PD-L1hi plasmablasts limit the T cell response during the acute phase of parasite infections
Gorosito Serran, M.; Fiocca Vernengo, F.; Almada, L.; Beccaria, C. G.; Canete, P. F.; Rocco Alegre, J.; Tosello Boari, J.; Ramello, M. C.; Wehrens, E.; Cai, Y.; Zuniga, E. I.; Montes, C. L.; Acosta Rodriguez, E. V.; Cockburn, I. A.; Vinuesa, C. G.; Gruppi, A.
Show abstract
During infections with protozoan parasites or virus, T cell immunosuppression is generated simultaneously with a high B cell activation. Here, we show that in T. cruzi infection, all plasmablasts detected had higher surface expression of PD-L1, than other mononuclear cells. PD-L1hi plasmablasts were induced in vivo in an antigen-specific manner and required help from Bcl-6+CD4+T cells. PD-L1hi expression was not a characteristic of all antibody-secreting cells since plasma cells found during the chronic phase of infection express PD-L1 but at lower levels. PD-L1hi plasmablasts were also present in mice infected with Plasmodium or with lymphocytic choriomeningitis virus, but not in mice with autoimmune disorders or immunized with T cell-dependent antigens. PD-L1hi plasmablasts suppressed T cell response, via PD-L1, in vitro and in vivo. Thus, this study reveals that extrafollicular PD-L1hi plasmablasts, which precede the germinal center (CG) response, are a suppressive population in infections that may influence T cell response. Brief summaryPathogens develop different strategies to settle in the host. We identified a plasmablats population induced by pathogens in acute infections which suppress T cell response.
Matching journals
The top 5 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Interferon-γ-producing CD4+ T cells drive monocyte activation in the bone marrow during experimental Leishmania donovani infection. 96%
- IFNγ and iNOS-mediated alterations in the bone marrow and thymus and its impact on Mycobacterium avium-induced thymic atrophy 96%
- Blockade of LAG-3 in PD-L1-deficient mice enhances clearance of blood stage malaria independent of humoral responses 96%
Similar papers in this journal
- The IL-12 and IL-23-Dependent NK Cell Response is Essential For Protective Immunity Against Secondary Toxoplasma gondii Infection. 95%
- Refined cell transfer model reveals roles for Ascl2 and Cxcr3 in splenic localization of mouse NK cells during virus infection 94%
- Deficiency in Bhlhe40 impairs resistance to H. polygyrus bakeri and reveals novel Csf2rb-dependent regulation of anti-helminth immunity 94%
Similar papers in this journal
- ILC1-derived IFN-gamma mediates cDC1-dependent host resistance against Toxoplasma gondii 95%
- The lectin-specific activity of Toxoplasma gondii microneme proteins 1 and 4 binds Toll-like receptor 2 and 4 N-glycans to regulate innate immune priming 95%
- Parasite-Induced IFN-g Regulates Host Defense via CD115 and mTOR-Dependent Mechanism of Tissue-Resident Macrophage Death 95%
Similar papers in this journal
- Cytotoxic CD4+ T cells driven by T-cell intrinsic IL-18R/MyD88 signaling predominantly infiltrate Trypanosoma cruzi-infected hearts 96%
- IL-33 promotes innate lymphoid cell-dependent IFN-γ production required for innate immunity to Toxoplasma gondii 95%
- IL-4 and helminth infection downregulate MINCLE-dependent macrophage response to mycobacteria and Th17 adjuvanticity 95%
Similar papers in this journal
- Effects of Low-level Persistent Infection on maintenance of immunity by CD4 T cell subsets and Th1 cytokines 96%
- Lymphotoxin β receptor: A crucial role in innate and adaptive immune responses against Toxoplasma gondii 95%
- ICOS expression is required for maintenance but not the formation of germinal centers in the spleen in response to P. yoelii infection. 95%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.