scholarly journals Interferon‐α curbs production of interleukin‐22 by human peripheral blood mononuclear cells exposed to live Borrelia burgdorferi

2015 ◽  
Vol 19 (10) ◽  
pp. 2507-2511
Author(s):  
Anika Berner ◽  
Malte Bachmann ◽  
Josef Pfeilschifter ◽  
Peter Kraiczy ◽  
Heiko Mühl
2001 ◽  
Vol 82 (8) ◽  
pp. 1899-1907 ◽  
Author(s):  
Wassim Chehadeh ◽  
Ahmed Bouzidi ◽  
Gunar Alm ◽  
Pierre Wattré ◽  
Didier Hober

Coxsackievirus B4 (CVB4) can be found in circulating blood of patients; however, the interaction of CVB4 with peripheral blood mononuclear cells (PBMCs) is poorly understood. CVB4 induced low levels of IFN-α synthesis in PBMCs from healthy donors. In contrast, preincubation of infectious CVB4 with plasma from these donors containing anti-CVB4 antibodies strongly enhanced the synthesis of IFN-α. IgG obtained from plasma by chromatography formed immune complexes with CVB4 and increased significantly the CVB4-induced production of IFN-α by PBMCs. These antibodies did not have a neutralizing effect on CVB4 infection of Hep-2 cells. The role of CVB and adenovirus receptor (CAR), FcγRII and FcγRIII in the increased synthesis of IFN-α induced by CVB4 preincubated with IgG was shown by inhibition with specific antibodies. The major interferon-α-producing cells in response to CVB4–IgG complexes were CD14+ cells and monocyte-enriched PBMCs. With the latter, detection of IFN-α by immunostaining was positive whereas in monocyte-depleted PBMCs it was not. This study shows that CVB4-induced synthesis of IFN-α by PBMCs can be enhanced by an antibody-dependent mechanism through interactions between the virus, non-neutralizing antivirus antibodies, FcγRII and III and CAR.


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