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| 1. |
Flavivirus‐Induced Up‐regulation of MHC Class I Antigens; Implications for the Induction of CD8+T‐Cell‐Mediated Autoimmunity |
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Immunological Reviews,
Volume 152,
Issue 1,
1996,
Page 5-19
Mario Lobigs,
Robert V. Blanden,
Arno Müllbacher,
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ISSN:0105-2896
DOI:10.1111/j.1600-065X.1996.tb00908.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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| 2. |
Immunopathology or Organ‐Specific Autoimmunity as a Consequence of Virus Infection |
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Immunological Reviews,
Volume 152,
Issue 1,
1996,
Page 21-45
Peter Aichele,
Martin F. Bachmann,
Hans Hengartner,
Rolf M. Zinkernagel,
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PDF (8038KB)
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ISSN:0105-2896
DOI:10.1111/j.1600-065X.1996.tb00909.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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| 3. |
Viruses, Hidden Self‐Epitopes and Autoimmunity |
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Immunological Reviews,
Volume 152,
Issue 1,
1996,
Page 47-66
Vincenzo Barnaba,
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PDF (1296KB)
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ISSN:0105-2896
DOI:10.1111/j.1600-065X.1996.tb00910.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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| 4. |
B‐Cell Activation by Superstimaulatory Influenza Virus Hemagglutinin: A Pathogenesis for Autoimmunity? |
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Immunological Reviews,
Volume 152,
Issue 1,
1996,
Page 67-88
Evelyne Cash,
Jeannine Charreire,
Oortwin Rott,
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ISSN:0105-2896
DOI:10.1111/j.1600-065X.1996.tb00911.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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| 5. |
Epstein‐Barr Virus Infection of T Cells: Implications for Altered T‐Lymphocyte Activation, Repertoire Development and Autoimmunity |
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Immunological Reviews,
Volume 152,
Issue 1,
1996,
Page 89-110
David H. Dreyfus,
Colm A. Kelleher,
James F. Jones,
Erwin W. Gelfand,
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ISSN:0105-2896
DOI:10.1111/j.1600-065X.1996.tb00912.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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| 6. |
Using Transgenic Mouse Models to Dissect the Pathogenesis of Virus‐Induced Autoimmune Disorders of the Islets of Langerhans and the Central Nervous System |
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Immunological Reviews,
Volume 152,
Issue 1,
1996,
Page 111-143
Matthias G. Herrath,
Claire F. Evans,
Marc S. Horwitz,
Michael B. A. Oldstone,
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ISSN:0105-2896
DOI:10.1111/j.1600-065X.1996.tb00913.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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| 7. |
Retroviruses and Systemic Lupus Erythematosus |
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Immunological Reviews,
Volume 152,
Issue 1,
1996,
Page 145-156
Martin Herrmann,
Manuel Hagenhofer,
Joachim R. Kalden,
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PDF (600KB)
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ISSN:0105-2896
DOI:10.1111/j.1600-065X.1996.tb00914.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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| 8. |
Human Herpes Viruses Latent Infection in the Nervous System |
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Immunological Reviews,
Volume 152,
Issue 1,
1996,
Page 157-173
Istael Steiner,
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ISSN:0105-2896
DOI:10.1111/j.1600-065X.1996.tb00915.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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| 9. |
A Novel Mechanism for Virus‐Induced Autoimmunity in Humans |
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Immunological Reviews,
Volume 152,
Issue 1,
1996,
Page 175-192
Cecilia Söderberg Nauclér,
Susanne Larsson,
Erna Möller,
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ISSN:0105-2896
DOI:10.1111/j.1600-065X.1996.tb00916.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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| 10. |
The Potential Roles of Endogenous Retroviruses in Autoimmunity |
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Immunological Reviews,
Volume 152,
Issue 1,
1996,
Page 193-236
Kaku Nakagawa,
Leonard C. Harrison,
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摘要:
SUMMARYEndogenous retroviruses (ERVs) are estimated to comprise up to 1% of human DNA. While the genome of many ERVs is interrupted by termination codons, deletions or frame shift mutations, some ERVs are transcriptionally active and recent studies reveal protein expression or particle formation by human ERVs.ERVs have been implicated as aetiological agents of autoimmune disease, because of their structural and sequence similarities to exogenous retroviruses associated with immune dysregulation and their tissue‐specific or differentiation‐dependent expression. In fact, retrovirus‐like particles distinct from those of known exogenous retroviruses and immune responses to ERV proteins have been observed in autoimmune disease. Quantitatively or structurally aberrant expression of normally cryptic ERVs, induced by environmental or endogenous factors, could initiate autoimmunity through direct or indirect mechanisms.ERVs may lead to immune dysregulation as insertional mutagens or cis‐regulatory elements of cellular genes involved in immune function. ERVs may also encode elements liketaxin human T‐lymphotrophic virus type I (HTLV‐I) ortatin human immunodeficiency virus‐I (HIV‐I) that are capable of transactivating cellular genes. More directly, human ERV gene products themselves may be immunologically active, by analogy with the superantigen activity in the long terminal repeat (LTR) of mouse mammary tumour viruses (MMTV) and the non‐specific immunosnppressive activity in mammalian type C retrovirusenvprotein. Alternatively, increased expression of an ERV protein, or expression of a novel ERV pro‐tissue the result could be autoimmune disease. The adjective, paraneoplastic, would only seem appropriate if autoimmunity and tumour were temporally associated. Thus, ERVs could be viewed as being at the interface between tumour immunity and autoimmunity, the pivotal balance depending on the prevailing overlap between 'self and‘non‐self. Although pure speculation, this hypothesis is consistent with the emerging body of molecular evidence that ERVs play a key role in regulating immune function
ISSN:0105-2896
DOI:10.1111/j.1600-065X.1996.tb00917.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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