Dendritic cells (DC) can be present at distinct stages of differentiation within the immune system. Sallusto and colleagues have recently described an in vitro culture system suitable for analyzing the maturation processes of DC (Sallusto and colleagues, J. Exp. Med. 1994;179:1109-1118). Monocytes cultured for 6 d in the presence of granulocyte macrophage colony-stimulating factor and interleukin-4 develop into immature DC with a high endocytic capacity but a low capacity to stimulate T cells. When challenged by lipopolysaccharide, these cells upregulate costimulatory molecules, express CD83, and become mature DC. CCR1 and CCR5 chemokine receptors are highly expressed on immature DC and downregulated on mature DC. This in vitro system was used to characterize human lung DC. Lung DC were shown to express some characteristics of in vitro immature DC. These are: (1) low expression of the costimulatory molecules CD40, CD80, and CD86; (2) poor expression of the differentiation marker CD83 and no CD1a; and (3) good capacity to incorporate dextran. Lung DC express moderate levels of CCR1 and CCR5. However, lung DC, like in vitro mature DC, express high levels of major histocompatibility complex Class II molecules, show low expression of CD14 and CD64, and are characterized by their high capacity to stimulate allogeneic T cells to proliferate during mixed leukocyte reactions (MLRs). Although lung DC express low levels of CD80 and CD86, the important role of these costimulatory molecules in inducing high MLR was demonstrated by using blocking antibodies. Therefore, while lung DC have overall a phenotype and an endocytic capacity close to in vitro immature DC, they share, like in vitro mature DC, a powerful capacity to stimulate T cells.

SUMMARYBackground: Lactobacillus johnsonii (Lj1) had an in vitro and in vivo inhibitory effect on Helicobacter pylori. Fermented milk containing Lj1 (LC 1 ), coadministered with antibiotics had a favourable effect on H. pylori gastritis. Aim: Evaluate the effect of LC 1 intake without antibiotics on H. pylori gastritis. Methods: Fifty H. pylori positive healthy volunteers were randomised in a double-blind study to LC 1 or placebo. Gastric biopsies from the antrum and corpus were obtained before, and after 3 and 16 weeks of treatment, for histology and quantitative cultures. Results: Severity and activity of antral gastritis was reduced after 16-week LC 1 intake (pretreatment and

This is the first report of successful induction of partial protection against H. felis with a mucosal prime-boost regimen in which recombinant Lactobacillus strains were used as antigen-delivery vehicles.

Alveolar macrophages (AM) from sarcoid patients have been shown to be good antigen presenting cells (APC) unlike normal AM which are usually ineffective. We demonstrate in ten consecutive sarcoid patients that most of their AM, unlike normal AM, do coexpress high levels of CD86, CD40, and CD30L, all known to be important for T-cell activation. CD80 is also slightly more expressed on sarcoid AM than on normal AM, but is detected on only 26 +/- 6% (mean +/- SEM) of sarcoid AM. A good correlation is present between the percentage of sarcoid AM expressing CD86 and CD40 or CD86 and CD30L. However, no correlation is found between the percentage of CD80 and CD86 positive AM in these same patients. Blocking antibodies against CD86 were able to reduce by more than 80% allogeneic T-cell proliferation induced by the AM of sarcoid patients. This study provides evidence that AM can, in pathologic states such as sarcoidosis, express functional costimulatory molecules for T-cell activation such as CD86, thought to be rather specific for more professional APC such as dendritic cells.

By releasing interleukin (IL)-12 in the lung, alveolar macrophages (AM) may profoundly modify an immune response. The autocrine regulation of the heterodimeric, biologically active form of IL-12 (IL-12 p70) by IL-10 was studied, as well as the expression of its subunits of 35 kD (p35) and 40 kD (p40). AM cultured in medium alone expressed only p35 mRNA. Both p35 and p40 mRNA levels were induced by lipopolysaccharide (LPS) and were further increased by interferon-gamma (IFN-gamma). LPS alone induced IL-12 p40 but not IL-12 p70 production in monocytes and in AM. However, IL-12 p70 was released when the autocrine production of IL-10 was neutralized by IL-10 blocking antibody, and IL-12 p40 production increased. Although IFN-gamma markedly decreased LPS-induced IL-10 production in AM, neutralizing IL-10 further enhanced the level of LPS and IFN-gamma-induced IL-12 p70 in AM. In contrast, neutralizing the trace amount of IL-10 released by AM stimulated by CD40 crosslinking and IFN-gamma did not increase IL-12 p70. Thus, IL-12 p70 production by AM appears to be tightly controlled by the autocrine release of IL-10 when stimulated by LPS, or by LPS and IFN-gamma, whereas CD40 crosslinking triggered IL-12 p70 production in the absence of autocrine regulation by IL-10.