HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Collins, C. Articles by Budd, R. C. Search for Related Content PubMed PubMed Citation Articles by Collins, C. Articles by Budd, R. C.

Activation of T Cells by Borrelia burgdorferi Is Indirect via a TLR- and Caspase-Dependent Pathway¹

Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, VT 50405

Activation of the innate immune system typically precedes engagement of adaptive immunity. Cells at the interface between these two arms of the immune response are thus critical to provide full engagement of host defense. Among the innate T cells at this interface are T cells. T cells contribute to the defense from a variety of infectious organisms, yet little is understood regarding how they are activated. We have previously observed that human T cells of the V1 subset accumulate in inflamed joints in Lyme arthritis and proliferate in response to stimulation with the causative spirochete, Borrelia burgdorferi. We now observe that murine T cells are also activated by B. burgdorferi and that in both cases the activation is indirect via TLR stimulation on dendritic cells or monocytes. Furthermore, B. burgdorferi stimulation of monocytes via TLR, and secondary activation of T cells, are both caspase-dependent.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grants AR43520 and AI 45666 (to R.C.B.), and P30CA22435 (Vermont Cancer Center) from the National Institutes of Health.

² Address correspondence and reprint requests to Dr. Ralph C. Budd, Immunobiology Program, The University of Vermont College of Medicine, Given Medical Building, D-305, Burlington, VT 05405-0068. E-mail address: ralph.budd{at}uvm.edu

³ Abbreviations used in this paper: DC, dendritic cell; BMDC, bone marrow-derived dendritic cell.

This article has been cited by other articles:

				M. M. Petzke, A. Brooks, M. A. Krupna, D. Mordue, and I. Schwartz Recognition of Borrelia burgdorferi, the Lyme Disease Spirochete, by TLR7 and TLR9 Induces a Type I IFN Response by Human Immune Cells J. Immunol., October 15, 2009; 183(8): 5279 - 5292. [Abstract] [Full Text] [PDF]

				C. M. Olson Jr., T. C. Bates, H. Izadi, J. D. Radolf, S. A. Huber, J. E. Boyson, and J. Anguita Local Production of IFN-{gamma} by Invariant NKT Cells Modulates Acute Lyme Carditis J. Immunol., March 15, 2009; 182(6): 3728 - 3734. [Abstract] [Full Text] [PDF]