Active immunization with complementary peptide PBM 9-1: preliminary evidence that it modulates experimental allergic encephalomyelitis in PL/J mice and Lewis rats

Zhou, Shuang; Whitaker, John N.

doi:10.1002/(sici)1097-4547(19960815)45:4<439::aid-jnr13>3.0.co;2-w

Cited by 8 publications

(4 citation statements)

References 19 publications

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“…Although the present and earlier studies have concentrated on MG, a model of a T cell-dependent, B cell-mediated autoimmune disease, recent studies have demonstrated that the procedure described here is also effective against two animal models of the human T cell-mediated autoimmune diseases: multiple sclerosis (24,25,62) and Guillain-Barré syndrome (68). mAb CTCR8 that recognized AChR 100 -116-specific T cells in the present report had no effect on rat T cells specific for the peripheral myelin protein P2 residues 60 -70 in the model of Guillain-Barré syndrome (68).…”

Section: Discussionmentioning

confidence: 99%

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A peptide vaccine that prevents experimental autoimmune myasthenia gravis by specifically blocking T cell help

Araga

Nakashima

et al. 2000

FASEB j.

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Myasthenia gravis (MG) and its animal model, experimental autoimmune (EA) MG, are caused by T cell-dependent autoantibodies that react with the nicotinic acetylcholine receptor (AChR) on muscle and interfere with neuromuscular transmission. Thus, selective inactivation of CD4(+) AChR-specific T helper cells should lower AChR Ab levels and ameliorate disease. In the Lewis rat model of EAMG, alpha chain residues 100-116 of the AChR represent the dominant T cell epitope, which is important in helping Ab responses to this autoantigen. In the present report, we have applied a new design technique that requires no knowledge of Ag receptor sequences on errant T cells in order to develop a synthetic peptide vaccine against T cells reactive with the aforementioned T cell epitope. Immunization with the peptide 1) induced polyclonal and monoclonal Ab, which inhibited AChR 100-116 stimulation of AChR-sensitized lymphocytes and recognized Vbeta15 containing T cell receptors on AChR 100-116-specific T cell lines and clones; 2) lowered AChR Ab levels; 3) reduced the loss of muscle AChR; and 4) lessened the incidence and severity of EAMG. These findings suggest a new strategy for the functional abrogation of epitope-specific T cells that could have potential application to human autoimmune diseases.

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Section: Discussionmentioning

confidence: 99%

“…Thus, the beneficial effect seems to be specific for RhCA 611-001. The effects are disease as well as peptide specific, since an AChR complementary peptide was previously shown to have no effect on the model of multiple sclerosis (experimental allergic encephalomyelitis) in Lewis rats (62).…”

Section: Prevention Of Eamgmentioning

confidence: 99%

A peptide vaccine that prevents experimental autoimmune myasthenia gravis by specifically blocking T cell help

Araga

Nakashima

et al. 2000

FASEB j.

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“…Both human and animal models of MS have a significant T-cell component to the disease and thus are ripe for attempts to use the MRT to address the condition. In a Lewis rat model of MS (experimental autoimmune encephalomyelitis (EAE)), inverse hydropathy peptide administration and the subsequent anti-Id response reduced severity of disease, and frequency of relapse (64). Finally, there have been recent studies showing the effectiveness of a complementary peptide to La/SSB, the main autoantigen in both systemic lupus erythematosus and Sjogren's syndrome (4, 65).…”

Section: Complementary Peptides Vaccinesmentioning

confidence: 99%

Molecular recognition theory and sense-antisense interaction therapeutic applications in autoimmunity

Blalock¹

2012

Front Biosci

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Perhaps behind only the understanding of the genetic code in importance is the comprehension of protein sequence and structure in its effect on modern scientific investigation. How proteins are structured and interact dictates a considerable amount of the body's processes in maintaining homeostasis. Unfortunately, in diseases of autoimmunity, these processes are directed against the body itself and most of the current clinical responses are severely lacking. This review addresses current therapeutics involved in the treatment of various autoimmune diseases and details potential future therapeutics designed with a more targeted approach. Detailed in this manuscript is the concept of utilizing peptides possessing an inverse hydropathy to the immunogenic region of proteins to generate anti-idiotypic (anti-Id) and anti-clonotypic T cell receptor (TCR) antibodies (Abs). Theoretically, the anti-Id Abs cross react with Id Abs and negate the powerful machinery of the adaptive immune response with little to no side effects. A series of studies by a number of groups have shown this to be an exciting and intriguing concept that will likely play a role in the future treatment of autoimmune diseases.

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“…Further evidence suggests that this general approach is effective in two animal models of human T cell-mediated autoimmune disease: MS [119,120,121] and Guillain-Barré syndrome [7]. Susceptibility to many autoimmune diseases is known to be associated with MHC class II alleles in both mice and humans [72,102].…”

Section: Anti-idiotype Antibodiesmentioning

confidence: 99%

Treating autoimmune diseases through restoration of antigen-specific immune tolerance

Wolfraim

2006

Arch. Immunol. Ther. Exp.

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The first line of treatment for many human autoimmune diseases involves the use of anti-inflammatory or immunosuppressive drugs such as prednisone or other steroids that not only suppress the underlying autoimmune disease, but lead to global suppression of the immune system. The sequelae of this approach include increased risk of infection, carcinogenesis, and osteoporosis. Moreover, such broad spectrum immunosuppression tends to have transient therapeutic benefit, as in many cases the disease becomes refractory to these drugs. There is a clear need for more specific means to restore immune tolerance to the specific autoantigens implicated in disease pathology. This review provides an overview of some of these newer, more specific therapeutic approaches to restoring immune tolerance to autoantigens, with an emphasis on those approaches that have been or will soon be tested in controlled clinical trials. Covered here are peptide- or protein-based therapeutics, oral tolerance, and cellular and gene therapy approaches to restoring antigen-specific immune tolerance.

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Active immunization with complementary peptide PBM 9-1: preliminary evidence that it modulates experimental allergic encephalomyelitis in PL/J mice and Lewis rats

Cited by 8 publications

References 19 publications

A peptide vaccine that prevents experimental autoimmune myasthenia gravis by specifically blocking T cell help

A peptide vaccine that prevents experimental autoimmune myasthenia gravis by specifically blocking T cell help

Molecular recognition theory and sense-antisense interaction therapeutic applications in autoimmunity

Treating autoimmune diseases through restoration of antigen-specific immune tolerance

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