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Your search keyword '"Firan, Mihail"' showing total 24 results
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24 results on '"Firan, Mihail"'

6. The Natural History of X-Linked Lymphoproliferative Disease (XLP1): Lessons from a Long-Term Survivor

Author

Jiang, Yike, Firan, Mihail, Nandiwada, Sarada L., Reyes, Anaid, Marsh, Rebecca A., Vogel, Tiphanie P., and Hajjar, Joud

Subjects
surgical procedures, operative, Article Subject
Abstract

X-linked lymphoproliferative disease (XLP1) is a rare primary immunodeficiency characterized by EBV-triggered immune dysregulation, lymphoproliferation, dysgammaglobulinemia, and lymphoma. Early childhood mortality from overwhelming inflammation is expected in most patients. The only curative therapy is hematopoietic stem cell transplant (HSCT); however, whether to perform HSCT on an asymptomatic patient remains debatable. This uncertainty arises because the natural history of XLP1 patients without transplantation is not clear. In this case report, we present the natural history of XLP1 in a 43-year-old male patient who did not receive HSCT. We also review the literature on untransplanted XLP1 patients who lived into mid-adulthood. Despite surviving childhood presentations that are typically fatal, we found that these rare patients remain susceptible to manifestations of XLP1 decades later.

Published
2020
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17. Reversal of tolerance induced by transplantation of skin expressing the immunodominant T cell epitope of rat type II collagen entitles development of collagen-induced arthritis but not graft rejection.

Author

Bäcklund, Johan, Treschow, Alexandra, Firan, Mihail, Malmström, Vivianne, Issazadeh-Navikas, Shohreh, Ward, E Sally, Holmdahl, Rikard, Bäcklund, Johan, Treschow, Alexandra, Firan, Mihail, Malmström, Vivianne, Issazadeh-Navikas, Shohreh, Ward, E Sally, and Holmdahl, Rikard

Abstract

Udgivelsesdato: 2002-Jun, Collagen-induced arthritis (CIA) is induced in H-2(q) mice after immunization with rat type II collagen (CII). The immunodominant T cell epitope on heterologous CII has been located to CII256-270. We have previously shown that TSC transgenic mice, which express the heterologous epitope in type I collagen (CI), e.g. in skin, are tolerized against rat CII and resistant to CIA. In this study we transplanted skin from TSC transgenic mice onto non-transgenic CIA-susceptible littermates to investigate whether introduction of this epitope to a naïve immune system would lead to T cell priming and graft rejection or instead to tolerance and arthritis protection. Interestingly, TSC grafts were accepted and not even immunization of recipient mice with CII in adjuvant induced graft rejection. Instead, TSC skin recipients displayed a reduced T and B cell response to CII and were also protected from arthritis. However, additional priming could break arthritis protection and was accompanied by an increased T cell response to the grafted epitope. Strikingly, despite the regained T cell response, development of arthritis was not accompanied by graft rejection, showing that these immune-mediated inflammatory responses involve different mechanisms.

Published
2002

24. CD8+ T Cells Are Required For Glatiramer Acetate Therapy in Autoimmune Demyelinating Disease.

Author

Tyler, Andrew F., Mendoza, Jason P., Firan, Mihail, and Karandikar, Nitin J.

Subjects
CD8 antigen, T cells, GLATIRAMER acetate, DEMYELINATION, AUTOIMMUNE diseases, IMMUNOREGULATION, IMMUNOLOGY, ANIMAL models in research
Abstract

The exact mechanism of glatiramer acetate (GA, Copaxone®), an FDA-approved immunomodulatory therapy for multiple sclerosis (MS), remains unclear after decades of research. Previously, we have shown that GA therapy of MS induces CD8+ T cell responses that can potentially suppress pathogenic CD4+ T cell responses. Using a murine model of MS, experimental autoimmune encephalomyelitis (EAE), we now demonstrate that CD8+ T cells are necessary in mediating the therapeutic effects of GA. Further, adoptive transfer of GA-induced CD8+ T cells resulted in amelioration of EAE, establishing a role as a viable immunotherapy in demyelinating disease. Generation of these cells required indoleamine-2,3-dioxygenase (IDO), while suppressive function depended on non-classical MHC class I, IFN-γ, and perforin expression. GA-induced regulatory myeloid cells, previously shown to activate CD4+ regulatory T cells in an antigen-independent manner, required CD8+ T cells for disease suppression in vivo. These studies demonstrate an essential role for CD8+ T cells in GA therapy and identify their potential as an adoptive immunotherapeutic agent. [ABSTRACT FROM AUTHOR]

Published
2013
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