IFN-γ production by antigen-presenting cells: mechanisms emerge

Frucht, David M.; Fukao, Takanori; Bogdan, Christian; Schindler, Heike; O’Shea, John J.; Koyasu, Shigeo

doi:10.1016/s1471-4906(01)02005-1

Cited by 418 publications

(322 citation statements)

References 45 publications

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“…analysed in adherent cells, from Peyer's patches, it was found that most of the IFN-g detected in the histological slices was not due to a release from Th1 cells but from the adherent cells like macrophages or dendritic cells. This observation agrees with recent evidences that macrophages or dendritic cells are IFN-g good producers (Frucht et al, 2001). Thus, the dose-dependent inflammatory response induced by the LAB assayed would be mediated by macrophage or dendritic activation, rather than by Th1 activation.…”

Section: Discussionsupporting

confidence: 92%

Interaction of lactic acid bacteria with the gut immune system

et al. 2002

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Health claims of lactic acid bacteria (LAB) used in functional foods and pharmaceutical preparations are based on the capacity of these microorganisms to stimulate the host immune system. In this study, the antigenic effect of LAB (Lactobacillus acidophilus, Lactobacillus casei, Lactobacillus delbrueckii ssp. bulgaricus and Streptococcus thermophilus) on the gut immune system of BALB=c mice was evaluated. A dose-dependent increase of the Bcl2 protein was observed with all LAB assayed. Furthermore, the analysis of cytokine-producing cells in the lamina propria of gut showed that TNFa and INFg values, determined in macrophages cultured from Peyer patches, were enhanced for all the LAB assayed. An important increase of interleukins IL-10 and IL-4 was observed mainly in mice fed with Lactobacillus delbrueckii ssp. bulgaricus or Lactobacillus casei, while a significant induction of IL-2 and IL-12 was only observed with L. acidophilus (P < 0.01). These effects were dose dependent. The role of produced cytokines in the balance Th1=Th2 was determined by a systemic antibody response against parenterally injected ovoalbumin. L. casei, L. delbrueckii ssp. bulgaricus and L. acidophilus enhanced the IgG1 response favouring Th2 balance, while L. acidophilus also increased the IgG2a response inducing Th1 balance. S. thermophilus did not influence the balance Th1=Th2. Our studies showed that lactic acid bacteria induce distinct mucosal cytokine profiles showing different adjuvant capacity among them. Thus, selection of probiotic strain with immunological properties must be well defined to influence cytokine expression that favour the claimed immune response.

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Section: Discussionsupporting

confidence: 92%

Interaction of lactic acid bacteria with the gut immune system

et al. 2002

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“…Macrophages contribute to innate immunity against foreign pathogens by their phagocytic as well as bactericidal activities. In addition, both DC and macrophages produce large amounts of IFN-+ in response to foreign pathogens as shown previously [14,22,[24][25][26][27][28][29]. NK cells have been considered as major IFN-+ producers in innate immune responses based on the observation that + c -/-(y) mice lacking all lymphoid cells are unable to produce IFN-+ and are highly susceptible to L. monocytogenes as well as T. gondii [32,34].…”

Section: Discussionmentioning

confidence: 58%

“…IFN-+ gene knockout (IFN-+ -/-) mice, IFN-+ receptor gene knockout (IFN-+ R -/-) mice, as well as other IFN-+ -related gene knockout mice are extremely susceptible to intracellular pathogens compared to SCID or wild-type (WT) mice [5][6][7][8][9][10][11][12][13]. Whereas NK cells among lymphoid cells had been believed to be a major source of IFN-+ during early phase of infection, we and others have shown that antigen-presenting cells (APC) such as dendritic cells (DC) and macrophages produce large amounts of IFN-+ in response to interleukin (IL)-12 that is produced by APC upon microbial infection [14][15][16][17][18][19][20][21][22][23][24][25][26][27]. In fact, amounts of IFN-+ produced by DC and macrophages are substantially larger than those produced by NK cells [14][15][16].…”

Section: Introductionmentioning

confidence: 99%

In vivo role of IFN‐γ produced by antigen‐presenting cells in early host defense against intracellular pathogens

et al. 2003

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Antigen-presenting cells (APC), including dendritic cells and macrophages, produce a large amount of interferon (IFN)-+ , a crucial cytokine for the control of infectious diseases. To elucidate the role of IFN-+ from APC in vivo, we employed cytokine receptor common + subunit ( + c) and recombination-activating gene (Rag)-2 double-knockout ( + c -/-(y) -Rag-2 -/-) mice, which are severely impaired in IFN-+ production and are extremely susceptible to infection of intracellular pathogens including Listeria monocytogenes and Toxoplasma gondii. Adoptive transfer of IFN-+ -producing APC increased levels of serum IFN-+ and the resistance to Listeria. Although depletion of NK cells from Rag-2 -/-mice slightly increased the susceptibility to bacterial infection, they are substantially more resistant than + c -/-(y) -Rag-2 -/-mice, which are also devoid of all lymphoid cells. These results demonstrate that the APC-derived IFN-+ contributes to the control of infectious agents in vivo.

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“…We have shown previously that systemic injection of the Th1-related, pro-inflammatory cytokines IL-12 or/and IL-18, accelerated lupus disease progression in MRL/lpr mice [16,38]. IL-12 and IL-18 are generally thought to act by stimulating T cells and NK cells to produce IFN-c, but recent evidence indicates that, apart from T (Th1) and NK cells, DC may also be a direct source of IFN-c [39]. Here we show that DC/nec from MRL/+ mice may directly release high levels of IFN-c independent of IL-12 and IL-18 activities.…”

Section: Discussionmentioning

confidence: 99%

Systemic autoimmune disease induced by dendritic cells that have captured necrotic but not apoptotic cells in susceptible mouse strains

Chan

Trendell-Smith

et al. 2005

Eur. J. Immunol.

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Systemic lupus erythematosus (SLE) is an autoimmune disorder of a largely unknown etiology. Anti-double-stranded (ds) DNA antibodies are a classic hallmark of the disease, although the mechanism underlying their induction remains unclear. We demonstrate here that, in both lupus-prone and normal mouse strains, strong anti-dsDNA antibody responses can be induced by dendritic cells (DC) that have ingested syngeneic necrotic (DC/nec), but not apoptotic (DC/apo), cells. Clinical manifestations of lupus were evident, however, only in susceptible mouse strains, which correlate with the ability of DC/nec to release IFN-c and to induce the pathogenic IgG2a anti-dsDNA antibodies. Injection of DC/nec not only accelerated disease progression in the MRL/MpJ-lpr/lpr lupus-prone mice but also induced a lupus-like disease in the MRL/MpJ-+/+ wild-type control strain. Immune complex deposition was readily detectable in the kidneys, and the mice developed proteinuria. Strikingly, female MRL/MpJ-+/+ mice that had received DC/nec, but not DC/apo, developed a 'butterfly' facial lesion resembling a cardinal feature of human SLE. Our study therefore demonstrates that DC/nec inducing a Th1 type of responses, which are otherwise tightly regulated in a normal immune system, may play a pivotal role in SLE pathogenesis.

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IFN-γ production by antigen-presenting cells: mechanisms emerge

Cited by 418 publications

References 45 publications

Interaction of lactic acid bacteria with the gut immune system

Interaction of lactic acid bacteria with the gut immune system

In vivo role of IFN‐γ produced by antigen‐presenting cells in early host defense against intracellular pathogens

Systemic autoimmune disease induced by dendritic cells that have captured necrotic but not apoptotic cells in susceptible mouse strains

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