4.7 Article

Regulatory B-cell induction by helminths: Implications for allergic disease

Journal

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 128, Issue 4, Pages 733-739

Publisher

MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2011.05.012

Keywords

Regulatory B cells; IL-10; regulatory T cells; helminths; allergy; asthma

Funding

  1. Dutch Organization for Scientific Research (NWO)
  2. ZONMW-VENI [016.066.093]
  3. Netherlands Asthma Foundation (NAF) [10.072]

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Chronic helminth infections are often associated with a reduced prevalence of inflammatory disorders, including allergic diseases. Helminths influence the host immune system by downregulating T-cell responses; the cytokine IL-10 appears to play a central role in this process. Over the last decade, evidence has emerged toward a new regulatory cell type: IL-10-producing B cells, capable of regulating immunity and therefore termed regulatory B cells. Initially, regulatory B cells have been described in autoimmunity models where they dampen inflammation, but recently they were also found in several helminth infection models. Importantly, regulatory B cells have recently been identified in humans, and it has been suggested that patients suffering from autoimmunity have an impaired regulatory B-cell function. As such, it is of therapeutic interest to study the conditions in which IL-10-producing B cells can be induced. Chronic helminth infections appear to hold promise in this context as emerging evidence suggests that helminth-induced regulatory B cells strongly suppress allergic inflammation. In this review, we will discuss the conditions under which regulatory B cells are present, leading to a state of tolerance, as well as the conditions where their absence or functional impairment leads to exacerbated disease. We will summarize their phenotypic characteristics and their mechanisms of action and elaborate on possible mechanisms whereby regulatory B cells can be induced or expanded, as this may open novel avenues for the treatment of inflammatory diseases, such as allergic asthma. (J Allergy Clin Immunol 2011;128:733-9.)

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