Reddy J

ORCID iD
https://orcid.org/0000-0003-4082-9254
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Jay Reddy,

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Reddy J (2014-09-14)

Jayagopala Reddy

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Reddy J (2014-09-14)

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United States

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Reddy J (2016-01-24)

  • Keywords
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Animal models of autoimmunity, cytokines, environmental triggers, epitope spreading, myocarditis, MHC tetramers and dextramers, molecular mimicry, T helper subsets, coxsackievirus, inflammation, Treg cells, EAE, EAM, and uveoretinitis

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Reddy J (2014-02-26)

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Jay Reddy

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Reddy J (2014-09-14)

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ResearcherID: K-7200-2014

Sources:
Clarivate Analytics (2014-09-14)

Biography

Introduction: Dr. Reddy received the bachelor (1985) and master's degrees in Veterinary Medicine (1990), University of Agricultural Sciences, Bangalore, India and PhD in Pathobiology (1998), University of Guelph, Ontario, Canada. He had his postdoctoral training at Pasteur Institute, Paris, France (1998-2000) and Brigham and Women's Hospital, Harvard Medical School, Boston, MA (2000-2006). He was a senior research investigator in multiple sclerosis drug discovery research groups at Sanofi-aventis, NJ before joining UNL in 2007. Dr. Reddy is also a member of Redox Biology Center and Nebraska Virology Center, UNL. His research interest is the cellular and molecular mechanisms underlying the development of human autoimmune diseases. Expertise: T cell immunology; autoimmunity Teaching: Course Director: Veterinary Immunology (VMED 680, 2 credits); Topics in Immunology (VBMS 910, 3 credits) Research: Most healthy humans have a propensity to develop autoimmune diseases, as evidenced by the presence of autoreactive T cells or autoantibodies in their naïve periphery. T cells are educated in the thymus, where high-affinity TCR-bearing cells that interact with self-antigens are deleted by negative selection while T cells with low-affinity TCR to self-antigens are selected positively and exported to the periphery. In spite of the high frequency of self-reactive T cells in the naïve peripheral repertoires, autoimmune responses do not ensue spontaneously. How this tolerance is maintained is a fundamental question. It has been suggested that the environmental antigens that bear similarities to self-antigens break self-tolerance by cross-reactivity. To this end, we focus our investigations on the identification of microbial products that can potentially induce autoimmunity in the heart and immunologically privileged sites such as central nervous system and eyes through antigenic mimicry.
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