot kill
without the activation from gamma IFN; b/c systmemic fungi and TB have lipid in the cell wall,
this leads to caseous necrosis. All the pink staining cells are ‘epthiloid’, which are activated
macrophages (which have been activated by gamma IFN); when they die, they die in style – they
fuse together and form multinucleated giant cells (like their ‘gravestone’). Therefore, epitheloid
cells are fused macrophages; black dots are helper T cells.
There are two types of helper T-cell:
a. Subset 1: involved in Type IV (delayed type) HPY; macrophages have IL-12; when it is
secreted, the subset 1 helper T cells are presented with the antigen; then, subset 1
become MEMORY T cells. IL-12 is involved in activating the memory of subset 1 helper t
cells. Most people in their primary dz usually recover with no problems, but the
granulomas can calcify, as seen on x-ray. A calcified granuloma is not dead b/c they are resistant to dying. Therefore, most cases of secondary TB are due to reactivation TB.
Granulomas necrosis is due to reactivation.
“+” PPD (purified protein derivative) – injected into the