36 research outputs found
Successful Prevention of Retrocochlear Hearing Loss in Murine Experimental Allergic Encephalomyelitis with T Cell Receptor Vβ8–Specific Antibody
No full textNo Evidence for TCR Vbeta Repertoire Changes Influencing Disease Protection in E-Transgenic NOD Mice
No full textT-Cell Receptor Identification of an Oligodendrocyte-Specific Autoreactive Cytotoxic T-Cell Clone Without Self Restriction
No full textA novel, native-format bispecific antibody triggering T-cell killing of B-cells is robustly active in mouse tumor models and cynomolgus monkeys
No full text
Co-Expression of T-Cell Receptor beta and delta mRNA detected at High Frequency in Hybridomas derived from Adult Thymus
No full textA hyman hybrid hybridoma producing a bispecific monoclonal antibody that can target tumor cells for attack by Pseudomonas aeruginosa exotoxin A
No full textDendritic Cells Armed With Anti-CD3 mAbs Reduce Pulmonary Metastases, Prolong Survival, and Engender Antitumor Effector Cells Demonstrable by Adoptive Transfer
No full textSELECTIVE KILLING OF HEPATITIS-B ENVELOPE ANTIGEN-SPECIFIC B-CELLS BY CLASS-I-RESTRICTED, EXOGENOUS ANTIGEN-SPECIFIC LYMPHOCYTES-T
No full textSpecific B lymphocytes can act as very efficient antigen-presenting cells. They bind antigen with high affinity via their immunoglobulin receptors, process it through the class II major histocompatibility complex (MHC) pathway, and present its fragments to class II-restricted T lymphocytes. In general, exogenous antigens and noninfectious viral particles enter the class II pathway and are selectively associated with class II MHC molecules. The presentation of an exogenous antigen in association with class I molecules has been reported for only a few antigens, including the hepatitis B envelope antigen (HBenvAg). Here we demonstrate that antigen-specific B cells can efficiently deliver HBenvAg to the class I pathway, presenting its fragments to class I-restricted cytotoxic T lymphocytes (CTLs) which kill the specific B cells. This could represent a mechanism of suppression of neutralizing anti-hepatitis B virus (HBV) antibody response, a phenomenon that accompanies the development of the chronic HBV-carrier state
