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corneal transplantation 197 corticosteroids
corneal transplantation
A corneal transplantation is different from most other transplants
in that the cornea is a “privileged site.” Such sites do not
have lymphatic drainage. The rejection rate in corneal transplants
depends on vascularization; if vascularization occurs,
the cornea becomes accessible to the immune system; human
leukocyte antigen (HLA) incompatibility increases the risk of
rejection if the cornea becomes vascularized. The patient can
be treated with topical steroids to cause local immunosuppression.
Certain anatomical sites within the animal body provide
an immunologically privileged environment that favors the prolonged
survival of alien grafts. The potential for development
of a blood and lymphatic vascular supply connecting graft and
host may be a determining factor in the qualification of an anatomical
site as an area that provides an environment favorable
to the prolonged survival of a foreign graft. Immunologically
privileged sites include: (1) the anterior chamber of the eye, (2)
the substantia propria of the cornea, (3) the meninges of the
brain, (4) the testes, and (5) the cheek pouch of the Syrian hamster.
Foreign grafts implanted in these sites show a diminished
ability to induce transplantation immunity in the host. These
immunologically privileged sites usually fail to protect alien
grafts from the immune rejection mechanism in hosts previously
or simultaneously sensitized with donor tissues.
coronavirus immunity
Neutralizing and fusion-inhibiting antibodies are directed
mainly against the protein S antigen. Antibodies against
HE, N, M, and sM are also significant in neutralization
together with complement factors. Among coronavirus antigens,
there is high antigenic variability of the S1 subunit of
IBV. This subunit induces neutralizing antibodies that bind
to discontinuous epitopes. The S2 subunit contains linear
epitopes and an amino-dominant region. The S1 subunit of
the molecule contains the most immunogenic sites of BCV
and MHV. The S2 subunit of MHV also induces neutralizing
and fusion-inhibiting antibodies. BCV-specific antibodies
against the HE protein participate in neutralization.
The M protein of MHV and TGEV stimulate complementdependent
neutralizing antibodies. The TGEV sM protein is
involved in neutralization. T lymphocyte responses against
SN protein facilitate virus elimination and may confer
protection against encephalomyelitis in mice and rats. An
immunodominant T cell antigenic site in the N protein of
MHV induces neutralizing S protein-specific antibodies.
cortex
The outer or peripheral layer of an organ.
cortical thymic epithelial cells (cTECs)
Refer to thymic epithelial cells.
corticosteroids
Lympholytic steroid hormones, such as cortisone derived
from the adrenal cortex, that are potent anti-inflammatory
and immunosuppressive agents following their linkage to
O
O
CH 3
CH 3
CH 2 OH
C O
Structure of cortisone.
OH
O
O
O
HO
CH 3
CH 3
CH 2 OH
C O
Structure of corticosterone.
HO
CH 3
CH 3
Structure of cortisol.
HO
CH 3
CH 2 OH
C O
OH
CH 2 OH
C O
OH
Structure of 6α-methylprednisolone.
O
HO
CH 3
CH 3
CH 2 OH
C O
Structure of prednisolone.
OH
glucocorticoid receptors and inactivation of transcription
factors including NF-KB, AP-1, NF-AT and the STATs.
Glucocorticoids such as prednisone or dexamethasone can
diminish the size and lymphocyte content of lymph nodes
and spleen while sparing proliferating myeloid or erythroid
stem cells of the bone marrow. Glucocortoids may interfere
with the cell cycle of the activated lymphocyte. They
are cytotoxic for selected T lymphocyte subpopulations
and able to suppress cell-mediated immunity and antibody
synthesis, as well as the formation of prostaglandins and
leukotrienes. Corticosteroids may lyse either suppressor
or helper T lymphocytes, but plasma cells may be more
resistant to their effects. However, precursor lymphoid cells
are sensitive to the drugs, which may lead to decreased antibody
responsiveness. The repeated administration of prednisone
diminishes the concentrations of specific antibodies
in the immunoglobulin G (IgG) class whose fractional
catabolic rates are increased by prednisone. Corticosteroids
interfere with the phagocytosis of antibody-coated cells by
C