Autoantibodies and defined target autoantigens in autoimmune hepatitis: an overview

Intravenous glucocorticoid therapy for Graves' ophthalmopathy and acute liver damage: an epidemiological study

“…Approximately 2 weeks before treatment, all patients underwent the following evaluation: i) routine blood tests, including, among others, total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, aspartate (AST) and alanine (ALT) aminotransferase, alkaline phosphatase (ALP), gamma-glutamyl transferase (gGT), total and direct bilirubin; ii) thyroid function tests, including free tri-iodothyronine, and thyrotropin; iii) serum markers of exposure to HBV and HCV; iv) serum autoantibodies known to be associated with autoimmune hepatitis (12,13,14), namely anti-nuclear (ANA), anti-mitochondrial (AMA), anti-centromeric, anti-liverkidney-microsomal (LKM), and anti-smooth muscle antibodies (ASMA); and v) liver ultrasound.…”

“…These two patients were treated with GC themselves, in order to re-establish a certain degree of immune suppression, with a favorable outcome of ALD. In order to predict and possibly prevent the risk of autoimmune hepatitis, patients were tested for nonorgan-specific autoantibodies known to be related to autoimmune hepatitis (12,13,14), and, in addition, they were all given oral GC after the end of i.v.GC to prevent immune rebound. Furthermore, patients who had positive tests for nonorgan-specific autoantibodies were given oral GC also during i.v.GC, in order to prevent immune rebound between i.v.GC pulses.…”

“…After the initial reports, we introduced empirically a series of exclusion criteria and preventive measures aimed at reducing ALD morbidity and mortality, namely: i) exclusion of patients with viral or alcohol-related cirrhosis, or with a severe liver steatosis, the latter as determined by liver ultrasound, all of which are to some extent known to represent risk factors for a possible direct toxic effect of GC (10,11); ii) reduction of the GC dose, frequency, and number of pulses; this measures was based on the knowledge that GC may exert a direct toxic effect on liver cells, which is expected to be dose-dependent (10,11); and iii) administration of oral GC after i.v.GC, and limited to patients positive for nonorgan-specific autoantibodies which can be associated with autoimmune hepatitis (12,13,14), also during i.v.GC, in order to prevent an autoimmune rebound and a consequent autoimmune hepatitis, as described in at least two patients given i.v.GC (6,7).…”

BREAKTHROUGH OF IMMUNE SELF-TOLERANCE TO CALRETICULIN INDUCED BY CpG-OLIGODEOXYNUCLEOTIDES AS ADJUVANT

“…However, many studi es have been made of autoantibodies in AUf 19,20). The CpG-ODN s can induce autoantibodies that are undetectable by convention al methods because CpG-ODNs are three times more efficient in producing autoantibodies than complete Freund's adjuvant 21 ).…”

Autoimmune hepatitis: Of host and pathogen

“…We noticed that reactivity to p3 CYP2D6 peptide, which had homology with CYP2A6 [8][9][10][11][12][13][14][15][16][17] and CYP2A7 [8][9][10][11][12][13][14][15][16][17] , correlated with biochemical markers of disease activity, suggesting that p3-specific CD8 T cells may be involved in liver damage. It is also of interest that both CYP2A6 [8][9][10][11][12][13][14][15][16][17] and CYP2A7 [8][9][10][11][12][13][14][15][16][17] have been reported to be cross-reactively recognized with HCV 178-187 by CD8 T cells in chronic hepatitis C virus, 2 whereas we have shown that anti-CYP2A6 antibody may be present in HCV patients. 3 Of note, p3-specific CD8 T cells were not as effective at the cytotoxicity level, 1 and this suggests a dichotomy between CD8 T-cell functions, which is a phenomenon reported in chronic HCV.…”