ArticleInfection and immunity2015
B cells modulate systemic responses to Pneumocystis murina lung infection and protect on-demand hematopoiesis via T cell-independent innate mechanisms when type I interferon signaling is absent.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Immune Responses toJournal of inflammation research · 2026Review
- Abrupt Breathlessness: Pneumocystis jirovecii Pneumonia Associated with Inebilizumab in Neuromyelitis Optica Spectrum Disorder: A Case Report and Literature Review.Infection and drug resistance · 2025Article
- Supplementary Role of Immunological Indicators in the Diagnosis and Prognosis ofInfection and drug resistance · 2022Article
- Immunosuppressive Mechanisms of Regulatory B Cells.Frontiers in immunology · 2021Review
- Interleukin-27 promotes CD8+ T cell reconstitution following antibody-mediated lymphoablation.JCI insight · 2019Article
- IL-17 Inversely Correlated with IL-10 via the STAT3 Gene inMediators of inflammation · 2019Article
- Interleukins-17 and 27 promote liver regeneration by sequentially inducing progenitor cell expansion and differentiation.Hepatology communications · 2018Article
- Hematopoietic Stem Cell Regulation by Type I and II Interferons in the Pathogenesis of Acquired Aplastic Anemia.Frontiers in immunology · 2016Review
- β-Glucan-Activated Human B Lymphocytes Participate in Innate Immune Responses by Releasing Proinflammatory Cytokines and Stimulating Neutrophil Chemotaxis.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Type I IFNs Act upon Hematopoietic Progenitors To Protect and Maintain Hematopoiesis during Pneumocystis Lung Infection in Mice.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
HIV infection results in a complex immunodeficiency due to loss of CD4(+) T cells, impaired type I interferon (IFN) responses, and B cell dysfunctions causing susceptibility to opportunistic infections such as Pneumocystis murina pneumonia and unexplained comorbidities, including bone marrow dysfunctions. Type I IFNs and B cells critically contribute to immunity to Pneumocystis lung infection. We recently also identified B cells as supporters of on-demand hematopoiesis following Pneumocystis infection that would otherwise be hampered due to systemic immune effects initiated in the context of a defective type I IFN system. While studying the role of type I IFNs in immunity to Pneumocystis infection, we discovered that mice lacking both lymphocytes and type I IFN receptor (IFrag(-/-)) developed progressive bone marrow failure following infection, while lymphocyte-competent type I IFN receptor-deficient mice (IFNAR(-/-)) showed transient bone marrow depression and extramedullary hematopoiesis. Lymphocyte reconstitution of lymphocyte-deficient IFrag(-/-) mice pointed to B cells as a key player in bone marrow protection. Here we define how B cells protect on-demand hematopoiesis following Pneumocystis lung infection in our model. We demonstrate that adoptive transfer of B cells into IFrag(-/-) mice protects early hematopoietic progenitor activity during systemic responses to Pneumocystis infection, thus promoting replenishment of depleted bone marrow cells. This activity is independent of CD4(+) T cell help and B cell receptor specificity and does not require B cell migration to bone marrow. Furthermore, we show that B cells protect on-demand hematopoiesis in part by induction of interleukin-10 (IL-10)- and IL-27-mediated mechanisms. Thus, our data demonstrate an important immune modulatory role of B cells during Pneumocystis lung infection that complement the modulatory role of type I IFNs to prevent systemic complications.
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