Polyclonal B Cell Activation and B Cell Cross-Reactivity During Autoantibody Production in Systemic Lupus Erythematosus

1994 ◽  
pp. 115-123 ◽  
Author(s):  
Dennis M. Klinman ◽  
Akira Shirai ◽  
Yoshiaki Ishigatsubo
Keyword(s):  
Systemic Lupus Erythematosus ◽  
B Cell ◽  
Lupus Erythematosus ◽  
Cell Activation ◽  
Cross Reactivity ◽  
B Cell Activation ◽  
Systemic Lupus ◽  
Autoantibody Production

scholarly journals Hidden autoantibodies against common serum proteins in murine systemic lupus erythematosus. Detection by in vitro plaque-forming cell assay.

1985 ◽  
Vol 161 (6) ◽  
pp. 1587-1592 ◽  
Author(s):  
P L Cohen ◽  
R G Rapoport ◽  
R A Eisenberg
Keyword(s):  
Systemic Lupus Erythematosus ◽  
B Cell ◽  
Lupus Erythematosus ◽  
Cell Activation ◽  
Serum Proteins ◽  
B Cell Activation ◽  
Systemic Lupus ◽  
Autoantibody Production ◽  
Murine Systemic Lupus Erythematosus

The autoantibodies found in human and murine systemic lupus erythematosus (SLE) are generally directed against cells or components of cells such as nuclear antigens. This predilection may be due to the unusual immunogenicity of certain autoantigens, or to unusual patterns of antibody crossreactivity. Alternatively, the observed spectrum of reactivities may reflect the in vivo absorption of those autoantibodies directed against soluble antigens. To test whether hitherto undetected autoantibodies against serum proteins might exist in murine SLE, we developed assays that were independent of the possibility of absorption of autoantibodies by serum autoantigens; large numbers of plaque-forming cells (PFC) directed against mouse albumin and mouse transferrin were easily detected in the spleens of MRL/Mp-lpr/lpr, BXSB, and NZB mice. The secreted antibodies were relatively specific for the mouse proteins, since only limited cross-reactivity was seen with albumin and transferrins of other species in inhibition experiments. The production of these hidden antibodies could not be the result of diffuse polyclonal B cell activation, since the PFC to mouse transferrins and albumin were not always accompanied by comparable numbers of PFC against related albumins and transferrins. The results indicate that autoantibody production in murine lupus is a generalized phenomenon, not limited to the production of autoantibodies to nuclear or other cell-bound antibodies. However, the relative specificity of the autoantibodies for self-antigens indicates that diffuse polyclonal B cell activation cannot be the mechanism responsible, and argues that a selective mechanism, probably driven by antigen, accounts for production of autoantibodies in SLE.

B Cell Activation and Plasma Cell Differentiation Are Promoted by IFN-λ in Systemic Lupus Erythematosus

2021 ◽  
Vol 207 (11) ◽  
pp. 2660-2672
Author(s):  
Jennifer L. Barnas ◽  
Jennifer Albrecht ◽  
Nida Meednu ◽  
Diana F. Alzamareh ◽  
Cameron Baker ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cell Differentiation ◽  
B Cell ◽  
Plasma Cell ◽  
Lupus Erythematosus ◽  
Cell Activation ◽  
B Cell Activation ◽  
Systemic Lupus ◽  
Plasma Cell Differentiation

Change in autoantibody and cytokine responses during the evolution of neuromyelitis optica in patients with systemic lupus erythematosus: A preliminary study

2016 ◽  
Vol 22 (9) ◽  
pp. 1192-1201 ◽  
Author(s):  
Katalin T Kovacs ◽  
Sudhakar Reddy Kalluri ◽  
Antonio Boza-Serrano ◽  
Tomas Deierborg ◽  
Tunde Csepany ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
B Cell ◽  
Neuromyelitis Optica ◽  
Lupus Erythematosus ◽  
Cell Activation ◽  
Rare Condition ◽  
B Cell Activation ◽  
Systemic Lupus ◽  
Cytokines And Chemokines ◽  
Ifn Γ

Background: Neuromyelitis optica (NMO)–systemic lupus erythematosus (SLE) association is a rare condition characterized by multiple autoantibodies. Objective: To examine if, during the evolution of NMO, anti-AQP4 responses are part of polyclonal B cell activation, and if T cell responses contribute. Methods: In 19 samples of six patients who developed NMO during SLE, we examined the correlation of AQP4-IgG1 and IgM with (i) anti-MOG IgG and IgM, (ii) anti-nuclear, anti-nucleosome and anti-dsDNA IgG antibodies, (iii) cytokines and chemokines in the serum and (iv) longitudinal relation to NMO relapses/remission. Results: AQP4-IgG1 was present 1–2–5 years before the first NMO relapse. During relapse, AQP4-IgG1, ANA, anti-dsDNA and anti-nucleosome antibodies were elevated. Anti-MOG IgG/IgM and AQP4-IgM antibodies were not detected. AQP4-IgG1 antibodies correlated with concentration of anti-nucleosome, IFN-γ,interferon-gamma-induced CCL10/IP-10 and CCL17/TARC ( p<0.05, respectively). CCL17/TARC correlated with levels of anti-nucleosome and anti-dsDNA ( p<0.05, respectively). Compared to healthy subjects, concentration of IFN-γ and CCL17/TARC was higher in NMO/SLE ( p<0.05). Conclusions: AQP4-IgG1 antibodies are present in the sera years before the first NMO attack in patients with SLE; elevation of anti-AQP4 is part of a polyclonal B cell response during NMO relapses; in spite of multiple autoantibodies in the serum, MOG antibodies were not present; Th1 responses accompany autoantibody responses in NMO/SLE.

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