ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Innate retroviral restriction by Apobec3 promotes antibody affinity maturation in vivo.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- SAMHD1 Promotes the Antiretroviral Adaptive Immune Response in Mice Exposed to Lipopolysaccharide.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Transcriptional signatures associated with rubella virus-specific humoral immunity after a third dose of MMR vaccine in women of childbearing age.European journal of immunology · 2021Article
- Mouse APOBEC3 Restriction of Retroviruses.Viruses · 2020Review
- Murine Leukemia Virus P50 Protein Counteracts APOBEC3 by Blocking Its Packaging.Journal of virology · 2020Article
- Friend retrovirus studies reveal complex interactions between intrinsic, innate and adaptive immunity.FEMS microbiology reviews · 2019Review
- Restriction Factors: From Intrinsic Viral Restriction to Shaping Cellular Immunity Against HIV-1.Frontiers in immunology · 2018Review
- Type I interferon signaling is required for the APOBEC3/Rfv3-dependent neutralizing antibody response but not innate retrovirus restriction.Retrovirology · 2017Article
- Restriction by SAMHD1 Limits cGAS/STING-Dependent Innate and Adaptive Immune Responses to HIV-1.Cell reports · 2016Article
- Tetherin/BST-2 promotes dendritic cell activation and function during acute retrovirus infection.Scientific reports · 2016Article
- Tetherin/BST-2: Restriction Factor or Immunomodulator?Current HIV research · 2016Review
- Requirement for Fc effector mechanisms in the APOBEC3/Rfv3-dependent neutralizing antibody response.Journal of virology · 2015Article
- Mouse knockout models for HIV-1 restriction factors.Cellular and molecular life sciences : CMLS · 2014Review
- Immunoglobulin somatic hypermutation by APOBEC3/Rfv3 during retroviral infection.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- AID and APOBECs span the gap between innate and adaptive immunity.Frontiers in microbiology · 2014Review
- Ribonuclease L is not critical for innate restriction and adaptive immunity against Friend retrovirus infection.Virology · 2013Article
- APOBEC3 inhibition of mouse mammary tumor virus infection: the role of cytidine deamination versus inhibition of reverse transcription.Journal of virology · 2013Article
- Humoral immunity in the Friend retrovirus infection model.Immunologic research · 2013Review
- IFN-α treatment inhibits acute Friend retrovirus replication primarily through the antiviral effector molecule Apobec3.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Article
- Negative impact of IFN-γ on early host immune responses to retroviral infection.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Apobec3/Rfv3 is an innate immune factor that promotes the neutralizing Ab response against Friend retrovirus (FV) in infected mice. Based on its evolutionary relationship to activation-induced deaminase, Apobec3 might directly influence Ab class switching and affinity maturation independently of viral infection. Alternatively, the antiviral activity of Apobec3 may indirectly influence neutralizing Ab responses by reducing early FV-induced pathology in critical immune compartments. To distinguish between these possibilities, we immunized wild-type and Apobec3-deficient C57BL/6 (B6) mice with (4-hydroxy-3-nitrophenyl) acetyl (NP) hapten and evaluated the binding affinity of the resultant NP-specific Abs. These studies revealed similar affinity maturation of NP-specific IgG1 Abs between wild-type and Apobec3-deficient mice in the absence of FV infection. In contrast, hapten-specific Ab affinity maturation was significantly compromised in Apobec3-deficient mice infected with FV. In highly susceptible (B6 x A.BY)F(1) mice, the B6 Apobec3 gene protected multiple cell types in the bone marrow and spleen from acute FV infection, including erythroid, B, T, and myeloid cells. In addition, B6 Apobec3 deficiency was associated with elevated Ig levels, but decreased induction of splenic germinal center B cells and plasmablasts during acute FV infection. These data suggest that Apobec3 indirectly influences FV-specific neutralizing Ab responses by reducing virus-induced immune dysfunction. These findings raise the possibility that enabling Apobec3 activity during acute infection with human pathogenic retroviruses, such as HIV-1, may similarly facilitate stronger virus-specific neutralizing Ab responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.