Nocardia rubra cell-wall skeleton promotes CD4 + T cell activation and drives Th1 immune response

2017 ◽  
Vol 101 ◽  
pp. 398-407 ◽  
Author(s):  
Guangchuan Wang ◽  
Jie Wu ◽  
Miao Miao ◽  
Heng Dou ◽  
Ning Nan ◽  
...  
2020 ◽  
Vol 4 (7) ◽  
pp. 1526-1537
Author(s):  
David R. Gruber ◽  
Amanda L. Richards ◽  
Heather L. Howie ◽  
Ariel M. Hay ◽  
Jenna N. Lebedev ◽  
...  

Abstract Antibodies are typically thought of as the endpoint of humoral immunity that occur as the result of an adaptive immune response. However, affinity-matured antibodies can be present at the initiation of a new immune response, most commonly because of passive administration as a medical therapy. The current paradigm is that immunoglobulin M (IgM), IgA, and IgE enhance subsequent humoral immunity. In contrast, IgG has a “dual effect” in which it enhances responses to soluble antigens but suppresses responses to antigens on red blood cells (RBCs) (eg, immunoprophylaxis with anti-RhD). Here, we report a system in which passive antibody to an RBC antigen promotes a robust cellular immune response leading to endogenous CD4+ T-cell activation, germinal center formation, antibody secretion, and immunological memory. The mechanism requires ligation of Fcγ receptors on a specific subset of dendritic cells that results in CD4+ T-cell activation and expansion. Moreover, antibodies cross-enhance responses to a third-party antigen, but only if it is expressed on the same RBC as the antigen recognized by the antibody. Importantly, these observations were IgG subtype specific. Thus, these findings demonstrate that antibodies to RBC alloantigens can enhance humoral immunity in an IgG subtype-specific fashion and provide mechanistic elucidation of the enhancing effects.


Author(s):  
Ivana von Metzler ◽  
Julia Campe ◽  
Sabine Huenecke ◽  
Marc S. Raab ◽  
Hartmut Goldschmidt ◽  
...  

Abstract Multiple myeloma patients are often treated with immunomodulatory drugs, proteasome inhibitors, or monoclonal antibodies until disease progression. Continuous therapy in combination with the underlying disease frequently results in severe humoral and cellular immunodeficiency, which often manifests in recurrent infections. Here, we report on the clinical management and immunological data of three multiple-myeloma patients diagnosed with COVID-19. Despite severe hypogammaglobulinemia, deteriorated T cell counts, and neutropenia, the patients were able to combat COVID-19 by balanced response of innate immunity, strong CD8+ and CD4+ T cell activation and differentiation, development of specific T-cell memory subsets, and development of anti-SARS-CoV-2 type IgM and IgG antibodies with virus-neutralizing capacities. Even 12 months after re-introduction of lenalidomide maintenance therapy, antibody levels and virus-neutralizing antibody titers remained detectable, indicating persisting immunity against SARS-CoV-2. We conclude that in MM patients who tested positive for SARS-CoV-2 and were receiving active MM treatment, immune response assessment could be a useful tool to help guide decision-making regarding the continuation of anti-tumor therapy and supportive therapy. Key messages Immunosuppression due to multiple myeloma might not be the crucial factor that is affecting the course of COVID-19. In this case, despite pre-existing severe deficits in CD4+ T-cell counts and IgA und IgM deficiency, we noticed a robust humoral and cellular immune response against SARS-CoV-2. Evaluation of immune response and antibody titers in MM patients that were tested positive for SARS-CoV-2 and are on active MM treatment should be performed on a larger scale; the findings might affect further treatment recommendations for COVID-19, MM treatment re-introduction, and isolation measures.


Vaccine ◽  
2007 ◽  
Vol 25 (6) ◽  
pp. 1023-1029 ◽  
Author(s):  
Angelo Martino ◽  
Rita Casetti ◽  
Fabrizio Poccia

2013 ◽  
Vol 86 (6) ◽  
pp. 770-781 ◽  
Author(s):  
Andrew J. Wiemer ◽  
Sarah A. Wernimont ◽  
Thai-duong Cung ◽  
David A. Bennin ◽  
Hilary E. Beggs ◽  
...  

2009 ◽  
Vol 182 (12) ◽  
pp. 8080-8093 ◽  
Author(s):  
Lachlan M. Moldenhauer ◽  
Kerrilyn R. Diener ◽  
Dougal M. Thring ◽  
Michael P. Brown ◽  
John D. Hayball ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document