pubmed-article:2476481 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2476481 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
pubmed-article:2476481 | lifeskim:mentions | umls-concept:C0018894 | lld:lifeskim |
pubmed-article:2476481 | lifeskim:mentions | umls-concept:C0009013 | lld:lifeskim |
pubmed-article:2476481 | lifeskim:mentions | umls-concept:C0012737 | lld:lifeskim |
pubmed-article:2476481 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
pubmed-article:2476481 | lifeskim:mentions | umls-concept:C0456387 | lld:lifeskim |
pubmed-article:2476481 | lifeskim:mentions | umls-concept:C1552861 | lld:lifeskim |
pubmed-article:2476481 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:2476481 | pubmed:dateCreated | 1989-10-18 | lld:pubmed |
pubmed-article:2476481 | pubmed:abstractText | In order to determine the involvement of T-B cell contact vs lymphokine production in mediating B cell cycle entry and progression, Th cell clones "defective" in lymphokine production were cloned. Th-3.1 is one such clone that required IL-2 to produce significant levels of IL-4 and IFN-gamma. Unlike conventional Th clones, Th-3.1 induced B cell proliferation only in the presence of Ag and IL-2. In contrast to the absolute requirement of IL-2 for Th-3.1-induced B cell proliferation, IL-2 was not required for the formation of stable Th-3.1-B cell conjugates or Th-3.1-induced B cell entry into the G1 phase of the cell cycle. In the absence of IL-2 and under conditions that promoted Th-B cell interactions, Th-3.1 induced 10 to 20% of resting B cells to enter G1. B cell entry into the cell cycle was not inhibited by anti-lymphokine mAb or promoted by exogenous lymphokines, suggesting that endogenous lymphokine activity was not required for Th-3.1-induced G0 to G1 transition. The data suggested that the IL-2-independent induction of B cells into G1 by Th-3.1 was a cell contact-dependent event. Direct proof that Th-3.1-B cell contact was necessary for B cell cycle entry was provided by comparative in situ analysis of the RNA synthetic activity and the RNA content of B cells that were in physical contact with Th-3.1 or not in contact with Th-3.1. In situ autoradiography of RNA synthesis illustrated that a high frequency of B cells in contact with Th-3.1 expressed heightened RNA synthetic activity, whereas "bystander" B cells were less frequently induced into cycle. In situ laser cytometry of B cell size and total RNA content showed that B cells in physical contact with Th-3.1 had a higher RNA content and were larger than "bystander" B cells present in the same microcultures. This model system has allowed the dissection of T cell help into IL-2-dependent and IL-2-independent phases. Early cell contact-dependent events and B cell cycle progression into G1 were IL-2 independent, whereas the production of lymphokines (IL-4, IFN-gamma) by Th-3.1 and Th-3.1-induced B cell proliferation was IL-2 dependent. | lld:pubmed |
pubmed-article:2476481 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2476481 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2476481 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2476481 | pubmed:language | eng | lld:pubmed |
pubmed-article:2476481 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2476481 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:2476481 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2476481 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:2476481 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2476481 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2476481 | pubmed:month | Sep | lld:pubmed |
pubmed-article:2476481 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:2476481 | pubmed:author | pubmed-author:YuanDD | lld:pubmed |
pubmed-article:2476481 | pubmed:author | pubmed-author:MichaelAA | lld:pubmed |
pubmed-article:2476481 | pubmed:author | pubmed-author:McCannJJ | lld:pubmed |
pubmed-article:2476481 | pubmed:author | pubmed-author:NoelleR JRJ | lld:pubmed |
pubmed-article:2476481 | pubmed:author | pubmed-author:ClaassenEE | lld:pubmed |
pubmed-article:2476481 | pubmed:author | pubmed-author:BartlettW CWC | lld:pubmed |
pubmed-article:2476481 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2476481 | pubmed:day | 15 | lld:pubmed |
pubmed-article:2476481 | pubmed:volume | 143 | lld:pubmed |
pubmed-article:2476481 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2476481 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2476481 | pubmed:pagination | 1745-54 | lld:pubmed |
pubmed-article:2476481 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:2476481 | pubmed:year | 1989 | lld:pubmed |
pubmed-article:2476481 | pubmed:articleTitle | Cognate interactions between helper T cells and B cells. II. Dissection of cognate help by using a class II-restricted, antigen-specific, IL-2-dependent helper T cell clone. | lld:pubmed |
pubmed-article:2476481 | pubmed:affiliation | Department of Microbiology, Dartmouth Medical School, Hanover, NH 03756. | lld:pubmed |
pubmed-article:2476481 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2476481 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:2476481 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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