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B Seed

Publications and source records attributed to B Seed.

95 records · Page 6Linked to original sources
PubMedDate not supplied

Expression of the CD6 T lymphocyte differentiation antigen in normal human brain.

Antigens shared by the immune and central nervous systems (CNS) have been described repeatedly. The present study reports the expression of the CD6 lymphocyte differentiation antigen in normal human brain evidenced by immunohistochemistry and Northern blot analysis. A panel of various anti-CD6 monoclonal antibodies (mabs) tested on serial cryostat sections identified CD6-positive cells randomly scattered in parenchyma of all examined brain areas. Northern blot analysis with a highly sensitive cRNA probe revealed a 3.1 kb CD6-specific mRNA in various brain regions, especially in basal ganglia and cortex cerebellum. Staining with mabs raised against different hematopoietic cell types, as well as hybridization with probes specific for the beta- and gamma-T cell receptor (TCR) chains support the notion that CD6 is expressed by original brain cells. The nature of the CD6-positive cell type and possible functions of shared antigens in immune and nervous systems are discussed.

Antibodies, Monoclonal↗
PubMedDate not supplied

Expression and function of CD4 in a murine T-cell hybridoma.

The CD4 (T4) antigen was originally described as a phenotypic marker specific for helper T cells, and has recently been shown to be the receptor for the human immunodeficiency virus (HIV). Functional studies using monoclonal antibodies directed at CD4 and major histocompatibility complex (MHC) class II molecules led to the suggestion that CD4 binds to the MHC class II molecules expressed on stimulator cells, enhancing T-cell responsiveness by increasing the avidity of T cell-stimulator cell interaction and/or by transmitting a positive intracellular signal. But recent evidence that antibodies to CD4 inhibit T-cell responsiveness in the absence of any putative ligand for CD4 has been interpreted as suggesting that antibody-mediated inhibition may involve the transmission of a negative signal via the CD4 molecule instead. We have infected a murine T-cell hybridoma that produces interleukin 2 (IL-2) in response to human class II HLA-DR antigens with a retroviral vector containing CD4 cDNA. The resulting CD4-expressing hybridoma cell lines produce 6- to 20-fold more IL-2 in response to HLA-DR antigens than control cell lines. Furthermore, when antigen levels are suboptimal, the response of the cell lines is entirely CD4-dependent. The data presented here clearly demonstrate that CD4 can enhance T-cell responsiveness and may be crucial in the response to suboptimal levels of antigen.

Animals↗
PubMedDate not supplied

An LFA-3 cDNA encodes a phospholipid-linked membrane protein homologous to its receptor CD2.

Recently the human T cell erythrocyte receptor CD2 has been shown to bind human erythrocytes through LFA-3, a heavily glycosylated surface protein of broad tissue distribution. CD2-LFA-3 interactions are important for cytolytic conjugate formation, for thymocyte adhesion, and for T cell activation. A complementary DNA clone encoding LFA-3 was isolated using a complementary DNA clone encoding LFA-3 was isolated using a novel transient expression system of mouse cells. The cDNA encodes a phospholipid-linked membrane protein whose extracellular domain shares significant homology with CD2. As CD2 is homologous with the neural cell adhesion molecule NCAM in immunoglobulin-like domains, cellular adhesion molecules in both neural and lymphoid tissues could have a common ancestor.

Amino Acid Sequence↗
PubMedDate not supplied

Monoclonal antibody and ligand binding sites of the T cell erythrocyte receptor (CD2).

The human T cell erythrocyte receptor (CD2 antigen) allows thymocytes and mature T cells to adhere to thymic epithelium and target cells through a cell surface protein, LFA-3 (refs 1-6). Monoclonal antibodies recognizing CD2 can either block adhesion or, in certain combinations, induce an antigen-independent T cell activation. We have identified the binding sites for 16 monoclonal antibodies against CD2 by a rapid and generally applicable mutational analysis. The binding sites fall in three discrete regions: antibodies that participate in activation and block erythrocyte adhesion bind to the first region; antibodies that block adhesion bind to the second region; and antibodies that participate in activation but do not block adhesion bind to the third region. A large number of mutations selected for loss of antibody reactivity in the first two regions also weaken the CD2-LFA-3 interaction. Good agreement was observed between mutational lesions blocking LFA-3 binding and lesions blocking binding by activating antibodies, which supports the view that such antibodies induce T cell activation by mimicking the effect of LFA-3 binding. CD2 sequences that participate in LFA-3 binding correspond to immunoglobulin variable region hypervariable sequences when the homologous domains are aligned.

Amino Acid Sequence↗