[Effect of plant polysaccharides on TH1-dependent immune response: screening investigation].

We have studied the influence of water-soluble polysaccharides isolated from Tussilago farfara L. leaves, Betula verrucosa Ehrh. leaves, Calendula officinalis L.

[Prospects for pharmacological regulation of macrophage activity by modulation of intracellular signal cascade].

This article is devoted to classical and alternative macrophage activation, and intracellular transmission of external signals onto genes. It presents data on postreceptor events resulting in the formation of classical or alternative properties of macrophages. The role of some molecules of intracellular signaling pathways (STAT1, NF-kappaB, IRAK, TRAF6, Jak1, Tyk2, STAT3, c-Maf, Sp1, C/EBP, CREB, STAT6, MAP-kinase, PI3-kinase, c P) in the development of proinflammatory and anti-inflammatory activities of macrophages is discussed.

[Antiallergic effect of D-glucuronic acid].

The influence of D-glucuronic acid (course administration) on a Thl and Th2 immune response was studied. It is established that D-glucuronic acid suppressed Th2-dependent immune response as it decreased the lethality from the anaphylactic shock, abolished the local anaphylactic reaction and strongly inhibited allergen-specific IgE and IgG1 production. In addition, D-glucuronic acid stimulated Thl-dependent immune response since it enhanced the delay-type hypersensitivity reaction, increased amount of antibody-forming cells and the number of antibodies in blood.

[Ehrlich tumor cells stimulate T-cell production of interferon-gamma and are resistant to autocrine nitric oxide].

Ehrlich tumor cells released factors which activated T-cell production of interferon-gamma and triggered a mechanism of nitric oxide (NO) production instead of interferon-gamma. When cultured in vitro, they produced NO without stimulation and responded to interferon-gamma by an output rate of NO significantly greater than that in bone marrow cells. Unlike P-815 cells, those of Ehrlich tumor proved resistant to autocrine NO.