title: Murine systemic autoimmune disease induced by mercuric chloride (HgCl2): Hg-specific helper T-cells react to antigen stored in macrophages.
abstract: The adoptive transfer popliteal lymph node assay (PLNA) was used to demonstrate Hg-specific T-cell responses of mice that were continuously treated with HgCl2 by a regimen known to induce a systemic autoimmune disease in H-2s (murine histocompatibility complex, haplotype s) mice, but not H-2d mice. We found that spleen cells of B10.S and A.SW donors (both H-2s) responded anamnestically to HgCl2 by inducing a significant increase in cellularity in the draining PLN of the recipient: In contrast, spleen cells of HgCl2-treated DBA/2 (H-2d) donors failed to induce an increase in PLN cellularity, and spleen cells of B10.D2/n (H-2d) donors induced no changes or even diminished PLN cellularity upon re-encounter with HgCl2. Kinetic studies showed that spleen cells of B10.S donors were stimulatory from day 3 until day 14 of donor HgCl2 treatment and, when purified splenic T-cells were tested, still on day 28, the last point in time tested. The Hg-specific T-cells prepared from HgCl2-treated B10.S mice not only induced an increased cellularity, but also B-cell activation to antibody secretion in the draining PLN of the recipient. Moreover, the Hg-specific donor T-cells transferred could specifically be restimulated by killed peritoneal cells obtained from the same donors or from syngeneic donors previously treated with HgCl2. Interestingly, when killed peritoneal cells were injected as antigen the amount of Hg required for T-cell restimulation was only 1/40 of that required when free HgCl2 was used. Taken together, these results show that an HgCl2 treatment schedule designed to induce systemic autoimmune disease primes Hg-specific T-helper (Th) cells and generates immunogenic material in peritoneal cells to which the T-cells react. The possible contribution to the pathogenesis of HgCl2-induced auto-immune disease of these Hg-specific T-cells and the autoreactive T-cells reported in the literature is discussed.
authors: Division of Immunology, Heinrich Heine University of Düsseldorf, F.R.G.
authors: M
authors: M
authors: Kubicka-Muranyi
authors: O
authors: O
authors: Behmer
authors: M
authors: M
authors: Uhrberg
authors: H
authors: H
authors: Klonowski
authors: J
authors: J
authors: Bister
authors: E
authors: E
authors: Gleichmann
mesh_terms: D000818:Animals; D001324:Autoantigens; D001327:Autoimmune Diseases / Q000139:chemically induced* / Q000276:immunology; D005260:Female; D006183:H-2 Antigens; D008213:Lymphocyte Activation; D008264:Macrophages / Q000276:immunology; D008627:Mercuric Chloride / Q000633:toxicity*; D008628:Mercury / Q000276:immunology; D051379:Mice; D008805:Mice, Inbred A; D008811:Mice, Inbred DBA; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*
chemical_list: D001324:Autoantigens; D006183:H-2 Antigens; D008627:Mercuric Chloride; D008628:Mercury