immunity

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.
These instantly
       degranulate and release active substances into the surrounding tissue.

              The reaction begins within seconds to minutes following antigen
exposure, and
              is over within a few hours.

              IgE protects us against worms. (Almost everyone gets allergic to
ascaris worm
              once they have met it.) The idea that type I hypersensitivity
was created to help
              protect us from worms has recently found good experimental
support: Nature
              349: 243, 1991.

              *IgE production is of course orchestrated by T-helper and T-
suppressor cells
              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
people with
       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
"allergen"), IgE
              binds to the mast cells and basophils. The person is now
allergic to the
              particular "allergen".

                    It will get worse every time the allergen is encountered,
and if the
                    allergen is carefully avoided, the allergy will become
less severe.


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
complement-fixers, the
              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
after several
              days.

TYPE III IMMUNE INJURY IN HUMAN DISEASE

       This sort of tissue injury is mediated by antigen-antibody complexes
("immune
       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
the right
              (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
and monos
              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
recognize a
       particular "altered self" antigen, are stimulated. They in turn
coordinate other
       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,
cells harboring
              intracellular parasites (TB, some fungi), and perhaps tumor
cells.

              It is also the way the body acute-rejects transplanted organs
(allografts).

       The TD-cell programmed to respond to a particular antigen meets it in
association with
       the class II histocompatibility antigens (MHC-II, HLA-D, DR; "Ia's") of
the dendritic
       macrophage that presents it. This is a big deal.

              The stimulated TD cell signals to other T-cells and macrophages,
telling them
              that it is time for a type IV hypersensitivity reaction.

              All nearby resting T-CTL cells of all specificities are readied,
and macrophages
              in the area are stimulated ("become angry").

              In addition, the TD cell produces interferon (helps anger the
macrophages) and
              probably other factors. (You will have to read about transfer
factor yourself).

       The now-stimulated T-CTL cell specialized for killing cells bearing a
particular antigen
       will attack when it encounters that antigen in association with the
class I
       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"
antigen
              bursts/undergoes apoptosis and dies. Unlike in complement-
mediated woes,
              "innocent bystanders" are spared. When this predominates, we
talk about
              "cell-mediated cytotoxicity"; some authorities call this "type V
immune injury".

              The molecular biology is now worked being worked out. A T-cell
"kisses" the
              cell to be destroyed on the fas antigen (J. Imm. 152: 1127,
1994), the common
              apoptosis trigger.

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