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Antigen‐specific B lymphocytes acquire proteoglycan aggrecan from cartilage extracellular matrix resulting in antigen presentation and CD 4 + T ‐cell activation
Author(s) -
Ciechomska Marzena,
Wilson Caroline L.,
Floudas Achilleas,
Hui Wang,
Rowan Andrew D.,
Eden Willem,
Robinson John H.,
Knight Andrew M.
Publication year - 2014
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12169
Subject(s) - antigen presentation , antigen , microbiology and biotechnology , aggrecan , extracellular matrix , antigen presenting cell , b cell , t cell , chemistry , autoimmunity , proteoglycan , antigen processing , immunology , biology , immune system , antibody , medicine , pathology , alternative medicine , osteoarthritis , articular cartilage
Summary The majority of studies examining antigen‐presenting cell ( APC ) function have focused on the capture and presentation of antigens released from pathogens or damaged cells. However, antigen‐specific B cells are also capable of efficiently extracting antigens that are either tethered to, or integrally part of the plasma membrane of various target cells. In this study we show that B cells are also highly efficient at extracting integral components of the extracellular matrix ( ECM ) for subsequent presentation. In particular we demonstrate that B cells specific for aggrecan, an integral component of cartilage ECM , acquire this rheumatoid arthritis candidate autoantigen in both a B ‐cell‐receptor‐dependent and a contact‐dependent manner. We also demonstrate that the subsequent presentation of aggregan from ECM leads to CD 4 + T ‐cell activation and effector cell formation. Recent studies have identified B‐cell‐mediated antigen presentation as essential for the development of autoimmunity, but a unique role for B cells compared with other APC has yet to be defined. Our findings lead us to propose that the acquisition of ECM ‐derived autoantigens represents a mechanism that defines the APC requirement for B cells in the development of autoimmunity.