Kanneboyina Nagaraju Kanneboyina Nagaraju
Adjunct Professor of Genomics and Precision Medicine

Office Phone: 202-476-6029
Email: Email
Department: Genomics and Precision Medicine


My primary research interest is to investigate molecular mechanisms of target tissue injury in muscle diseases. For the past fifteen years, I have focused my research on understanding skeletal muscle cell damage and dysfunction in various genetic and inflammatory myopathies. Subsequent to my Doctor of Veterinary Medicine training, I received both Masters and Ph.D. degrees in Immunology. Later I joined the laboratory of Dr. Paul Plotz, who is an authority on autoimmune rheumatic diseases especially autoimmune muscle diseases at the National Institutes of Health. Soon after joining his laboratory I learned that there is very little mechanistic information regarding muscle fiber damage and dysfunction in inflammatory myopathy. Delineation of pathogenic mechanisms in humans is hindered by the heterogeneity of the population, the complexity and chronicity of the disease. Therefore, I realized an immediate need to develop and standardize animal models for genetic and autoimmune muscle diseases to help define mechanistic pathways and explore promising new therapies for this disease. My independent laboratory both at Johns Hopkins Medical school and at Children’s National Medical Center  continue  to study a) molecular mechanisms regulating the initiation, natural remission and progression of  inflammation in muscle disease pathology, b) identification of unique disease or function-related pathways using genomic and proteomic technologies in human and in mouse models of  these diseases, c) interrogation of these pathways using immunological, pharmacological and genetic approaches in vitro in cell culture models and in vivo in relevant mouse models, and d) developing novel therapies to treat these rare  autoimmune and genetic muscle diseases.

Additional Education

College of Veterinary Sciences, AP, India   DVM  1986 Veterinary Medicine
Indian Veterinary Research Institute, India   MVSc 1989 Immunology
National Institutes of Health, Bethesda, MD, USA  Post-Doc 1999 Immunology


From a total of 54; in chronological order;

  • Nagaraju K, Casciola-Rosen L, Rosen A, Thompson C, Loeffler L, Parker T, Danning C, Rochon PJ, Gillespie J and Plotz P. The inhibition of apoptosis in myositis and in normal muscle cells. J Immunol. (2000) 164, 5459.
  • Nagaraju K, Raben N, Loeffler L, Parker T, Rochon PJ, Lee E, Danning C, Wada R, Thompson C, Bahtiyar G, Craft J, Hooft van Huijsduijnen  R and Plotz P. The conditional up-regulation of MHC class I in skeletal muscle leads to self-sustaining autoimmune myositis and myositis-specific autoantibodies. Proc. Natl. Acad. Sci. USA  (2000) 97, 9209-9214.
  • Casciola-Rosen L, Nagaraju K, Plotz P, Wang K, Levine S, Gabrielson E, Corse A, and Rosen A.  Enhanced autoantigen expression in regenerating muscle cells in idiopathic inflammatory myopathy. J. Exp. Med. (2005) 201, 591-601.  (see also comment on pg 487 of the same issue).
  • Nagaraju K, Casciola-Rosen L, Lundberg I, Rawat R, Cutting S, Thapliyal R, Chang J, Dwivedi S, Mitsak M, Chen YW, Plotz P, Rosen A, Hoffman E, Raben N. Activation of the endoplasmic reticulum stress response in autoimmune myositis: Potential role in muscle fiber damage and dysfunction. Arthritis Rheum. (2005) 52, 1824-1835.
  • Lamason R, Po Z, Rawat R, Davis A, Hall J, Chae JJ, Agarwal R, Cohen P, Rosen R, Hoffman E, and Nagaraju K. Sexual dimorphism in immune resp. genes as a function of puberty. BMC Immunol. (2006) 7:2. PMCID: PMC1402325
  • Nagaraju K, Rawat R, Veszelovszky E, Thapliyal R, Kesari A, Sparks S, Raben N, Plotz P, and Hoffman E. Dysferlin deficiency enhances phagocytosis by monocytes: A model for the inflammatory onset of limb-girdle muscular dystrophy 2B. Am J Pathol 2008,172(3):774-85. PMCID: PMC2258254
  • Wu B, Moulton HM, Iversen PL, Jiang J, Li J, Li J, Spurney CF, Sali A, Guerron AD, Nagaraju K, Doran T, Lu P, Xiao X, Lu QL. Effective rescue of dystrophin improves cardiac function in dystrophin-deficient mice by a modified morpholino oligomer. Proc Natl Acad Sci U S A. 2008;105(39):14814-9. PMCID: PMC2546441.
  • Spurney CF, Gordish-Dressman H, Guerron AD, Sali A, Pandey GS, Rawat R, Van Der Meulen JH, Cha HJ, Pistilli EE, Partridge TA, Hoffman EP, Nagaraju K. Preclinical drug trials in the mdx mouse: Assessment of reliable and sensitive outcome measures. Muscle Nerve. 2009; 39(5):591-602.
  • Baudy AR, Saxena N, Gordish H, Hoffman EP, Nagaraju K. A robust in vitro screening assay to identify NF-kappaB inhibitors for inflammatory muscle diseases. Int Immunopharmacol. 2009;9(10):1209-14. PMCID: PMC2745946
  • Spurney CF, Cha HJ, Sali A, Pandey GS, Pistilli E, Guerron AD, Gordish-Dressman H, Hoffman EP, Nagaraju K. Evaluation of skeletal and cardiac muscle function after chronic administration of thymosin beta-4 in the dystrophin deficient mouse. PLoS One. 2010 Jan 29;5(1):e8976.


Pathogenesis of genetic and inflammatory myopathies: My laboratory is interested in studying pathogenic mechanism of muscle fiber damage and dysfunction in inflammatory myositis, dysferlin deficiency (LGMD2B) and Duchenne muscular dystrophy. We have developed a mouse model for inflammatory myositis by over expressing MHC class I skeletal muscle. These mice develop clinical, biochemical, histological, and immunological features very similar to human myositis. The disease is inflammatory, limited to skeletal muscles, self-sustaining, more severe in females, and often accompanied by autoantibodies. The MHC class I mouse model of myositis is a powerful tool to identify and define molecular pathways. Using global gene expressing profiling we have identified endoplasmic reticulum stress response as the major non-immune pathway that is highly active in muscle tissue of human myositis patients and in our mouse model. We are currently defining the role of non-immune pathways in causing muscle weakness and damage in vivo in this mouse model. Similarly we are also investigating the role of inflammasome and NF-kB pathways in dysferlin and dystrophin deficient mouse models. These translational research studies will help us to identify new targets for therapeutic intervention in human muscle diseases.

Sex-based differences in immune response genes and autoimmunity: It is known that autoimmune diseases are more prevalent in females than in males, whereas males have higher mortality due to parasitic diseases.  The biological basis of this sexual dimorphism is unclear. Using global gene expression profiling, we have studied immune response programs in murine spleen as a function of age and sex, and show expression of innate and adaptive immune response genes consistent with the observed immune function phenotypes; innate immune response gene expression was higher in post-pubertal male mice, while adaptive immune response was higher in post-pubertal female mice.  We are currently investigating strategies to alter ratios of innate and adaptive immune responsive genes as a method to treat autoimmune diseases.

Link to pubmed publications: http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=search&db=pubmed&term= Nagaraju+K

Industry Relationships and Collaborations

This faculty member (or a member of their immediate family) has reported a financial interest with the health care related companies listed below. These relations have been reported to the University and, when appropriate, management plans are in place to address potential conflicts.

  • None