Secondary autoimmune diseases following alemtuzumab therapy for multiple sclerosis

References

• The International Multiple Sclerosis Genetics Consortium and the Wellcome Trust Case Control Consortium 2. Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis. Nature476, 214–219 (2011).
   PubMed Web of Science ®Google Scholar
• Coles AJ, Cox A, LePage E et al. The window of therapeutic opportunity in multiple sclerosis: evidence from monoclonal antibody therapy. J. Neurol.253, 98–108 (2006).
   PubMed Web of Science ®Google Scholar
• CAMMS 223 Trial Investigators. Alemtuzumab vs. interferon beta-1a in early multiple sclerosis. N. Engl. J. Med.359, 1786–1801 (2008).
   PubMed Web of Science ®Google Scholar
• Coles AJ, Fox E, Vladic A et al. Alemtuzumab treatment of multiple sclerosis: five-year follow-up of the CAMMS223 trial. Neurology (2012) (In Press).
   PubMed Web of Science ®Google Scholar
• Jones JL, Anderson JM, Phuah C-L. Improvement in disability after alemtuzumab treatment of multiple sclerosis is associated with neuroprotective autoimmunity. Brain133, 2232–2247 (2010).
   PubMed Web of Science ®Google Scholar
• Coles AJ, Wing M, Smith S et al. Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis. Lancet354, 1691–1695 (1999).
   PubMed Web of Science ®Google Scholar
• De Keyser J. Autoimmunity in multiple sclerosis. Neurology38, 371–374 (1988).
   PubMed Web of Science ®Google Scholar
• Schwid SR, Goodman AD, Mattson DH. Autoimmune hyperthyroidism in patients with multiple sclerosis treated with interferon-beta 1b. Arch. Neurol.54, 1169–1170 (1997).
   PubMed Web of Science ®Google Scholar
• Cossburn M, Pace AA, Jones J et al. Autoimmune diseases after alemtuzumab treatment for multiple sclerosis in a multicentre cohort. Neurology77, 573–579 (2011).
   PubMed Web of Science ®Google Scholar
• Coles AJ, Brinar V, Arnold DL et al.; the CARE-MS I investigators. Efficacy and safety results from CARE-MS I: a Phase 3 study comparing alemtuzumab and interferon Beta-1a Presented at: ECTRIMS 2011: 27th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Amsterdam, The Netherlands, 19–22 October 2011.
   Google Scholar
• Niederwieser G, Buchinger W, Bonelli RM et al. Prevalance of autoimmune thyroiditis and non-immune thyroid disease in multiple sclerosis. J. Neurol.250, 672–675 (2003).
   PubMed Web of Science ®Google Scholar
• Hale G, Rebello P, Brettman LR et al. Blood concentration of alemtuzumab and anti-globulin responses in patients with chronic lymphocytic leukemia following intravenous or subcutaneous routes of administration. Blood104, 948–955 (2004).
   PubMed Web of Science ®Google Scholar
• Hill-Cawthorne GA, Button T, Tuohy O et al. Long-term lymphocyte reconstitution after alemtuzumab treatment of multiple sclerosis. J. Neurol. Neurosurg Psychiatry doi:10.1136/jnnp-2011-300826 (2011) (Epub ahead of print).
   PubMed Web of Science ®Google Scholar
• Thompson SAJ, Jones JL, Cox AL et al. B-cell reconstitution and BAFF after alemtuzumab (Campath-1H) treatment of multiple sclerosis. J. Clin. Immunol.30, 99–105 (2010).
   PubMed Web of Science ®Google Scholar
• Cox AL, Thompson SAJ, Jones JL et al. Lymphocyte homeostasis following lymphocyte depletion in multiple sclerosis. Eur. J. Immunol.35, 3332–3342 (2005).
   PubMed Web of Science ®Google Scholar
• Hakim FT, Memon SA, Cepeda R et al. Age-dependent incidence, time course, and consequences of thymic renewal in adults. J. Clin. Invest.115(4), 930–939 (2005).
   PubMed Web of Science ®Google Scholar
• Cho BK, Rao VP, Ge Q, Eisen HN, Chen J. Homeostasis-stimulated proliferation drives naive T cells to differentiate directly into memory T cells. J. Exp. Med.192(4), 549–556 (2000).
   PubMed Web of Science ®Google Scholar
• Goldrath AW, Bogatski LY, Bevan MJ. Naive T cells transiently acquire a memory-like phenotype during homeostasis driven proliferation. J. Exp. Med.192, 557–564 (2000).
   PubMed Web of Science ®Google Scholar
• Murali-Krishna K, Ahmed R. Cutting edge: naive T cells masquerading as memory cells. J. Immunol.165, 1733–1737 (2000).
   PubMed Web of Science ®Google Scholar
• Baccala R, Thiofilopoulos AN. The new paradigm of T cell homeostatic proliferation-induced autoimmunity. Trends Immunol.26, 5–8 (2005).
   PubMed Web of Science ®Google Scholar
• Loh Y, Oyama Y, Statkute L et al. Development of a secondary autoimmune disorder after haematopoietic stem cell transplantation for autoimmune diseases: role of conditioning regimen used. Blood109, 2643–2648 (2007).
   PubMed Web of Science ®Google Scholar
• Ting SS, Zeigler JB, Vowels MR. Acquired autoimmune thrombocytopenia post bone marrow transplant for severe combined immunodeficiency. Bone Marrow Transplant.21, 841–843 (1998).
   PubMed Web of Science ®Google Scholar
• DeSimone PR, Babinchak TJ. Inflammatory reactions in HIV-1-infected persons after initialtion of highly active anti-retroviral therapy. Ann. Intern. Med.133, 447–454 (2000).
   PubMed Web of Science ®Google Scholar
• Chen F, Day SL, Metcalfe RA et al. Characteristics of autoimmune thyroid disease occurring as a late complication of immune reconstitution in patients with advanced human immunodeficiency virus (HIV) disease. Medicine84, 98–106 (2005).
   PubMed Web of Science ®Google Scholar
• Krupica T, Fry TJ, Mackall CL. Autoimmunity during lymphopenia: a two-hit model. Clin. Immunol.120, 121–128 (2006).
   PubMed Web of Science ®Google Scholar
• Alderuccio F, Toh BH, Tan SS et al. An autoimmune disease with multiple molecular targets abrogated by the transgenic expression of a single autoantigen in the thymus. J. Exp. Med.178, 419–426 (1993).
   PubMed Web of Science ®Google Scholar
• McHugh RS, Shevach EM. Cutting edge: depletion of CD4+CD25+ regulatory T cells is necessary, but not sufficient, for induction of organ specific autoimmune disease. J. Immunol.168, 5979–5983 (2002).
   PubMed Web of Science ®Google Scholar
• Powrie F, Leach MW, Mauze S et al. Phenotypically distinct subsets of CD4+ T cells induce or protect from chronic intestinal inflammation in C. B-17 scid mice. Int. Immunol.5, 1461–1471 (1993).
   PubMed Web of Science ®Google Scholar
• King C, Ilic A, Koelsch K et al. Homeostatic expansion of T cells during immune insufficiency generates autoimmunity. Cell117, 265–277 (2004).
   PubMed Web of Science ®Google Scholar
• Jones JL, Phuah C-L, Cox AL et al. IL-21 drives secondary autoimmunity in patients with multiple sclerosis, following therapeutic lymphocyte depletion with alemtuzumab (Campath-1H). J. Clin. Invest.119, 2052–2061 (2009).
   PubMed Web of Science ®Google Scholar