Antibody

About: Antibody is a research topic. Over the lifetime, 113941 publications have been published within this topic receiving 4130181 citations. The topic is also known as: Ab & antibodies.

Anti-Mac-1 selectively inhibits the mouse and human type three complement receptor.

Abstract: Anti-Mac-1 (M1/70), a rat monoclonal antibody that reacts with mouse and human macrophages, polymorphonuclear leukocytes (PMNL), and natural killer cells, selectively inhibited complement receptor-mediated rosetting by murine macrophages and human PMNL. Preincubation of macrophages with anti-Mac-1 inhibited formation of rosettes with sheep erythrocytes bearing IgM antibody and murine C3 fragments. No inhibition was observed when other monoclonal antibodies that react with macrophages (such as anti-Ly5, anti-H-2, or anti-pan-leukocyte) were tested at 10-fold higher concentrations. Anti-Mac-1 did not affect macrophage Fc receptor-mediated rosetting. Erythrocytes bearing homogeneous human C3 fragments C3b (EC3b) or C3bi (EC3bi) were used to test the specificity of the murine macrophage and human PMNL complement receptor inhibited by anti-Mac-1. In both cases, anti-Mac-1 inhibited CR3-mediated rosetting of EC3bi but not CR1-dependent rosetting of EC3b. The results show that Mac-1 is either identical to CR3 or closely associated with CR3 function. This is one of the first cases in which a monoclonal antibody-defined differentiation antigen has been associated with a specific cell surface function.

Rituximab and Intravenous Immune Globulin for Desensitization during Renal Transplantation

Abstract: Background Few options for transplantation currently exist for patients highly sensitized to HLA. This exploratory, open-label, phase 1–2, single-center study examined whether intravenous immune globulin plus rituximab could reduce anti-HLA antibody levels and improve transplantation rates. Methods Between September 2005 and May 2007, a total of 20 highly sensitized patients (with a mean [±SD] T-cell panel-reactive antibody level, determined by use of the complement-dependent cytotoxicity assay, of 77±19% or with donor-specific antibodies) were enrolled and received treatment with intravenous immune globulin and rituximab. We recorded rates of transplantation, panel-reactive antibody levels, cross-matching results at the time of transplantation, survival of patients and grafts, acute rejection episodes, serum creatinine values, adverse events and serious adverse events, and immunologic factors. Results The mean panel-reactive antibody level was 44±30% after the second infusion of intravenous immune globul...

Characterization of a murine monoclonal antibody specific for an allotypic determinant on T cell antigen receptor.

Abstract: Repeated immunization of normal C57L/J (H-2b) mice with peripheral T cells from BALBB (H-2b) mice results in the production of antibodies which react with the T cell receptor A monoclonal antibody-producing hybridoma, F231, was isolated from immunized C57L/J mice showing this property This monoclonal antibody recognizes approximately 25% of peripheral T cells in BALB mice It stains approximately the same fraction of T cells and precipitates the same heterodimer as the rat monoclonal antibody described previously that was made against isolated receptor material The allotypic determinant recognized by this monoclonal antibody is present in most common laboratory strains (BALB, C57BL, CBA, A, DBA, C3H) and is absent in C57L, C57BR, and SJL mice Sorting peripheral T cells from BALBB or (SJL X BALB/c)F1 mice for the F231+ and F231- subsets revealed that both populations contain approximately the same CTL precursor frequency for alloantigen Thus, the T cell receptor allotype defined by F231 is present on CTL Furthermore, cytotoxicity mediated by an F231+ CTL line could be blocked specifically by the F231 monoclonal antibody Under appropriate conditions, the monoclonal antibody F231 bound to Sepharose 4B beads can induce resting peripheral T lymphocytes of allotype-positive strains to proliferate

Immune cell profiling of COVID-19 patients in the recovery stage by single-cell sequencing

Abstract: COVID-19, caused by SARS-CoV-2, has recently affected over 1,200,000 people and killed more than 60,000. The key immune cell subsets change and their states during the course of COVID-19 remain unclear. We sought to comprehensively characterize the transcriptional changes in peripheral blood mononuclear cells during the recovery stage of COVID-19 by single-cell RNA sequencing technique. It was found that T cells decreased remarkably, whereas monocytes increased in patients in the early recovery stage (ERS) of COVID-19. There was an increased ratio of classical CD14++ monocytes with high inflammatory gene expression as well as a greater abundance of CD14++IL1β+ monocytes in the ERS. CD4+ T cells and CD8+ T cells decreased significantly and expressed high levels of inflammatory genes in the ERS. Among the B cells, the plasma cells increased remarkably, whereas the naive B cells decreased. Several novel B cell-receptor (BCR) changes were identified, such as IGHV3-23 and IGHV3-7, and isotypes (IGHV3-15, IGHV3-30, and IGKV3-11) previously used for virus vaccine development were confirmed. The strongest pairing frequencies, IGHV3-23-IGHJ4, indicated a monoclonal state associated with SARS-CoV-2 specificity, which had not been reported yet. Furthermore, integrated analysis predicted that IL-1β and M-CSF may be novel candidate target genes for inflammatory storm and that TNFSF13, IL-18, IL-2, and IL-4 may be beneficial for the recovery of COVID-19 patients. Our study provides the first evidence of an inflammatory immune signature in the ERS, suggesting COVID-19 patients are still vulnerable after hospital discharge. Identification of novel BCR signaling may lead to the development of vaccines and antibodies for the treatment of COVID-19.