Here's the link to the free full report.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270541/?tool=pubmed
And here's the pubmed abstract. I found this very interesting. I'm not too good with the technical discussion of immunology, but if I understand correctly, the gist of this article is the hypothesis that IBD sufferers, like many other autoimmune sufferers, are infected with Epstein-Barr virus, and that this, in combination with a genetic problem regulating CD8+ T-Cells within the setting of a deficiency of sunlight/vitamin D, auto-immune disease occurs within a target organ(s). It sounds like a really persuasive report, at least when reading the full report.
The author's final comment makes me wonder, "...successful treatment of chronic autoimmune diseases by controlling EBV infection." Does anyone know anything about how EBV infection can be "controlled"? I found this, which talks about EBV, but I saw no mention of how it can be "controlled". Mainly it just mentions that 95% of the population is infected with EBV.
http://www.cdc.gov/ncidod/diseases/ebv.htm
Autoimmune Dis. 2012;2012:189096. Epub 2012 Jan 24.
CD8+ T-Cell Deficiency, Epstein-Barr Virus Infection, Vitamin D Deficiency, and Steps to Autoimmunity: A Unifying Hypothesis.
Pender MP.
SourceSchool of Medicine, The University of Queensland, Brisbane, QLD 4072, Australia.
Abstract
CD8+ T-cell deficiency is a feature of many chronic autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, Sjögren's syndrome, systemic sclerosis, dermatomyositis, primary biliary cirrhosis, primary sclerosing cholangitis, ulcerative colitis, Crohn's disease, psoriasis, vitiligo, bullous pemphigoid, alopecia areata, idiopathic dilated cardiomyopathy, type 1 diabetes mellitus, Graves' disease, Hashimoto's thyroiditis, myasthenia gravis, IgA nephropathy, membranous nephropathy, and pernicious anaemia. It also occurs in healthy blood relatives of patients with autoimmune diseases, suggesting it is genetically determined. Here it is proposed that this CD8+ T-cell deficiency underlies the development of chronic autoimmune diseases by impairing CD8+ T-cell control of Epstein-Barr virus (EBV) infection, with the result that EBV-infected autoreactive B cells accumulate in the target organ where they produce pathogenic autoantibodies and provide costimulatory survival signals to autoreactive T cells which would otherwise die in the target organ by activation-induced apoptosis. Autoimmunity is postulated to evolve in the following steps: (1) CD8+ T-cell deficiency, (2) primary EBV infection, (3) decreased CD8+ T-cell control of EBV, (4) increased EBV load and increased anti-EBV antibodies, (5) EBV infection in the target organ, (6) clonal expansion of EBV-infected autoreactive B cells in the target organ, (7) infiltration of autoreactive T cells into the target organ, and (8) development of ectopic lymphoid follicles in the target organ. It is also proposed that deprivation of sunlight and vitamin D at higher latitudes facilitates the development of autoimmune diseases by aggravating the CD8+ T-cell deficiency and thereby further impairing control of EBV. The hypothesis makes predictions which can be tested, including the prevention and successful treatment of chronic autoimmune diseases by controlling EBV infection.
PMID:22312480[PubMed - in process] PMCID
MC3270541
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270541/?tool=pubmed
And here's the pubmed abstract. I found this very interesting. I'm not too good with the technical discussion of immunology, but if I understand correctly, the gist of this article is the hypothesis that IBD sufferers, like many other autoimmune sufferers, are infected with Epstein-Barr virus, and that this, in combination with a genetic problem regulating CD8+ T-Cells within the setting of a deficiency of sunlight/vitamin D, auto-immune disease occurs within a target organ(s). It sounds like a really persuasive report, at least when reading the full report.
The author's final comment makes me wonder, "...successful treatment of chronic autoimmune diseases by controlling EBV infection." Does anyone know anything about how EBV infection can be "controlled"? I found this, which talks about EBV, but I saw no mention of how it can be "controlled". Mainly it just mentions that 95% of the population is infected with EBV.
http://www.cdc.gov/ncidod/diseases/ebv.htm
Autoimmune Dis. 2012;2012:189096. Epub 2012 Jan 24.
CD8+ T-Cell Deficiency, Epstein-Barr Virus Infection, Vitamin D Deficiency, and Steps to Autoimmunity: A Unifying Hypothesis.
Pender MP.
SourceSchool of Medicine, The University of Queensland, Brisbane, QLD 4072, Australia.
Abstract
CD8+ T-cell deficiency is a feature of many chronic autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, Sjögren's syndrome, systemic sclerosis, dermatomyositis, primary biliary cirrhosis, primary sclerosing cholangitis, ulcerative colitis, Crohn's disease, psoriasis, vitiligo, bullous pemphigoid, alopecia areata, idiopathic dilated cardiomyopathy, type 1 diabetes mellitus, Graves' disease, Hashimoto's thyroiditis, myasthenia gravis, IgA nephropathy, membranous nephropathy, and pernicious anaemia. It also occurs in healthy blood relatives of patients with autoimmune diseases, suggesting it is genetically determined. Here it is proposed that this CD8+ T-cell deficiency underlies the development of chronic autoimmune diseases by impairing CD8+ T-cell control of Epstein-Barr virus (EBV) infection, with the result that EBV-infected autoreactive B cells accumulate in the target organ where they produce pathogenic autoantibodies and provide costimulatory survival signals to autoreactive T cells which would otherwise die in the target organ by activation-induced apoptosis. Autoimmunity is postulated to evolve in the following steps: (1) CD8+ T-cell deficiency, (2) primary EBV infection, (3) decreased CD8+ T-cell control of EBV, (4) increased EBV load and increased anti-EBV antibodies, (5) EBV infection in the target organ, (6) clonal expansion of EBV-infected autoreactive B cells in the target organ, (7) infiltration of autoreactive T cells into the target organ, and (8) development of ectopic lymphoid follicles in the target organ. It is also proposed that deprivation of sunlight and vitamin D at higher latitudes facilitates the development of autoimmune diseases by aggravating the CD8+ T-cell deficiency and thereby further impairing control of EBV. The hypothesis makes predictions which can be tested, including the prevention and successful treatment of chronic autoimmune diseases by controlling EBV infection.
PMID:22312480[PubMed - in process] PMCID
MC3270541