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Type I interferon signaling and B cells maintain hemopoiesis during Pneumocystis infection of the lung.

Type I interferon signaling and B cells maintain hemopoiesis during Pneumocystis infection of the lung. Research Abstract Details 

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  • Type I interferon signaling and B cells maintain hemopoiesis during Pneumocystis infection of the lung. Abstract Text:

    nicole meissnerNicole Meissner,melanie rutkowskiMelanie Rutkowski,ann l harmsenAnn L Harmsen,soo hanSoo Han,allen g harmsenAllen G Harmsen,

    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.

    Type I interferon signaling and B cells maintain hemopoiesis during Pneumocystis infection of the lung. Publishing Authors By Initials

    n meissnerN Meissner,m rutkowskiM Rutkowski,al harmsenAL Harmsen,s hanS Han,ag harmsenAG Harmsen,

    For similar tissues: lymphoid tissue: spleen research abstracts see: tissues: lymphoid tissue: spleen research

    PUBMED ID PMID:

    MEDLINE DATE:

    Type I interferon signaling and B cells maintain hemopoiesis during Pneumocystis infection of the lung. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    VOLUME: 178

    Page Numbers: 6604-15

    Journal Abbreviation:

    ISSN: 0022-1767

    DAY: 15

    MONTH: May

    YEAR: 2007

    Type I interferon signaling and B cells maintain hemopoiesis during Pneumocystis infection of the lung. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985117

    Type I interferon signaling and B cells maintain hemopoiesis during Pneumocystis infection of the lung. Keywords Mesh Terms:

    KEYWORDS: Spleen

    MESH TERMS: transplantation

    Chemical & Substance for Abstract: Type I interferon signaling and B cells maintain hemopoiesis during Pneumocystis infection of the lung. Information

    Substance Name: Interferon-beta

    Registry Number: 77238-31-4

    Grant and Affiliation Information for Type I interferon signaling and B cells maintain hemopoiesis during Pneumocystis infection of the lung.

    AFFILIATION: Department of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59718, USA. nicolem@montana.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States PHS

    GRANT: RP020185

    ACRONYM: HL

    MEDLINETA: J Immunol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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