The Journal of Experimental Medicine
Torrey Pines Biolabs
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 6582K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cutler, A. J.
Right arrow Articles by Walport, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cutler, A. J.
Right arrow Articles by Walport, M. J.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?
© The Rockefeller University Press, 0022-1007/1998/6/1789/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 11, June 1, 1998 1789-1797

Articles

T Cell–dependent Immune Response in C1q-deficient Mice: Defective Interferon {gamma} Production by Antigen-specific T Cells

Antony J. Cutler*, Marina Botto*, Dominic van Essen{ddagger}, Roberta Rivi§, Kevin A. Davies*, David Gray{ddagger}, and Mark J. Walport*

From the * Rheumatology Section and {ddagger} Immunology Department, Division of Medicine, Imperial College School of Medicine, Hammersmith Hospital, London W12 ONN, United Kingdom; and the § Department of Human Genetics, Sloan Kettering Institute, New York 10021

The role of the classical complement pathway in humoral immune responses was investigated in gene-targeted C1q-deficient mice (C1qA–/–). Production of antigen-specific immunoglobulin (Ig)G2a and IgG3 in primary and secondary responses to T cell–dependent antigen was significantly reduced, whereas IgM, IgG1, and IgG2b responses were similar in control and C1qA–/– mice. Despite abnormal humoral responses, B cells from C1qA–/– mice proliferated normally to a number of stimuli in vitro. Immune complex localization to follicular dendritic cells within splenic follicles was lacking in C1qA–/– mice. The precursor frequency of antigen-specific T cells was similar in C1qA–/– and wild-type mice. However, analysis of cytokine production by primed T cells in response to keyhole limpet hemocyanin revealed a significant reduction in interferon-{gamma} production in C1qA–/– mice compared with control mice, whereas interleukin 4 secretion was equivalent. These data suggest that the classical pathway of complement may influence the cytokine profile of antigen-specific T lymphocytes and the subsequent immune response.

Key Words: complement • deficiency • immune response • interferon {gamma} • gene targeting

Address correspondence to Mark J. Walport, Division of Medicine, Rheumatology Section, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Rd., London W12 ONN, UK. Phone: 0044-181-383-3299; Fax: 0044-181-743-3109; E-mail: mwalport{at}rpms.ac.uk

Abbreviations used: FDC, follicular dendritic cell; GCDC, dendritic cell identified within murine germinal center; HAGG, heat-aggregated human {gamma}-globulin; IDC, interdigitating dendritic cell; PNA, peanut agglutinin; TD, T cell–dependent.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS