Linda Bockenstedt, M.D.

Harold W. Jockers Professor of Medicine
Director, Professional Development & Equity
Yale School of Medicine
Rheumatology

Research Activities

My laboratory studies the pathogenesis of Lyme disease, a tick-borne infection with the spirochete Borrelia burgdorferi. We have used the murine model of Lyme borreliosis to investigate the host immune response to the spirochete and mechanisms by which the spirochete persists in the host. Using molecular genomic, proteomic and imaging approaches, we are studying 1) host-spirochete interactions that modulate cellular and humoral immune responses to spirochetal antigens; 2) host genetic factors that determine disease severity; and 3) mechanisms of spirochete persistence despite host protective immunity. Our results have led us to examine the interface between innate and adaptive immunity as the key to effective pathogen control, T and B cell effector functions in disease pathogenesis and in its regression, and variation in gene expression by persisting spirochetes. Opportunities for research training in these areas are available for interested students and fellows.

Publications

Kumar H, A Belperron, SW Barthold, A Bendelac, and LK Bockenstedt (2000) CD1d deficiency impairs host defense against the spirochete, Borrelia burgdorferi. Cutting Edge, J Immunol 165:4797

Bockenstedt LK, I Kang, C Chang, D Persing, A Hayday, and SW Barthold (2001)  CD4+ Th1 cells facilitate regression of murine Lyme carditis.  Infect Immun  69:5264

Belperron AA, D. Fish, and LK Bockenstedt. (2001)  Natural antibody affects the survival of the spirochete Borrelia burgdorferi within feeding ticks. Infect Immun  69:6456.

Bockenstedt LK, J Mao, E Hodzic, SW Barthold, D Fish (2002) Detection of attenuated, non-infectious spirochetes after antibiotic treatment of Borrelia burgdorferi infected mice. J Infect Dis  186:1430-7

Bockenstedt LK, M-C Shanafelt, A Belperron, J Mao, and SW Barthold (2003) Humoral immunity reflects altered T helper cell bias in Borrelia burgdorferi-infected gd T cell-deficient mice. Infect Immun 71:2938

Pal U, X Yang, M Chen, LK Bockenstedt, J.F. Anderson, RA Flavell, M.V. Norgard, E Fikrig. (2004) OspC facilitates Borrelia burgdorferi invasion of Ixodes scapularis salivary glands. J. Clin. Invest. 113:220.

Liu N, RR Montgomery, SW Barthold, LK Bockenstedt (2004) Myeloid differentiation antigen 88 deficiency impairs pathogen clearance but does not alter inflammation in Borrelia burgdorferi-infected mice. Infect Immun 72:3195.

Belperron AA, CM Dailey, and LK Bockenstedt (2005)  Infection-induced marginal zone B cell production of Borrelia hermsii-specific antibody is impaired in the absence of CD1d. J Immunol 174:5681.

Bockenstedt LK, N Liu, I Schwartz, and D Fish (2006)  MyD88 deficiency enhances acquisition and transmission of Borrelia burgdorferi by Ixodes scapularis ticks. Infect Immun 74:2154.

Belperron, AA, CM Dailey, CJ Booth, and LK Bockenstedt (2007) Marginal zone B-cell depletion impairs murine host defense against Borrelia burgdorferi infection. Infect. Immun. 75:3354.

Lab Members

Research Assistants
Ming Li	(203) 785-7660
Research Associates
Jialing Mao	(203) 785-7660
Postdoctoral Fellows
Diana Vesely	(203) 785-7660
Associate Research Scientists
Nengyin Liu, M.D.	(203) 785-7660
Alexia Belperron, Ph.D.	(203) 785-7660

Contact

Campus Address
300 Cedar Street
TAC S-525C

Mailing Address
Yale University School of Medicine
P.O. Box 208031
New Haven, CT 06520-8031

E-mail
linda.bockenstedt@yale.edu

Office Phone
(203) 785-2453

Fax
(203) 785-7053