Viral infection can induce the production of autoantibodies

Barzilai, Ori; Ram, Maya; Shoenfeld, Yehuda

doi:10.1097/bor.0b013e3282f0ad25

Cited by 139 publications

(131 citation statements)

References 69 publications

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“…The next mechanism involves the over activation and indiscriminate expansion of self reactive T-cells that are initially considered to be inefficient but can cause the disease in the presence of elevated levels of cytokines. Finally, microbes express super antigens on their surfaces that are unique in coupling T-cells with MHC complexes irrespective of their relativities (Barzilai et al, 2007a(Barzilai et al, , 2007b. On the contrary when correlations were made between autoimmune diseases and infections, the incidences were found to be increased in the subjects who are at reduced risk of infections.…”

Section: Role Of Infectionsmentioning

confidence: 92%

Recent Advances in the Treatment of Neurological Autoimmune Disorders

Kanwar¹,

Sriramoju²,

Kanwar³

2011

Autoimmune Disorders - Current Concepts and Advances From Bedside to Mechanistic Insights

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Section: Role Of Infectionsmentioning

confidence: 92%

Recent Advances in the Treatment of Neurological Autoimmune Disorders

Kanwar¹,

Sriramoju²,

Kanwar³

2011

Autoimmune Disorders - Current Concepts and Advances From Bedside to Mechanistic Insights

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“…Considering our data, altered BAFF expression levels may lead to increased immune responses during viral infections. These mechanisms could also contribute to induction of autoantibodies observed during viral infections (50,51).…”

Section: Discussionmentioning

confidence: 99%

Deficiency of the B Cell-Activating Factor Receptor Results in Limited CD169+ Macrophage Function during Viral Infection

Huang²,

Häussinger

et al. 2015

Z Gastroenterol

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The B cell-activating factor (BAFF) is critical for B cell development and humoral immunity in mice and humans. While the role of BAFF in B cells has been widely described, its role in innate immunity remains unknown. Using BAFF receptor (BAFFR)-deficient mice, we characterized BAFFR-related innate and adaptive immune functions following infection with vesicular stomatitis virus (VSV) and lymphocytic choriomeningitis virus (LCMV). We identified a critical role for BAFFR signaling in the generation and maintenance of the CD169 ؉ macrophage compartment. Consequently, Baffr ؊/؊ mice exhibited limited induction of innate type I interferon production after viral infection. Lack of BAFFR signaling reduced virus amplification and presentation following viral infection, resulting in highly reduced antiviral adaptive immune responses. As a consequence, BAFFR-deficient mice showed exacerbated and fatal disease after viral infection. Mechanistically, transient lack of B cells in Baffr ؊/؊ animals resulted in limited lymphotoxin expression, which is critical for maintenance of CD169 ؉ cells. In conclusion, BAFFR signaling affects both innate and adaptive immune activation during viral infections. IMPORTANCEViruses cause acute and chronic infections in humans resulting in millions of deaths every year. Innate immunity is critical for the outcome of a viral infection. Innate type I interferon production can limit viral replication, while adaptive immune priming by innate immune cells induces pathogen-specific immunity with long-term protection. Here, we show that BAFFR deficiency not only perturbed B cells, but also resulted in limited CD169 ؉ macrophages. These macrophages are critical in amplifying viral particles to trigger type I interferon production and initiate adaptive immune priming. Consequently, BAFFR deficiency resulted in reduced enforced viral replication, limited type I interferon production, and reduced adaptive immunity compared to BAFFRcompetent controls. As a result, BAFFR-deficient mice were predisposed to fatal viral infections. Thus, BAFFR expression is critical for innate immune activation and antiviral immunity.

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“…Up till now, attempts to develop an effective vaccine to prevent CMV infection by several researches around the world, either in the general population or in some special groups, have not been successfully (Gandhi & Khanna, 2004). Epstein-Barr virus (EBV) infection importance resides in its temporal relationship with lupus initiation; moreover, EBV infection is relevant because of the immunological abnormalities found during and after exposure to this virus (Barzilai et al, 2007), the defective control of latent infection seen in lupus patients (I. Kang, 2004) and the higher prevalence of serum antibodies against EBV observed in subjects with SLE as compared with other patient groups.…”

Section: Opportunistic Infections Of Viral Originmentioning

confidence: 99%