Abstract
As part of an investigation into the question of whether virus-induced autoreactivity might contribute to liver damage in viral hepatitis, serial studies (from onset through recovery) of circulating liver autoantibodies have been performed in patients with uncomplicated acute virus A (AVH-A), B (AVH-B) and non-A, non-B (AVH-NANB) hepatitis in whom the time of onset of symptoms could be precisely documented. One hundred and forty-four sera from 35 patients were tested by radioimmunoassay for autoantibodies against the liver-derived lipoprotein complex, LSP, and also against one of its costituents - the asialoglycoprotein receptor, known as hepatic lectin (HL). Anti-LSP antibodies were found in all 10 patients with AVH-A in 17/18 with AVH-B and in 3/7 with AVH-NANB at titres that declined during recovery. Anti-HL antibodies were detected concurrently in 6 of the AVH-A patients and in 5 with AVH-B but on only 1 occasion in 1 patient with AVH-NANB. Transient cellular immunity to LSP, assayed by a T-lymphocyte migration inhibitory factor test, was detected in 4 of the 6 AVH-B patients tested, 2 of whom also showed concurrent reactivity to HL, but these cellular immune responses did not correlate with production of anti-LSP and/or anti-HL. The findings indicate that humoral immune responses to liver cell surface antigens are frequently triggered by hepatitis A and B viruses, possibly via induction of autoreactive, T-cell independent, liver antigen-specific B lymphocytes. These liver-specific autoreactions have the potential to contribute to hepatocellular damage in virus A and B hepatitis but it seems unlikely that autoimmunity plays a significant pathogenic role in NANB viral infections.
| Original language | English |
|---|---|
| Pages (from-to) | 1-7 |
| Number of pages | 7 |
| Journal | Journal of Clinical and Laboratory Immunology |
| Volume | 25 |
| Issue number | 1 |
| Publication status | Published - 1988 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Immunology
Cite this
Liver autoreactivity in acute virus A, B and non-A, non-B hepatitis. / Vento, S.; McFarlane, B. M.; McSorley, C. G.; Ranieri, S.; Giuliani-Piccari, G.; Dal Monte, P. R.; Verucchi, G.; Williams, R.; Chiodo, F.; McFarlane, I. G.
In: Journal of Clinical and Laboratory Immunology, Vol. 25, No. 1, 1988, p. 1-7.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Liver autoreactivity in acute virus A, B and non-A, non-B hepatitis
AU - Vento, S.
AU - McFarlane, B. M.
AU - McSorley, C. G.
AU - Ranieri, S.
AU - Giuliani-Piccari, G.
AU - Dal Monte, P. R.
AU - Verucchi, G.
AU - Williams, R.
AU - Chiodo, F.
AU - McFarlane, I. G.
PY - 1988
Y1 - 1988
N2 - As part of an investigation into the question of whether virus-induced autoreactivity might contribute to liver damage in viral hepatitis, serial studies (from onset through recovery) of circulating liver autoantibodies have been performed in patients with uncomplicated acute virus A (AVH-A), B (AVH-B) and non-A, non-B (AVH-NANB) hepatitis in whom the time of onset of symptoms could be precisely documented. One hundred and forty-four sera from 35 patients were tested by radioimmunoassay for autoantibodies against the liver-derived lipoprotein complex, LSP, and also against one of its costituents - the asialoglycoprotein receptor, known as hepatic lectin (HL). Anti-LSP antibodies were found in all 10 patients with AVH-A in 17/18 with AVH-B and in 3/7 with AVH-NANB at titres that declined during recovery. Anti-HL antibodies were detected concurrently in 6 of the AVH-A patients and in 5 with AVH-B but on only 1 occasion in 1 patient with AVH-NANB. Transient cellular immunity to LSP, assayed by a T-lymphocyte migration inhibitory factor test, was detected in 4 of the 6 AVH-B patients tested, 2 of whom also showed concurrent reactivity to HL, but these cellular immune responses did not correlate with production of anti-LSP and/or anti-HL. The findings indicate that humoral immune responses to liver cell surface antigens are frequently triggered by hepatitis A and B viruses, possibly via induction of autoreactive, T-cell independent, liver antigen-specific B lymphocytes. These liver-specific autoreactions have the potential to contribute to hepatocellular damage in virus A and B hepatitis but it seems unlikely that autoimmunity plays a significant pathogenic role in NANB viral infections.
AB - As part of an investigation into the question of whether virus-induced autoreactivity might contribute to liver damage in viral hepatitis, serial studies (from onset through recovery) of circulating liver autoantibodies have been performed in patients with uncomplicated acute virus A (AVH-A), B (AVH-B) and non-A, non-B (AVH-NANB) hepatitis in whom the time of onset of symptoms could be precisely documented. One hundred and forty-four sera from 35 patients were tested by radioimmunoassay for autoantibodies against the liver-derived lipoprotein complex, LSP, and also against one of its costituents - the asialoglycoprotein receptor, known as hepatic lectin (HL). Anti-LSP antibodies were found in all 10 patients with AVH-A in 17/18 with AVH-B and in 3/7 with AVH-NANB at titres that declined during recovery. Anti-HL antibodies were detected concurrently in 6 of the AVH-A patients and in 5 with AVH-B but on only 1 occasion in 1 patient with AVH-NANB. Transient cellular immunity to LSP, assayed by a T-lymphocyte migration inhibitory factor test, was detected in 4 of the 6 AVH-B patients tested, 2 of whom also showed concurrent reactivity to HL, but these cellular immune responses did not correlate with production of anti-LSP and/or anti-HL. The findings indicate that humoral immune responses to liver cell surface antigens are frequently triggered by hepatitis A and B viruses, possibly via induction of autoreactive, T-cell independent, liver antigen-specific B lymphocytes. These liver-specific autoreactions have the potential to contribute to hepatocellular damage in virus A and B hepatitis but it seems unlikely that autoimmunity plays a significant pathogenic role in NANB viral infections.
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M3 - Article
VL - 25
SP - 1
EP - 7
JO - Journal of Clinical and Laboratory Immunology
JF - Journal of Clinical and Laboratory Immunology
SN - 0141-2760
IS - 1
ER -