New aspects of IFN‐α/β signalling in immunity, oncogenesis and bone metabolism

Takaoka, Akinori; Taniguchi, Tadatsugu

doi:10.1111/j.1349-7006.2003.tb01455.x

Cited by 68 publications

(63 citation statements)

References 69 publications

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“…IFN-␤ serum levels were not increased in LM-infected IFN␣R1 Ϫ/Ϫ mice (Fig. 6A), consistent with the notion that IFN␣R signaling provides an amplification loop for type I IFN production (33). In contrast to IFN-␤, LM infection did not result in detectable serum levels of IFN-␣ in any of these three mouse strains (data not shown).…”

Section: Prevention Of Tolerance By Lm Infection Is Mediated By Type supporting

confidence: 86%

Prevention of Allograft Tolerance by Bacterial Infection with Listeria monocytogenes

Wang¹,

Chen

Ahmed³

et al. 2008

The Journal of Immunology

101

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Exposure to certain viruses and parasites has been shown to prevent the induction of transplantation tolerance in mice via the generation of cross-reactive memory T cell responses or the induction of bystander activation. Bacterial infections are common in the perioperative period of solid organ allograft recipients in the clinic, and correlations between bacterial infections and acute allograft rejection have been reported. However, whether bacterial infections at the time of transplantation have any effect on the generation of transplantation tolerance remains to be established. We used the Gram-positive intracellular bacterium Listeria monocytogenes (LM) as a model pathogen because its effects on immune responses are well described. Perioperative LM infection prevented cardiac and skin allograft acceptance induced by anti-CD154 and donor-specific transfusion in mice. LM-mediated rejection was not due to the generation of cross-reactive T cells and was largely independent of signaling via MyD88, an adaptor for most TLRs, IL-1, and IL-18. Instead, transplant rejection following LM infection was dependent on the expression of the phagosome-lysing pore former listeriolysin O and on type I IFN receptor signaling. Our results indicate that bacterial exposure at the time of transplantation can antagonize tolerogenic regimens by enhancing alloantigen-specific immune responses independently of the generation of cross-reactive memory T cells.

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Section: Prevention Of Tolerance By Lm Infection Is Mediated By Type supporting

confidence: 86%

Prevention of Allograft Tolerance by Bacterial Infection with Listeria monocytogenes

Wang¹,

Chen

Ahmed³

et al. 2008

The Journal of Immunology

101

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“…IFNAR Ϫ/Ϫ mice reportedly have decreased bone density and their bones fracture more easily compared with those of wild-type animals (23,53,54). Indeed, we observed in our IFrag Ϫ/Ϫ mice increased bone brittleness in response to Pneumocystis infection of the lung compared with wild-type and uninfected IFrag Ϫ/Ϫ animals when the femur is removed from the hip joint (results not shown).…”

Section: Discussionmentioning

confidence: 52%

Type I Interferon Signaling and B Cells Maintain Hemopoiesis during Pneumocystis Infection of the Lung

Meissner

Rutkowski

Harmsen

et al. 2007

The Journal of Immunology

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Loss of CD4 T cells is the hallmark of HIV infection. However, type I IFN-producing plasmacytoid dendritic cells may also be lost. This results in susceptibility to an opportunistic infection such as Pneumocystis pneumonia. In addition, regenerative bone marrow failure resulting in pancytopenia is another common problem in advanced stage AIDS. This may be linked to both the failing immune system and recurrent opportunistic infections. We generated lymphocyte-deficient type I IFN receptor-deficient mice (IFrag−/−) to study the effects on Pneumocystis infection of the lung. When IFrag−/− animals were infected with Pneumocystis they died between days 16 and 21 postinfection with minimal pneumonia but severe anemia due to complete bone marrow failure. This included the loss of uncommitted hemopoietic precursor cells. Bone marrow failure was prevented by the reconstitution of IFrag−/− mice with wild-type lymphocytes, especially B cells. T and B cells lacking type I IFN receptor signaling could only partially prevent bone marrow failure in response to Pneumocystis infection. However, the presence of T and B cells lacking type I IFN signaling resulted in compensatory extramedullary hemopoiesis in the liver and spleen. Lymphocyte support of the regenerative capacity of the bone marrow was provided by both type I IFN-dependent and -independent mechanisms that acted synergistically. Our findings point to the requirement of both type I IFNs and lymphocytes in the regenerative capabilities of the hemopoietic system under the pressure of Pneumocystis infection, but not during steady-state hemopoiesis. This may have implications in the management of pancytopenia in AIDS.

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“…The role of Nfatc and the Ap1 family of transcription that includes Fos and Jun has also been established for osteoclastogenesis (Ikeda et al, 2004;Matsuo et al, 2004). Transcription factor of the Irf and Ifi families were first discovered in interferon signaling, and their role in osteoclast function has previously been described (Takayanagi et al, 2000;Takaoka and Taniguchi, 2003). All of the previously identified transcription factors in osteoclastogenesis are represented in the microarray data set, but in addition, we discovered 50 additional transcription factors (Table 3) that are differentially expressed during osteoclastogenesis.…”

Section: Regulation Of and By Transcription Regulatorsmentioning

confidence: 71%

Systems level analysis of osteoclastogenesis reveals intrinsic and extrinsic regulatory interactions

Kiesel

Miller

Abu‐Amer

et al. 2007

Developmental Dynamics

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New aspects of IFN‐α/β signalling in immunity, oncogenesis and bone metabolism

Cited by 68 publications

References 69 publications

Prevention of Allograft Tolerance by Bacterial Infection with Listeria monocytogenes

Prevention of Allograft Tolerance by Bacterial Infection with Listeria monocytogenes

Type I Interferon Signaling and B Cells Maintain Hemopoiesis during Pneumocystis Infection of the Lung

Systems level analysis of osteoclastogenesis reveals intrinsic and extrinsic regulatory interactions

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