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Articles |
Production by Antigen-specific T Cells



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