da_bruva at hotmail.com
da_bruva at hotmail.com
Wed Mar 25 09:49:38 EST 1998
In article <1998032504265000.XAA01563 at ladder03.news.aol.com>,
redi11 at aol.com (Redi11) wrote:
> i need to know the 4 different types of immunity
[tricky question but I think this is what you mean...if not let me know...
TYPE I IMMUNE INJURY IN HUMAN DISEASE (* ahh--CHOO!)
Type I hypersensitivity ("anaphylactic" or "immediate
hypersensitivity") is the result of
antigen binding to IgE on the surface of mast cells and basophils.
degranulate and release active substances into the surrounding tissue.
The reaction begins within seconds to minutes following antigen
is over within a few hours.
IgE protects us against worms. (Almost everyone gets allergic to
once they have met it.) The idea that type I hypersensitivity
was created to help
protect us from worms has recently found good experimental
349: 243, 1991.
*IgE production is of course orchestrated by T-helper and T-
that specialize in just this.
*A few unusual types of IgG attached to mast cells can do
exactly the same
thing that IgE does.
Some people make IgE much more readily than others, and these are the
allergies ("atopic disease").
"Atopy" means "strange". It's strange that some, but not all,
people get asthma
from something as trivial as cat dander.
By far the most interesting piece of news in allergy lately is
the discovery that
"allergy freaks" (like the author of these notes) seem to carry
a different allele
for the mast-cell IgE receptor (* 11q13 codes for the beta-
subunit). See Lancet
341: 1121, 1993.
Once induced (by one or more encounters with the antigen, or
binds to the mast cells and basophils. The person is now
allergic to the
It will get worse every time the allergen is encountered,
and if the
allergen is carefully avoided, the allergy will become
YPE II IMMUNE INJURY IN HUMAN DISEASE
In this type of hypersensitivity, antibodies attach to antigens on the
surfaces of a cell,
and then something injures or destroys the cell.
If the antibodies are already circulating and fast-acting
damage may be complete within minutes.
If the antibodies need to be made for the occasion or are slow-
acting, or if an
anamnestic response must take place, the injury will begin only
TYPE III IMMUNE INJURY IN HUMAN DISEASE
This sort of tissue injury is mediated by antigen-antibody complexes
If there is a great excess of either antigen or of antibody,
mixtures of the two are
readily soluble and easily disposed of by the body (why?).
The problem occurs when antigen and antibody are present in just
(wrong?) proportion. They form huge lattices ("complexes").
The complexes get deposited around the body, typically in the
walls of blood
vessels. Complement is fixed, vessels leak and spazz shut, polys
arrive and find nothing to attack (but attack anyway), C9
punches holes in
healthy membranes, and general havoc results.
TYPE IV IMMUNE INJURY IN HUMAN DISEASE
In type IV hypersensitivity, special T-helper cells (TD) programmed to
particular "altered self" antigen, are stimulated. They in turn
lymphocytes, macrophages, and other tissue elements. The object is to
destroy every cell
bearing the "altered self" antigen.
This is great for ridding the body of virally infected cells,
intracellular parasites (TB, some fungi), and perhaps tumor
It is also the way the body acute-rejects transplanted organs
The TD-cell programmed to respond to a particular antigen meets it in
the class II histocompatibility antigens (MHC-II, HLA-D, DR; "Ia's") of
macrophage that presents it. This is a big deal.
The stimulated TD cell signals to other T-cells and macrophages,
that it is time for a type IV hypersensitivity reaction.
All nearby resting T-CTL cells of all specificities are readied,
in the area are stimulated ("become angry").
In addition, the TD cell produces interferon (helps anger the
probably other factors. (You will have to read about transfer
The now-stimulated T-CTL cell specialized for killing cells bearing a
will attack when it encounters that antigen in association with the
histocompatibility antigens (HLA-A, B, C).
The T-CTL binds to the cell bearing the "altered self" antigen,
and then may
leave. A few hours later, the cell bearing the "altered self"
bursts/undergoes apoptosis and dies. Unlike in complement-
"innocent bystanders" are spared. When this predominates, we
"cell-mediated cytotoxicity"; some authorities call this "type V
The molecular biology is now worked being worked out. A T-cell
cell to be destroyed on the fas antigen (J. Imm. 152: 1127,
1994), the common
-----== Posted via Deja News, The Leader in Internet Discussion ==-----
http://www.dejanews.com/ Now offering spam-free web-based newsreading
More information about the Immuno