Linked Life Data

8294884

Source:http://linkedlifedata.com/resource/pubmed/id/8294884

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1994-3-3
pubmed:abstractText
Class II major histocompatibility complex encoded proteins (MHC class II or Ia molecules) are principal plasma membrane proteins involved in activation of both B and T cells during antigen-driven immune responses. Recent data indicate that class II molecules are more than simply recognition elements that provide a ligand for the T cell antigen receptor. Changes in B cell physiology that follow class II binding are now recognized as being required not only for the induction of T cell activation, but also for B cell activation and proliferation. It is interesting to note that class II molecules appear to transduce signals via two distinct mechanisms depending upon the differentiative state of the B cell on which they are expressed. While one of these pathways, involving cAMP generation and protein kinase C localization in the cytoskeletal/nuclear compartment, is seen in resting B cells, the second is seen in primed B cells and involves tyrosine kinase activation, inositol lipid hydrolysis, and Ca2+ mobilization. Use of this pathway is correlated with ability of class II to transduce signals leading to B cell proliferation. To begin to address the molecular basis of this unique, activation-dependent, differential coupling of class II to signaling pathways, we conducted mutational analysis of class II structural requirements for signal transduction. Here we report that the cytoplasmic (Cy) domains of I-Ak class II molecules are not required for either receptor-mediated activation of protein tyrosine phosphorylation or Ca2+ mobilization. This is in contrast to the requirement of the Cy domain of beta chain of class II for the alternate signaling pathway and efficient antigen presentation to autoreactive T cell lines. Disparate distribution of functional motifs within the MHC class II molecules may reflect use of distinct receptor associated effector molecules to sustain different modes of signal transduction in various class II-expressing cells.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-1351058, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-1531041, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-1680921, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-1719635, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-1846320, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-1848577, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-2158859, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-2212953, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-2307834, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-2473111, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-2503831, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-2557353, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-2653373, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-2788709, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-2838848, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-2918224, http://linkedlifedata.com/resource/pubmed/commentcorrection/8294884-3935317
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1007
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
179
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
763-8
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Distinct structural compartmentalization of the signal transducing functions of major histocompatibility complex class II (Ia) molecules.
pubmed:affiliation
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.