Molecular mimicry: frequency of reactivity of monoclonal antiviral antibodies with normal tissues

Srinivasappa, Javaraiah; Saegusa, Junzo; Prabhakar, Bellur S.; Gentry, Mary K.; Buchmeier, Michael J.; Wiktor, T J; Koprowski, Hilary; Oldstone, Michael B. A.; Notkins, A L

doi:10.1128/jvi.57.1.397-401.1986

Cited by 227 publications

(61 citation statements)

References 26 publications

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“…Monoclonal antibodies generated against various virus-specific proteins have been shown to cross-react with host cell components, thus serving as additional examples of molecular mimicry at the level of antibodies. Studies have shown that monoclonal antibodies generated against viral proteins from measles, HSV-1, and VV react with host cell components (Dales et al, 1983;Fujinami et al, 1983); common determinants existed between viruses and cellular-or tissue-specific elements (Srinivasappa et al, 1986). In another report, a monoclonal antibody, H8, to the TMEV Daniels (DA) strain reacted with both TMEV viral protein-1 and lipid-like moieties including galactocerebroside, a major component of myelin (Fujinami et al, 1988).…”

Section: Antibody and Mimicrymentioning

confidence: 99%

Molecular Mimicry in Multiple Sclerosis

Libbey

McCoy

Fujinami

2007

International Review of Neurobiology

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One of the most common demyelinating central nervous system (CNS) diseases in humans is multiple sclerosis (MS). The disease can be very debilitating with vision loss, motor and sensory disturbances, and cognitive impairment. The clinical course may present as a relapsing-remitting disease course, a progressive disease course, or a combination thereof. The etiology of MS is unknown. Though many viruses have been shown to be associated with MS, no one virus has ever been demonstrated to be the cause of MS. In addition, MS is thought to have an autoimmune component. Molecular mimicry is one hypothesis put forth which could reconcile the diverse pathology and etiology of MS. Molecular mimicry occurs when peptides from pathogens share sequence or structural similarities with self-antigens. Infection with various pathogens, each with its individual molecular mimic to a CNS antigen, may explain the inability of investigators to link one specific virus to MS. Molecular mimicry may be mediated through human leukocyte antigen class I- and class II-restricted T cells and antibodies, which may explain the diversity in phenotype. Aspects of molecular mimicry will be discussed in relation to each of these immune system components. Examples of various molecular mimics will be discussed with a particular focus on the CNS and MS. Molecular mimicry alone may not be able to induce disease; priming of the immune system by infection with a pathogen that carries a molecular mimic to self may have to be followed by a later nonspecific immunologic challenge in order for disease to be initiated. Recent research into this priming and triggering of disease will be discussed in relation to an animal model for MS.

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Section: Antibody and Mimicrymentioning

confidence: 99%

Molecular Mimicry in Multiple Sclerosis

Libbey

McCoy

Fujinami

2007

International Review of Neurobiology

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“…Carlo Garzelli et al found that the monoclonal antibody secreted by Epstein-Barr virus-transformed lymphocytes could react with multiple organs including the thyroid, pancreas, stomach, muscles and nerves, indicating that Epstein-Barr virus can induce autoantibodies (Naundorf et al, 2002). Srinivasappa et al (1968) reported that 600 mAb clones prepared using 11 viral antigens were able to react with 14 different organs from normal uninfected mice. Approximately 3.5% of these mAbs (21/600) reacted with specific types of cells from these organs.…”

Section: Discussionmentioning

confidence: 99%

Development and characterization of a panel of cross-reactive monoclonal antibodies generated using H1N1 influenza virus

Guo

Tang

et al. 2015

Immunobiology

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To characterize the antigenic epitopes of the hemagglutinin (HA) protein of H1N1 influenza virus, a panel consisting of 84 clones of murine monoclonal antibodies (mAbs) were generated using the HA proteins from the 2009 pandemic H1N1 vaccine lysate and the seasonal influenza H1N1(A1) vaccines. Thirty-three (39%) of the 84 mAbs were found to be strain-specific, and 6 (7%) of the 84 mAbs were subtype-specific. Twenty (24%) of the 84 mAbs recognized the common HA epitopes shared by 2009 pandemic H1N1, seasonal A1 (H1N1), and A3 (H3N2) influenza viruses. Twenty-five of the 84 clones recognized the common HA epitopes shared by the 2009 pandemic H1N1, seasonal A1 (H1N1) and A3 (H3N2) human influenza viruses, and H5N1 and H9N2 avian influenza viruses. We found that of the 16 (19%) clones of the 84 mAbs panel that were cross-reactive with human respiratory pathogens, 15 were made using the HA of the seasonal A1 (H1N1) virus and 1 was made using the HA of the 2009 pandemic H1N1 influenza virus. Immunohistochemical analysis of the tissue microarray (TMA) showed that 4 of the 84 mAb clones cross-reacted with human tissue (brain and pancreas). Our results indicated that the influenza virus HA antigenic epitopes not only induce type-, subtype-, and strain-specific monoclonal antibodies against influenza A virus but also cross-reactive monoclonal antibodies against human tissues. Further investigations of these cross-reactive (heterophilic) epitopes may significantly improve our understanding of viral antigenic variation, epidemics, pathophysiologic mechanisms, and adverse effects of influenza vaccines.

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“…82 For example, it was found that several human monoclonal antibodies can react specifically with infectious agents as well as with human antigens. 83 These antibodies are believed to be at least partially responsible for initiating a pathogenic process that eventually results in autoimmunity. Those studies led to the suggested criteria for 'diagnosing' the role of molecular mimicry in autoimmune diseases.…”

Section: Parasitesmentioning

confidence: 99%