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spliceosomal snRNP autoantibodies 665 spontaneous autoimmune thyroiditis (SAT)
spliceosomal snRNP autoantibodies
Sm autoantibodies are reactive with Sm core proteins (B, V,
E) common to U1 snRNP, U2 snRNP, and other uridinerich
snRNPs (U4/U6, U5, U7, and U11/U12). Use of the U1
snRNP autoantibodies term should be restricted to autoantibodies
reactive with non-Sm protein epitopes characteristic
of individual snRNPs (70K, A, and C for U1; AN and
BO for U2; 120-kDa/150-kDa for U4/U6). Sm autoantibodies
occur in 20 to 30% of Caucasian adults and children
with systemic lupus erythematosus (SLE) and in 30 to 40%
of Asians and blacks with SLE. Mixed connective tissue
disease (MCTD) is characterized by U1 snRNP (100%) and
occasionally accompanied by U2 snRNP (approximately
15%) autoantibodies.
SS-A/Ro antibodies.
splits
Human leukocyte antigen (HLA) subtypes. For example,
the base antigen HLA-B12 can be subdivided into splits
HLA-B44 and HLA-B45. The split term designates an HLA
initially believed to be a private antigen but later shown to
be a public antigen. The former designation can be placed in
parentheses following its new designation, e.g., HLA-B44(12).
split thickness graft
A skin graft that is only 0.25 to 0.35 mm thick and consists
of epidermis and a small layer of dermis. These grafts
vascularize rapidly and last longer than regular grafts. They
are especially useful for burns, contaminated skin areas,
and sites that are poorly vascularized. Thick split thickness
grafts are further resistant to trauma, produce minimal
contraction, and permit some sensation, but graft survival
is poor.
split tolerance
(1) Specific immunological unresponsiveness (tolerance)
affecting the B cell (antibody) limb or the T lymphocyte
(cell-mediated) limb of the immune response. The unaffected
limb is left intact to produce antibody or respond
with cell-mediated immunity, depending on which limb
has been rendered specifically unresponsive to the antigen
in question. (2) The induction of immunologic tolerance
to some epitopes of allogeneic cells, leaving the remaining
epitopes capable of inducing an immune response
characterized by antibody production and/or cell-mediated
immunity. (3) T cell tolerance to a specific tolerogen may be
induced, whereas B cell reactivity remains intact.
sponges
Even the most primitive invertebrates (marine sponges)
can discriminate self from nonself, leading to rejection
Splits
Original Broad Specificities
Splits and
Associated Antigens
A2 A203#, A210#
A9 A23, A24, A2403#
A10 A25, A26, A34, A66
A19 A29, A30, A31, A32, A33, A74
A28 A68, A69
B5 B51, B52
B7 B703#
B12 B44, B45
B14 B64, B65
B15 B62, B63, B75, B76, B77
B16 B38, B39, B3901#, B3902#
B17 B57, B58
B21 B49, B50, B4005#
B22 B54, B55, B56
B40 B60, B61
B70 B71, B72
Cw3 Cw9, Cw10
DR1 DR103#
DR2 DR15, DR16
DR3 DR17, DR18
DR5 DR11, DR12
DR6 Dr13, DR14, DR1403#, DR1404#
DQ1 DQ5, DQ6
DQ3 DQ7, DQ8, DQ9
Dw6 Dw18, Dw19
Dw7 Dw11, Dw17
of parabiosed fingers of different colonies in 7 to 9 days.
Species-specific glycoproteins of sponge cells are used
for identification of self and inhibition of hybrid colony
formation. Placed in apposition to one another, nonidentical
sponge colonies become necrotic at interfaces. Second
grafts undergo accelerated rejection.
spongiform encephalopathies
Fatal prion diseases. The brain becomes sponge-like. This
category includes variant Creutzfeldt-Jakob disease (vCJD)
in humans, scrapie in sheep, and bovine spongiform encephalopathy
(BSE, also known as mad cow disease) in cattle.
spontaneous autoimmune thyroiditis (SAT)
Spontaneous autoimmune thyroiditis (SAT) in the obese
strain (OS) of chicken constitutes an animal model of
Hashimoto’s thyroiditis in humans. Many mononuclear
cells infiltrate the thyroid gland, leading to disruption of
the follicular architecture. Immunodysregulation is critical
in the etiopathogenesis of SAT. Endocrine abnormalities
play a role in pathogenesis. Disturbances in communication
between the immune and endocrine systems occur.
Dysregulation leads to hyperreactivity of the immune
system which, combined with a primary genetic defectinduced
alteration of the thyroid gland, leads to autoimmune
thyroiditis. Both T and B lymphocytes are significant
in the pathogenesis of SAT. T cell effector mechanisms
have greater influence than humoral factors in initiating the
disease, and most lymphocytes infiltrating the autoimmune
thyroid are mature cells. Autoantibodies play a minor role
S