Steven N. Emancipator, M.D.

Professor

Mailing Address:
2103 Cornell Rd.
WRB 5134
Cleveland, OH 44106-7288

phone: (216) 368-1598
fax: (216) 368-0494
email: Steven.Emancipator@Case.edu

Biography

1974 ScB at Brown University
1977 MD at Brown University


Following straight internship and residency in Pathology at New York University-Bellevue Medical Center, where he was appointed Instructor of Pathology, Dr. Emancipator undertook research training in mucosal immunology in the laboratory led by Dr. Michael E. Lamm. Joining the faculty as Assistant Professor in 1982, Steve remained at Case Western Reserve University, where he is now Professor of Pathology.

Research
Currently, focusing on four issues:

  • The character and quality of immune responses differ if the immunogen enters a mammalian host via mucosal surfaces (i.e. the airways and the gut) as opposed to parenteral routes; these differences have ramifications for genesis of disease. We seek to learn the mechanistic basis for such differences, especially as they relate to the pathogenesis of IgA nephropathy.
  • Abnormally glycosylated IgA, more effective at promoting inflammatory sequelae than normal IgA, is observed in patients with IgA nephropathy. We reported that the T cell products IL-4 and IL-5, in combination, lead to synthesis of abnormally glycosylated IgA, whereas the T cell product IFN-g blunts the effect of IL-4 plus IL-5. We are probing the mechanism(s) of such T cell imbalances, and the role they play in genesis of IgA nephropathy.
  • Proteolytic enzymes have therapeutic effects on a variety of immune mediated diseases. Originally, enzyme efficacy was ascribed to digestion of immune complexes deposited in tissues, but such proteases are now known to act by interfering with immunoregulatory and pro-inflammatory chemical signals (cytokines, chemokines and adhesion molecules). In murine models of rheumatoid arthritis and glomerulonephritis, we are examining the effect of therapy with proteolytic enzymes on IL-4, IL-5 and IFN-g production by immune cells in response to antigenic stimulation, and the effect of these cytokines on the glycosylation of articular cartilage in culture.
  • Both membranous glomerulonephritis and IgA nephropathy progress to end-stage kidney in ~33% of cases. Both diseases are apparently caused by immune complex deposition in the kidney (i.e. mediated by humoral immunity), but the quality and quantity of immune complexes deposited does not differ between patients who progress to chronic kidney failure versus those that do not. We are beginning to probe the hypothesis that the participation of T cells (i.e cellular immunity) distinguishes those patients who progress from those who do not progress to chronic renal failure.

Publications
Gómez-Chiarri M, Ortiz A, González-Cuadrado S, Serón D, Emancipator SN, Hamilton TA, Barat A, Plaza JJ, González E, Egido J (1996). Interferon-inducible protein-10 (IP-10) is highly expressed in rats with experimental nephrosis. Am J Pathol 148, 301-311.

Bagheri N, Chintalacharuvu SR, Emancipator SN (1997). Proinflammatory cytokines regulate FcaR expression by human mesangial cells in vitro. Clin Exp Immunol 107, 404-409.

Chintalacharuvu SR, Emancipator SN (1997). The glycosylation of IgA produced by murine B cells is altered by Th2 cytokines. J Immunol 159, 2327-2333.

Amore A, Roccatello D, Picciotto G, Emancipator SN, Ropolo R, Cacace G, Suriani A, Gianoglio B, Sena LM, Cirina P, Mazzucco G, Alfieri V, Piccoli G, Coppo R, De Filippi PG (1997). Processing of IgA aggregates in a rat model of chronic liver disease. Clin Immunol Immunopathol 84, 107-114.

Fujioka H, Emancipator SN, Aikawa M, Huang DS, Blatnik F, Karban T, DeFife K, Mazanec MB (1998). Immunocytochemical co-localization of IgA with Sendai virus protein in infected polarized epithelium. J Exp Med 188, 1223-1229.

Simonson MS, Emancipator SN, Knauss TC, Hricik D (1998). Elevated neointimal endothelin 1 in transplantation-associated arteriosclerosis of renal allograft recipients. Kid Int 54, 960-971.