Soren T Hoff1, Ahmed M Salman2, Morten Ruhwald3, Pernille Ravn4, Inger Brock5, Nabila Elsheikh6, Peter Andersen7, Else Marie Agger8. 1. Statens Serum Institut, Department of Infectious Disease Immunology, Copenhagen, Denmark. Electronic address: SHO@ssi.dk. 2. Ain Shams University, Faculty of Science, Department of Biochemistry, Cairo, Egypt. Electronic address: amasy_salman@yahoo.com. 3. Statens Serum Institut, Department of Infectious Disease Immunology, Copenhagen, Denmark. Electronic address: MORU@ssi.dk. 4. Copenhagen University Hospital Hillerød, Department of Infectious Diseases, Denmark. Electronic address: peravn@gmail.com. 5. Copenhagen University Hospital Hillerød, Department of Clinical Microbiology, Denmark. Electronic address: Inger.Brock@regionh.dk. 6. Al Azhar University, Molecular Immunology Unit, Faculty of Medicine, Cairo, Egypt. Electronic address: bolbol47cairo@yahoo.com. 7. Statens Serum Institut, Department of Infectious Disease Immunology, Copenhagen, Denmark. Electronic address: PA@ssi.dk. 8. Statens Serum Institut, Department of Infectious Disease Immunology, Copenhagen, Denmark. Electronic address: EAG@ssi.dk.
Abstract
BACKGROUND: The role of B cells in human host response to Mycobacterium tuberculosis (Mtb) infection is still controversial, but recent evidence suggest that B cell follicle like structures within the lung may influence host responses through regulation of the local cytokine environment. A candidate for such regulation could be the chemokine CXCL10. CXCL10 is mainly produced by human monocytes, but a few reports have also found CXCL10 production by human B cells. The objective of this study was to investigate CXCL10 production by human B cells in response to in vitro stimulation with Mtb antigens. METHODOLOGY/PRINCIPAL FINDINGS: We analyzed human blood samples from 30 volunteer donors using multiparameter flow cytometry, and identified a subgroup of B cells producing CXCL10 in response to in vitro stimulation with antigens. T cells did not produce CXCL10, but CXCL10 production by B cells appeared to be mediated via IFN-γ and dependent on contact with antigen-specific T cells recognizing the antigen. CONCLUSION: Human B cells are able to produce CXCL10 in an IFN-γ and T cell contact-dependent manner. The present findings suggest a possible mechanism through which B cells in part may influence granuloma formation in human tuberculosis (TB) and participate in infection control.
BACKGROUND: The role of B cells in human host response to Mycobacterium tuberculosis (Mtb) infection is still controversial, but recent evidence suggest that B cell follicle like structures within the lung may influence host responses through regulation of the local cytokine environment. A candidate for such regulation could be the chemokine CXCL10. CXCL10 is mainly produced by human monocytes, but a few reports have also found CXCL10 production by human B cells. The objective of this study was to investigate CXCL10 production by human B cells in response to in vitro stimulation with Mtb antigens. METHODOLOGY/PRINCIPAL FINDINGS: We analyzed human blood samples from 30 volunteer donors using multiparameter flow cytometry, and identified a subgroup of B cells producing CXCL10 in response to in vitro stimulation with antigens. T cells did not produce CXCL10, but CXCL10 production by B cells appeared to be mediated via IFN-γ and dependent on contact with antigen-specific T cells recognizing the antigen. CONCLUSION:Human B cells are able to produce CXCL10 in an IFN-γ and T cell contact-dependent manner. The present findings suggest a possible mechanism through which B cells in part may influence granuloma formation in human tuberculosis (TB) and participate in infection control.
Authors: Eduard O Roos; Leeré A Scott; Sedzani Ndou; Francisco Olea-Popelka; Peter E Buss; Lin-Mari de Klerk-Lorist; Robin M Warren; Paul D van Helden; Tashnica T Sylvester; Michele A Miller; Sven D C Parsons Journal: Sci Rep Date: 2019-11-11 Impact factor: 4.379