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Sentences for "autoimmunity "
, [ 15 ] several lines of evidence indicate that amino acids 9-23 of the insulin B chain also represent a major target of anti-islet autoimmunity in T1DM.
Taken together with the findings reported herein, this work indicates that anaphylactic reactions can be elicited in mice that have been immunized with pancreatic islet-associated self-peptides that also represent significant targets of autoimmunity in T1DM.
We report the results of a review of cases undertaken to determine the prevalence of abnormal liver function tests (LFTs) and liver disease in patients with 1°SS referred to a tertiary care center and the association of abnormal LFTs with other systemic features and autoimmunity markers of 1°SS.
Other markers of systemic inflammation or autoimmunity did not correlate with the presence or absence of LFT abnormalities.
Expression of autoimmunity markers also tends to differ between HCV-infection and 1°SS.
Simple and accurate methods exist to determine for a single pair of alleles how the three possible genotypes (2 homozygotes and one heterozygote) affect disease outcome, and these methods have been used frequently in the literature on autoimmunity and HLA [ 28 29 30 ] and once (to our knowledge) in the HLA-infectious disease literature [ 33 ] .
txt Background Autoimmunity is a well-established mechanism of premature ovarian failure.
A false positive diagnostic test indicating autoimmunity as the mechanism of spontaneous premature ovarian failure could put young women at risk for inappropriate therapy.
These mice also develop autoimmunity against thyroid and gastric parietal cells [ 22 ] .
It is well established that these mice with ovarian autoimmunity also develop circulating autoantibodies against the oocyte cytoplasm, the zona pellucida, and against steroid producing cells [ 22 ] .
It is noteworthy that immune serum from mice with ovarian autoimmunity reacts specifically with an oocyte-specific protein called MATER [ 24 25 ] .
This tendency toward autoimmunity in females is often ascribed to hormonal differences, because in a number of experimental disease models estrogens exacerbated disease, and androgens can inhibit disease activity [ 3, 4].
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