concanavalin-a and Mucocutaneous-Lymph-Node-Syndrome

The liver remains a hematopoietic organ after birth and can produce all leukocyte lineages from resident hematopoietic stem cells. Hepatocytes produce acute phase proteins and complement in bacterial infections. Liver Kupffer cells are activated by various bacterial stimuli, including bacterial lipopolysaccharide (LPS) and bacterial superantigens, and produce interleukin (IL)-12. IL-12 and other monokines (IL- 18 etc.) produced by Kupffer cells activate liver natural killer (NK) cells and NK1.1 Ag+ T cells to produce interferon-gamma and thereby acquire cytotoxicity against tumors and microbe-infected cells. These liver leukocytes and the T helper 1 immune responses induced by them thus play a crucial role in the first line of defense against bacterial infections and hematogenous tumor metastases. However, if this defense system is inadequately activated, shock associated with multiple organ failure takes place. Activated liver NK1.1 Ag+ T cells and NK cells also cause hepatocyte injury. NK1.1 Ag+ T cells and another T-cell subset with an intermediate T-cell receptor, CD 122+CD8+ T cells, can develop independently of thymic epithelial cells. Liver NK cells and NK1.1 Ag+ T cells physiologically develop in situ from their precursors, presumably due to bacterial antigens brought from the intestine via the portal vein. NK cells activated by bacterial superantigens or LPS are also probably involved in the vascular endothelial injury in Kawasaki disease.

Topics: Animals; Antigens, Bacterial; Cell Lineage; Child, Preschool; Concanavalin A; Gram-Positive Bacteria; Humans; Intestinal Absorption; Killer Cells, Natural; Kupffer Cells; Lipopolysaccharides; Liver; Liver Circulation; Lymphocyte Activation; Lymphokines; Macrophage Activation; Mice; Mice, SCID; Mucocutaneous Lymph Node Syndrome; Multiple Organ Failure; Neoplasm Metastasis; Neoplastic Cells, Circulating; Peritonitis; Receptors, Antigen, T-Cell; Receptors, Antigen, T-Cell, gamma-delta; Shock, Septic; Shwartzman Phenomenon; Superantigens; T-Lymphocyte Subsets; T-Lymphocytes, Cytotoxic; Th1 Cells

Plasma obtained from patients with Kawasaki disease during the acute phase markedly inhibited DNA synthesis in autologous peripheral blood lymphocytes (PBLs) stimulated by phytohaemagglutinin-P (PHA-P) or concanavalin A (Con A). The inhibition became less marked with the progression of the disease and there was no effect on DNA synthesis in PBLs stimulated by pokeweed mitogen (PWM). The plasma also inhibited DNA synthesis in PBLs obtained from healthy adults. The postulated suppressors markedly inhibited DNA synthesis in PBLs from healthy adults stimulated by PHA-P, Con A, purified protein derivative (PPD) or mixed lymphocyte culture reaction (MLR) but they had little effect on the DNA synthesis stimulated by PWM or protein A. With respect to the mechanism, the suppression was found to be potentiated by an increase in the concentration of the patients' plasma, and not to be associated with cytotoxicity nor with a deficiency of factor(s) indispensable for PBL proliferation. It was also evident that the suppression was not related to the concentration of the stimulant, to the lengths of the culturing period nor to the presence of prostaglandins.

Topics: Adult; Child; Child, Preschool; Concanavalin A; DNA; Humans; Indomethacin; Infant; Lymphocytes; Mucocutaneous Lymph Node Syndrome; Phytohemagglutinins