# Michael C. Carroll Professor of Pediatrics (Pathology) ![Michael Carroll](/sites/g/files/omnuum3501/files/styles/hwp_4_5__480x600/public/dms/files/carroll_michael_0.jpg?itok=jAMpyeWk) location\_on Boston Children's Hospital 200 Longwood Ave. WAB, Room 251 Boston, MA 02115 smartphone [617-713-8700](tel:617-713-8700) email laptop\_windows [Lab Website](http://www.michaelcarrolllab.com/) laptop\_windows [Publications](https://pubmed.ncbi.nlm.nih.gov/?term=carroll%20mc%20[author]) The B cell receptor (BCR) is essential for survival of mature B cells and its specificity dictates the cells' fate from early development through final differentiation into an effector or memory cell. For example, immature B cells bearing a self-reactive BCR may be eliminated in the bone marrow (check-point I) or spleen (check point II). Escape at either checkpoint could result in autoimmune disease. A long-standing interest of the Carroll lab is how B cells encounter antigens, both self- and non-self, and how the local environment influences the outcome. Antigens are“presented”to B cells in large part by follicular dendritic cells (FDC) via a pathway dependent on complement C3 and receptors CD21 and CD35. Antigen recognition by antibody or pattern recognition receptors such as the C-type lectins can activate complement resulting in covalent attachment of the third component (C3) to the antigen. Activated C3 provides a molecular tag that identifies the antigen as foreign. C3-tagged antigens are transported to FDC via cells bearing complement receptors. By a mechanism that is not clear, foreign antigens are retained in their native form and made available to cognate B cells over extensive periods. Whether a similar pathway is involved in “presenting” self-antigen to immature B cells is not known. In summary, understanding how foreign antigens are made available to B cells at varying stages in their differentiation would be useful in the design of vaccines and programming of an optimal humoral response to specific pathogens. Similarly, disrupting B cell access to self-antigen would be desirable in tuning-down the humoral response in autoimmunity. - ## Faculty [BBS](/faculty/bbs) [Immunology](/faculty/immunology)