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Untitled - D Ank Unlimited

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self antigen 644 senescent cell antigen<br />

have been substantiated by scientific evidence. The selective<br />

theories maintained that cells were genetically programmed<br />

to react to certain antigenic specificities prior to antigen<br />

exposure. These theories are in sharp contrast to the instructive<br />

theories postulating that antigen was necessary to serve<br />

as a template around which polypeptide chains were folded to<br />

yield specific antibodies. The template theory was abandoned<br />

when antibody was demonstrated in the absence of antigen.<br />

self antigen<br />

Autoantigen. All normal body constituents to which the<br />

immune response would respond were it not for immunologic<br />

tolerance to these self epitopes.<br />

self MHC<br />

The major histocompatibility complex (MHC) molecules of<br />

a single individual.<br />

self marker hypothesis (historical)<br />

A concept suggested by Burnet and Fenner in 1949 to<br />

account for the failure of the body to react against its own<br />

antigens. They proposed that cells contained markers that<br />

identified them to the host’s immunologically competent<br />

cells as self. This recognition system was supposed to<br />

prevent the immune cells of the host from rejecting its<br />

own tissue cells. This hypothesis was later abandoned by<br />

the authors and replaced by the clonal selection theory of<br />

acquired immunity that Burnet proposed in 1957.<br />

self MHC restriction<br />

The confinement of antigens that an individual’s T cells can<br />

recognize to complexes of peptides bound to major histocompatibility<br />

complex (MHC) molecules in the thymus during T<br />

lymphocyte maturation (i.e., self MHC molecules). Positive<br />

selection leads to self MHC restriction of the T cell repertoire.<br />

self peptides<br />

Peptides formed from proteins of the body. In the absence<br />

of infection, these peptides occupy the peptide binding sites<br />

of major histocompatibility complex (MHC) molecules on<br />

cell surfaces.<br />

Thymus<br />

T<br />

DELETION<br />

T<br />

SUPPRESSION<br />

T<br />

T<br />

T<br />

B<br />

T<br />

T<br />

TCR against self<br />

TCR against non-self<br />

HELP<br />

T<br />

T<br />

self recognition<br />

The identification of autoantigens by lymphoid cells of the<br />

immune system. This is a consequence of the establishment<br />

of immunological tolerance of self antigens during<br />

fetal development.<br />

self renewal<br />

The capacity of a cell population to restore itself.<br />

self restriction<br />

Refer to MHC restriction.<br />

self tolerance<br />

The body’s acceptance of its own epitopes as self antigens.<br />

The body is tolerant to these autoantigens that are exposed<br />

to lymphoid cells of the host immune system without<br />

eliciting an immune response. Tolerance to self antigens<br />

is developed during fetal life. Thus, a host is immunologically<br />

tolerant to self or autoantigens. Self tolerance is due<br />

mainly to inactivation or killing of self-reactive lymphocytes<br />

induced by exposure to self antigens. Failure of<br />

self tolerance in the normal immune system may lead to<br />

autoimmune diseases. Refer also to tolerance and immunologic<br />

tolerance.<br />

semisyngeneic graft<br />

A graft that is ordinarily accepted from an individual of one<br />

strain into an F 1 hybrid of an individual of that strain mated<br />

with an individual of a different strain.<br />

senescent cell antigen<br />

A neoantigen appearing on old red blood cells that binds<br />

immunoglobulin G (IgG) autoantibodies. Senescent cell<br />

antigen is also found on lymphocytes, platelets, neutrophils,<br />

adult human liver cells (in culture), and human embryonic<br />

renal cells (in culture). Its appearance on aging somatic<br />

cells probably represents a physiologic process to remove<br />

senescent and injured cells that fulfilled their functions.<br />

Macrophages can identify and phagocytize dying and aging<br />

self cells that are no longer functional without disturbing<br />

mature healthy cells.<br />

T<br />

T<br />

CLONAL<br />

ANERGY<br />

Mechanism of self tolerance.<br />

Inactivation<br />

APC<br />

unable to<br />

produce<br />

costimulators

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