Four monoclonal antibodies (mAbs), UC-A4, UC-D3, UC-H9, and IL-A21, specific for bovine major histocompatibility complex class II proteins are described. Sequential immunoprecipitation experiments using biotin-labeled peripheral blood mononuclear cells suggested, but did not conclusively establish, that each of these antibodies recognized a different epitope. The epitope identified by IL-A21 appeared to be common to all of the class II proteins precipitated by the four mAbs, and UC-D3 and UC-H9 each appeared to react with distinct epitopes on separate subsets of these class II proteins. Monoclonal antibody UC-A4 appeared to identify an epitope on a subset of the class II molecules identified by UC-H9. Differences found in the expression by lymphoid cells of class II proteins identified by the four mAbs were indicative of each mAb recognizing a different epitope. UC-H9 and IL-A21 class II proteins were detected on all surface immunoglobulin (S'Ig) positive cells in peripheral blood, but UC-A4 and UC-D3 class II proteins were not. Expression of UC-A4 class II proteins, detected at low density on a strikingly reduced number of S'Ig+ cells from the blood of some bovine leukosis virus-infected cattle, could be increased by culturing these B cells with lipopolysaccharide. All peripheral blood monocytes expressed UC-H9 and IL-A21 class II proteins, but only a proportion of monocytes expressed detectable UC-A4 and UC-D3 class II proteins. Almost all mitogen-stimulated BoCD4+ and BoCD8+ T cells expressed UC-H9 and IL-A21 class II proteins, whereas fewer stimulated T cells of both subsets expressed UC-A4 and UC-D3 class II proteins. All gamma/delta receptor (gamma/delta R) T cells expressed UC-D3, UC-H9, and IL-A21 class II proteins, but no cells (of gamma/delta R+ or CD4+/CD2+ phenotype) from gamma/delta R+ T cell-enriched cultures expressed UC-A4 class II proteins.

Download full-text PDF

Source
http://dx.doi.org/10.1002/jlb.53.5.479DOI Listing

Publication Analysis

Top Keywords

class proteins
52
uc-h9 il-a21
20
uc-a4 uc-d3
16
il-a21 class
16
class
15
proteins
13
uc-d3 uc-h9
12
peripheral blood
12
uc-d3 class
12
cells
9

Similar Publications

Pancreatic ductal adenocarcinoma (PDAC) driven by the mutation presents a formidable health challenge because of limited treatment options. MRTX1133 is a highly selective and first-in-class KRAS-G12D inhibitor under clinical development. Here, we report that the advanced glycosylation end product-specific receptor (AGER) plays a key role in mediating MRTX1133 resistance in PDAC cells.

View Article and Find Full Text PDF

Cancer immunotherapies rely on CD8 cytolytic T lymphocytes (CTLs) in recognition and eradication of tumor cells via antigens presented on major histocompatibility complex class I (MHC-I) molecules. However, we observe MHC-I deficiency in human and murine urologic tumors, posing daunting challenges for successful immunotherapy. We herein report an unprecedented nanosonosensitizer of one-dimensional bamboo-like multisegmented manganese dioxide@manganese-bismuth vanadate (BMMBV) to boost multiple branches of immune responses targeting MHC-I-deficient tumors.

View Article and Find Full Text PDF

Microglia-mediated neuroinflammation plays a crucial role in Alzheimer's disease (AD). Tinosinenside A (Tis A) is a novel sesquiterpene glycoside isolated from the dried rattan stem of Tinospora sinensis (Lour.) Merr.

View Article and Find Full Text PDF

Rare inherited diseases caused by mutations in the copper transporters (CTR1) or induce copper deficiency in the brain, causing seizures and neurodegeneration in infancy through poorly understood mechanisms. Here, we used multiple model systems to characterize the molecular mechanisms by which neuronal cells respond to copper deficiency. Targeted deletion of CTR1 in neuroblastoma cells produced copper deficiency that produced a metabolic shift favoring glycolysis over oxidative phosphorylation.

View Article and Find Full Text PDF

Streptococcal pyogenic exotoxins (Spe proteins) secreted by (group A , GAS) are responsible for scarlet fever and streptococcal toxic shock syndrome. Most Spes are superantigens that cause excessive inflammation by activating large numbers of T cells. However, Streptococcal pyogenic exotoxin B (SpeB) is an exception, which is pro-inflammatory through its protease activity.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!